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Savko C, Esquer C, Molinaro C, Rokaw S, Shain AG, Jaafar F, Wright MK, Phillips JA, Hopkins T, Mikhail S, Rieder A, Mardani A, Bailey B, Sussman MA. Myocardial Infarction Injury Is Exacerbated by Nicotine in Vape Aerosol Exposure. J Am Heart Assoc 2025; 14:e038012. [PMID: 39704237 DOI: 10.1161/jaha.124.038012] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/30/2024] [Accepted: 11/12/2024] [Indexed: 12/21/2024]
Abstract
BACKGROUND Vaping is touted as a safer alternative to traditional cigarette smoking, but the full spectrum of harm reduction versus comparable risk remains unresolved. Elevated bioavailability of nicotine in vape aerosol together with known risks of nicotine exposure may result in previously uncharacterized cardiovascular consequences of vaping. The objective of this study is to assess the impact of nicotine exposure via vape aerosol inhalation upon myocardial response to infarction injury. METHODS AND RESULTS Flavored vape juice containing nicotine (5 mg/mL) or vehicle alone (0 mg) was delivered using identical 4-week treatment protocols. Mice were subjected to acute myocardial infarction injury and evaluated for outcomes of cardiac structure and function. Findings reveal that nicotine exposure leads to worse outcomes with respect to contractile performance regardless of sex. Nonmyocyte interstitial cell accumulation following infarction significantly increased with exposure to vape aerosol alone, but a comparable increase was not present when nicotine was included. CONCLUSIONS Myocardial function after infarction is significantly decreased after exposure to nicotine vape aerosol irrespective of sex. Comparable loss of contractile function was not observed in mice exposed to vape aerosol alone, highlighting the essential role of nicotine in loss of contractile function. Increased vimentin immunoreactivity was observed in the vape alone group compared with control and vape nicotine. The correlation between vaping, interstitial cell responses, and cardiac remodeling leading to impaired contractility warrants further investigation. Public health experts seeking to reduce vaping-related health risks should consider messaging that highlights the increased cardiovascular risk especially with nicotine-containing aerosols.
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Affiliation(s)
- Clarissa Savko
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Carolina Esquer
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Claudia Molinaro
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Sophie Rokaw
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Abraham G Shain
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Faid Jaafar
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Morgan K Wright
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Joy A Phillips
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Tyler Hopkins
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Sama Mikhail
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Abigail Rieder
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Ariana Mardani
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
| | - Barbara Bailey
- SDSU Department of Mathematics San Diego State University San Diego CA
| | - Mark A Sussman
- SDSU Integrated Regenerative Research Institute and Biology Department San Diego State University San Diego CA
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Kuang Z, Lin L, Kong R, Wang Z, Mao X, Xiang D. The correlation between cumulative cigarette consumption and infarction-related coronary spasm in patients with ST-segment elevation acute myocardial infarction across different age groups. Sci Rep 2025; 15:253. [PMID: 39747215 PMCID: PMC11697210 DOI: 10.1038/s41598-024-84125-5] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/18/2024] [Accepted: 12/20/2024] [Indexed: 01/04/2025] Open
Abstract
Coronary artery spasm (CAS) is a key contributor to the pathogenesis of acute ST-segment elevation myocardial infarction (STEMI). While smoking is recognized as a major risk factor for CAS, the relationship between cumulative cigarette consumption and infarction-related CAS across different age groups in STEMI patients remains unclear. This study aimed to investigate the correlation between cumulative cigarette consumption and infarction-related CAS across different age groups through a retrospective analysis. This retrospective study included STEMI patients who underwent coronary angiography (CAG) at the General Hospital of Southern Theater Command, between December 2014 and March 2018. STEMI was diagnosed based on the 2017 European Society of Cardiology (ESC) guidelines. Patients were divided into CAS and non-CAS groups according to CAG results, and further categorized by age into three groups: young (≤ 45 years), middle-aged (46-59 years), and elderly (≥ 60 years). Cumulative cigarette consumption was calculated using the smoking index (cigarettes/day × years). Smoking status was graded as follows: grade 0 (non-smokers), grade 1 (index ≤ 100), grade 2 (index > 100 and ≤ 200), and grade 3 (index > 200). Statistical analyses, including Chi-square tests, Spearman correlation, and multivariate logistic regression were conducted to evaluate the relationship between smoking and CAS in different age groups. Among the 1156 STEMI patients analyzed, 80 (6.9%) were diagnosed with CAS. The CAS group exhibited a higher proportion of young adults (35.0% vs. 13.8%, P < 0.001) and grade 3 smokers (62.5% vs. 46.6%, P < 0.001) compared to the non-CAS group. A positive correlation between cumulative cigarette consumption and CAS was observed in all patients (r = 0.124, P < 0.001), heavy smoking (grade 2 and grade 3) was significantly associated with CAS in young adults (r = 0.321, P < 0.001) and middle-aged adults (r = 0.127, P = 0.006) but not in elderly patients. Logistic regression demonstrated that heavy smoking significantly increased CAS risk, with adjusted odds ratios of 6.397 for grade 2 smokers and 6.926 for grade 3 smokers, relative to non-smokers. Among heavy smokers( grade 2 and grade 3), young adults had a 4.912-fold higher CAS risk, while middle-aged adults had a 2.041-fold higher risk, compared to elderly individuals. Cumulative cigarette consumption is closely linked to infarction-related CAS in STEMI patients. Heavy smoking (grade 2 and grade 3) is a key factor linked to infarction-related coronary spasm, especially in younger and middle-aged adults. Effective smoking control is essential for preventing and managing STEMI, particularly among younger and middle-aged populations in China. Further validation of our findings using prospective studies and large registries is warranted.
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Affiliation(s)
- Zhihui Kuang
- Department of Cardiology, The First People's Hospital of Chenzhou, Chenzhou, 423000, Hunan, China
- The First Clinical College of Jinan University，Jinan University, Guangzhou, 510000, Guangdong, China
| | - Lin Lin
- Department of Cardiology, Puning People's Hospital, Puning, 515300, Guangdong, China
| | - Ranran Kong
- Southern Medical University, Guangzhou, 510000, Guangdong, China
| | - Zhonghua Wang
- Department of Cardiology, The First People's Hospital of Chenzhou, Chenzhou, 423000, Hunan, China
| | - Xianjun Mao
- Department of Cardiology, The First People's Hospital of Chenzhou, Chenzhou, 423000, Hunan, China
| | - Dingcheng Xiang
- Department of Cardiology, General Hospital of Southern Theater Command, No.111, Liuhua Road, Liuhuaqiao Community, Liuhua Street, Yuexiu District, Guangzhou, 510000, Guangdong, China.
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Tao Y, Li G, Wang Z, Wang S, Peng X, Tang G, Li X, Liu J, Yu T, Fu X. MiR-1909-5p targeting GPX4 affects the progression of aortic dissection by modulating nicotine-induced ferroptosis. Food Chem Toxicol 2024; 191:114826. [PMID: 38897284 DOI: 10.1016/j.fct.2024.114826] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/15/2023] [Revised: 03/21/2024] [Accepted: 06/16/2024] [Indexed: 06/21/2024]
Abstract
OBJECTIVE Aortic dissection (AD) is a prevalent and acute clinical catastrophe characterized by abrupt manifestation, swift progression, and elevated fatality rates. Despite smoking being a significant risk factor for AD, the precise pathological process remains elusive. This investigation endeavors to explore the mechanisms by which smoking accelerates AD through ferroptosis induction. METHODOLOGY In this novel study, we detected considerable endothelial cell death by ferroptosis within the aortic inner lining of both human AD patients with a smoking history and murine AD models induced by β-aminopropionitrile, angiotensin II, and nicotine. Utilizing bioinformatic approaches, we identified microRNAs regulating the expression of the ferroptosis inhibitor Glutathione peroxidase 4 (GPX4). Nicotine's impact on ferroptosis was further assessed in human umbilical vein endothelial cells (HUVECs) through modulation of miR-1909-5p. Additionally, the therapeutic potential of miR-1909-5p antagomir was evaluated in vivo in nicotine-exposed AD mice. FINDINGS Our results indicate a predominance of ferroptosis over apoptosis, pyroptosis, and necroptosis in the aortas of AD patients who smoke. Nicotine exposure instigated ferroptosis in HUVECs, where the miR-1909-5p/GPX4 axis was implicated. Modulation of miR-1909-5p in these cells revealed its regulatory role over GPX4 levels and subsequent endothelial ferroptosis. In vivo, miR-1909-5p suppression reduced ferroptosis and mitigated AD progression in the murine model. CONCLUSIONS Our data underscore the involvement of the miR-1909-5p/GPX4 axis in the pathogenesis of nicotine-induced endothelial ferroptosis in AD.
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Affiliation(s)
- Yan Tao
- Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, Qingdao, 266000, People's Republic of China
| | - Gang Li
- Department of Vascular Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, 324 Jingwu Road, Jinan, Shandong, 250021, People's Republic of China; Department of Vascular Surgery, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, 324 Jingwu Road, Jinan, Shandong, 250021, People's Republic of China
| | - Zhibin Wang
- Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, Qingdao, 266000, People's Republic of China
| | - Shizhong Wang
- The Department of Cardiology Surgery, The Affiliated Hospital of Qingdao University, Qingdao, 266000, People's Republic of China
| | - Xingang Peng
- The Department of Emergency General Surgery, The Affiliated Hospital of Qingdao University, Qingdao, 266000, People's Republic of China
| | - Guozhang Tang
- Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, Qingdao, 266000, People's Republic of China
| | - Xiaolu Li
- Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, Qingdao, 266000, People's Republic of China
| | - Jianhua Liu
- Ultrasound Medicine Department, Guangzhou First People's Hospital, Guangzhou, 510000, People's Republic of China.
| | - Tao Yu
- Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, Qingdao, 266000, People's Republic of China; Institute for Translational Medicine, The Affiliated Hospital of Qingdao University, No. 38 Dengzhou Road, Qingdao, 266021, People's Republic of China.
| | - Xiuxiu Fu
- Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, Qingdao, 266000, People's Republic of China.
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Santos EW, Khatoon S, Di Mise A, Zheng YM, Wang YX. Mitochondrial Dynamics in Pulmonary Hypertension. Biomedicines 2023; 12:53. [PMID: 38255160 PMCID: PMC10813473 DOI: 10.3390/biomedicines12010053] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/20/2023] [Revised: 12/12/2023] [Accepted: 12/19/2023] [Indexed: 01/24/2024] Open
Abstract
Mitochondria are essential organelles for energy production, calcium homeostasis, redox signaling, and other cellular responses involved in pulmonary vascular biology and disease processes. Mitochondrial homeostasis depends on a balance in mitochondrial fusion and fission (dynamics). Mitochondrial dynamics are regulated by a viable circadian clock. Hypoxia and nicotine exposure can cause dysfunctions in mitochondrial dynamics, increases in mitochondrial reactive oxygen species generation and calcium concentration, and decreases in ATP production. These mitochondrial changes contribute significantly to pulmonary vascular oxidative stress, inflammatory responses, contractile dysfunction, pathologic remodeling, and eventually pulmonary hypertension. In this review article, therefore, we primarily summarize recent advances in basic, translational, and clinical studies of circadian roles in mitochondrial metabolism in the pulmonary vasculature. This knowledge may not only be crucial to fully understanding the development of pulmonary hypertension, but also greatly help to create new therapeutic strategies for treating this devastating disease and other related pulmonary disorders.
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Affiliation(s)
- Ed Wilson Santos
- Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA; (E.W.S.); (S.K.); (A.D.M.)
| | - Subika Khatoon
- Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA; (E.W.S.); (S.K.); (A.D.M.)
| | - Annarita Di Mise
- Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA; (E.W.S.); (S.K.); (A.D.M.)
- Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Via Orabona, 4, 70125 Bari, Italy
| | - Yun-Min Zheng
- Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA; (E.W.S.); (S.K.); (A.D.M.)
| | - Yong-Xiao Wang
- Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA; (E.W.S.); (S.K.); (A.D.M.)
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Liu J, Du X, Yao Q, Jiang T, Cui Q, Xie X, Zhao Z, Lai B, Wang N, Xiao L. Procyanidin B2 ameliorates endothelial dysfunction induced by nicotine via the induction of tetrahydrobiopterin synthesis. J Funct Foods 2022. [DOI: 10.1016/j.jff.2022.105306] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/05/2022] Open
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Chen J, Yao Y, Wang Y, Wang X, Peng X, Li T, Liu Y, Du J. Autophagy triggered by the ROS/ERK signaling pathway protects mouse embryonic palatal cells from apoptosis induced by nicotine. ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH INTERNATIONAL 2022; 29:81909-81922. [PMID: 35739442 DOI: 10.1007/s11356-022-21496-0] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 02/17/2022] [Accepted: 06/12/2022] [Indexed: 06/15/2023]
Abstract
Maternal cigarette smoking during pregnancy is a known high-risk factor for having a child with a cleft lip and/or palate (CLP), a common congenital malformation. Nicotine is the major teratogen component of cigarettes and e-cigarettes, and nicotine plays an important role in the development of CLP. However, the mechanism underlying nicotine's effect on CLP remains unclear. Here, we aimed to determine the role and molecular mechanisms of nicotine-induced autophagy, an important process involved in regulating the cellular stress response in mouse embryonic palatal cells (MEPCs). First, we found that nicotine promoted MEPCs proliferation and inhibited their apoptosis from 0 to 12 h. After 12 h, the proliferation was inhibited, and apoptosis was promoted. The migration of MEPCs was also inhibited by nicotine. Simultaneously, long-term nicotine stimulation inhibited the osteogenic differentiation of MEPCs. We then found that nicotine significantly increased autophagy flux in MEPCs at 12 h by increasing the expression of microtubule-associated protein light chain 3 (LC3) and reducing P62 expression levels. After nicotine exposure, intracellular reactive oxygen species (ROS) and extracellular signal-regulated kinase-1/2 (ERK1/2) expression significantly increased, and the expression of ERK1/2 was reversed by the ROS scavenging agent N-acetylcysteine (NAC). Moreover, the autophagy induced by nicotine was reversed by SCH772984, a specific inhibitor of ERK1/2, and the autophagy inhibitor chloroquine (CQ). These results suggest that in the early stage of nicotine exposure, MEPCs may trigger autophagy through the ROS/ERK1/2 signaling pathway to avoid cell damage caused by nicotine.
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Affiliation(s)
- Jing Chen
- Laboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China
| | - Yaxia Yao
- Laboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China
| | - Yijia Wang
- Laboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China
| | - Xiaotong Wang
- Laboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China
| | - Xia Peng
- Laboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China
| | - Tianli Li
- Laboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China
| | - Ying Liu
- Laboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China
| | - Juan Du
- Laboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, 100050, China.
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Correia TML, Almeida AA, da Silva DA, Coqueiro RDS, Pires RA, de Magalhães ACM, Queiroz RF, Brito LL, Marques LM, Machado M, Pereira R. Interaction between cigarette smoke exposure and physical training on inflammatory and oxidative profile in mice muscle. Chem Biol Interact 2022; 358:109913. [PMID: 35339431 DOI: 10.1016/j.cbi.2022.109913] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/27/2022] [Revised: 03/07/2022] [Accepted: 03/21/2022] [Indexed: 11/03/2022]
Abstract
Regular physical training and cigarette smoke exposure (CSE) have opposite effects on physical performance, antioxidant, and inflammatory profile. However, the interaction between these events is not well studied. We aimed to investigate how regular physical training and CSE interact, and in what is the outcome of this interaction on the physical performance, skeletal muscle antioxidant defense and molecular profile response of pro and anti-inflammatory cytokines. Male C57BL/6 mice were randomly divided into 4 groups (n = 8/group): 1) Sedentary group (SED); 2) 4 weeks of control, followed by 4 weeks of CSE (SED + CSEG); 3) Physically active (PA) along 8 weeks (forced swim training, 5 times a week); 4) Physically active and exposed to the cigarette smoke (PA + CSEG), group submitted to forced swim training for 4 weeks, followed by 4 weeks of concomitant training and CSE. Physical performance was evaluated before and after the experimental period (8 weeks), total peroxidase and glutathione peroxidase (GPx) activities, expression of genes encoding TNF-α, MCP-1, IL1β, IL-6, IL-10, TGF-β, HO-1 and the TNF-α/IL-10 ratio were determined from gastrocnemius muscle at the end of experimental period. The CSE attenuated the aerobic capacity adaptation (time to exhaustion in swimming forced test) promoted by physical training and inhibit the improvement in local muscle resistance (inverted screen test). The regular physical training enhanced the antioxidant defense, but the CSE abrogated this benefit. The CSE induced a harmful pro-inflammatory profile in skeletal muscle from sedentary animals whereas the regular physical training induced an opposite adaptation. Likewise, the CSE abolished the protective effect of physical training. Together, these results suggest a negative effect of CSE including, at least in part, the inhibition/attenuation of beneficial adaptations from regular physical training.
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Affiliation(s)
- Thiago Macêdo Lopes Correia
- Integrative Physiology Research Center, Department of Biological Sciences, State Universidade Estadual do Sudoeste da Bahia (UESB), Jequie, 45210-506, Bahia, Brazil; Multicentric Postgraduate Program in Physiological Sciences (Brazilian Society of Physiology), Universidade Federal da Bahia (UFBA), Vitoria da Conquista, Bahia, Brazil
| | - Amanda Alves Almeida
- Integrative Physiology Research Center, Department of Biological Sciences, State Universidade Estadual do Sudoeste da Bahia (UESB), Jequie, 45210-506, Bahia, Brazil; Multicentric Postgraduate Program in Physiological Sciences (Brazilian Society of Physiology), Universidade Federal da Bahia (UFBA), Vitoria da Conquista, Bahia, Brazil
| | - Danielba Almeida da Silva
- Postgraduate Program in Biosciences, Universidade Federal da Bahia, Campus Anísio Teixeira, Vitória da Conquista, Brazil
| | - Raildo da Silva Coqueiro
- Integrative Physiology Research Center, Department of Biological Sciences, State Universidade Estadual do Sudoeste da Bahia (UESB), Jequie, 45210-506, Bahia, Brazil
| | - Ramon Alves Pires
- Integrative Physiology Research Center, Department of Biological Sciences, State Universidade Estadual do Sudoeste da Bahia (UESB), Jequie, 45210-506, Bahia, Brazil; Multicentric Postgraduate Program in Biochemistry and Molecular Biology (Brazilian Society of Biochemistry and Molecular Biology), Universidade Estadual do Sudoeste da Bahia (UESB), Vitoria da Conquista, Bahia, Brazil
| | - Amelia Cristina Mendes de Magalhães
- Multicentric Postgraduate Program in Physiological Sciences (Brazilian Society of Physiology), Universidade Federal da Bahia (UFBA), Vitoria da Conquista, Bahia, Brazil
| | - Raphael Ferreira Queiroz
- Multicentric Postgraduate Program in Biochemistry and Molecular Biology (Brazilian Society of Biochemistry and Molecular Biology), Universidade Estadual do Sudoeste da Bahia (UESB), Vitoria da Conquista, Bahia, Brazil; Postgraduate Program in Biosciences, Universidade Federal da Bahia, Campus Anísio Teixeira, Vitória da Conquista, Brazil
| | - Lorena Lôbo Brito
- Multicentric Postgraduate Program in Physiological Sciences (Brazilian Society of Physiology), Universidade Federal da Bahia (UFBA), Vitoria da Conquista, Bahia, Brazil
| | - Lucas Miranda Marques
- Multicentric Postgraduate Program in Physiological Sciences (Brazilian Society of Physiology), Universidade Federal da Bahia (UFBA), Vitoria da Conquista, Bahia, Brazil
| | - Marco Machado
- Universitary Foundation of Itaperuna (FUNITA), Itaperuna, RJ, Brazil; Laboratory of Physiology and Biokinetic, Faculty of Biological Sciences and Health, Iguaçu University, Campus V, Itaperuna, RJ, Brazil
| | - Rafael Pereira
- Integrative Physiology Research Center, Department of Biological Sciences, State Universidade Estadual do Sudoeste da Bahia (UESB), Jequie, 45210-506, Bahia, Brazil; Multicentric Postgraduate Program in Physiological Sciences (Brazilian Society of Physiology), Universidade Federal da Bahia (UFBA), Vitoria da Conquista, Bahia, Brazil; Multicentric Postgraduate Program in Biochemistry and Molecular Biology (Brazilian Society of Biochemistry and Molecular Biology), Universidade Estadual do Sudoeste da Bahia (UESB), Vitoria da Conquista, Bahia, Brazil; Postgraduate Program in Nursing and Health, Universidade Estadual do Sudoeste da Bahia (UESB), Jequie, 45210-506, Bahia, Brazil.
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Yang W, Li F, Li C, Meng J, Wang Y. Focus on Early COPD: Definition and Early Lung Development. Int J Chron Obstruct Pulmon Dis 2021; 16:3217-3228. [PMID: 34858022 PMCID: PMC8629909 DOI: 10.2147/copd.s338359] [Citation(s) in RCA: 18] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/08/2021] [Accepted: 11/03/2021] [Indexed: 12/24/2022] Open
Abstract
Chronic obstructive pulmonary disease (COPD) is a disease with high incidence rate and mortality rates worldwide. It is the third leading cause of death in the world. Nevertheless, little progress has been made in treating and preventing the disease. Under these circumstances, the concept of “early COPD” was proposed. Although this concept is not new, most health-care workers do not fully understand early COPD and tend to confuse it with mild COPD. In this review, we mainly discuss the definition of early COPD and the developmental trajectory of lung function. Although patients with early COPD have no symptoms, their lung function is already lower than that of normal people. A relatively complete definition is needed to identify this group of people. Reduced lung function is the diagnostic criterion for COPD, but lung development is a long-term dynamic process. In addition to smoking and air pollution, we should pay more attention to prenatal and childhood risk factors, for example, parents smoking, birth weight, preterm birth, mode of delivery, childhood respiratory infections and childhood asthma. Health-care workers need to be fully aware of early COPD, to reduce the morbidity of COPD and take effective measures to prevent these risk factors.
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Affiliation(s)
- Weichang Yang
- Department of Respiratory and Critical Care Medicine, Nanchang First Hospital, Nanchang University, Nanchang, 330000, Jiangxi, People's Republic of China
| | - Fengyuan Li
- Department of Respiratory and Critical Care Medicine, Nanchang First Hospital, Nanchang University, Nanchang, 330000, Jiangxi, People's Republic of China
| | - Can Li
- Department of Respiratory and Critical Care Medicine, Nanchang First Hospital, Nanchang University, Nanchang, 330000, Jiangxi, People's Republic of China
| | - Jiaqi Meng
- Department of Respiratory and Critical Care Medicine, Nanchang First Hospital, Nanchang University, Nanchang, 330000, Jiangxi, People's Republic of China
| | - Ying Wang
- Department of Respiratory and Critical Care Medicine, Nanchang First Hospital, Nanchang University, Nanchang, 330000, Jiangxi, People's Republic of China
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Grondin CJ, Davis AP, Wiegers JA, Wiegers TC, Sciaky D, Johnson RJ, Mattingly CJ. Predicting molecular mechanisms, pathways, and health outcomes induced by Juul e-cigarette aerosol chemicals using the Comparative Toxicogenomics Database. Curr Res Toxicol 2021; 2:272-281. [PMID: 34458863 PMCID: PMC8379377 DOI: 10.1016/j.crtox.2021.08.001] [Citation(s) in RCA: 48] [Impact Index Per Article: 12.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/11/2021] [Revised: 06/16/2021] [Accepted: 08/02/2021] [Indexed: 11/22/2022] Open
Abstract
There is a critical need to understand the health risks associated with vaping e-cigarettes, which has reached epidemic levels among teens. Juul is currently the most popular type of e-cigarette on the market. Using the Comparative Toxicogenomics Database (CTD; http://ctdbase.org), a public resource that integrates chemical, gene, phenotype and disease data, we aimed to analyze the potential molecular mechanisms of eight chemicals detected in the aerosols generated by heating Juul e-cigarette pods: nicotine, acetaldehyde, formaldehyde, free radicals, crotonaldehyde, acetone, pyruvaldehyde, and particulate matter. Curated content in CTD, including chemical-gene, chemical-phenotype, and chemical-disease interactions, as well as associated phenotypes and pathway enrichment, were analyzed to help identify potential molecular mechanisms and diseases associated with vaping. Nicotine shows the most direct disease associations of these chemicals, followed by particulate matter and formaldehyde. Together, these chemicals show a direct marker or mechanistic relationship with 400 unique diseases in CTD, particularly in the categories of cardiovascular diseases, nervous system diseases, respiratory tract diseases, cancers, and mental disorders. We chose three respiratory tract diseases to investigate further, and found that in addition to cellular processes of apoptosis and cell proliferation, prioritized phenotypes underlying Juul-associated respiratory tract disease outcomes include response to oxidative stress, inflammatory response, and several cell signaling pathways (p38MAPK, NIK/NFkappaB, calcium-mediated).
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Key Words
- A, acetaldehyde
- AC, acetone
- C, crotonaldehyde
- CGPD, chemical-gene-phenotype-disease
- COPD, chronic obstructive pulmonary disease
- CTD, Comparative Toxicogenomics Database
- Cr, chromium
- Database
- E-cigarettes
- Environmental exposure
- F, formaldehyde
- FR, free radicals
- Juul
- M, marker/mechanism relationship
- MIE, molecular initiating event
- MOA, mode-of-action
- Mn, manganese
- N, nicotine
- NAFFCAPP, nicotine, acetaldehyde, formaldehyde, free radicals, crotonaldehyde, acetone, pyruvaldehyde, and particulate matter chemical mixture
- NAFP, nicotine, acetaldehyde, formaldehyde, particulate matter chemical mixture
- Ni, nickel
- P, pyruvaldehyde
- PM, particulate matter
- Pb, lead
- ROS, reactive oxygen species
- Respiratory disease
- Vaping
- Zn, zinc
- nAChR, nicotinic acetylcholine receptor
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Affiliation(s)
- Cynthia J. Grondin
- Department of Biological Sciences, North Carolina State University, Raleigh, NC, USA
| | - Allan Peter Davis
- Department of Biological Sciences, North Carolina State University, Raleigh, NC, USA
| | - Jolene A. Wiegers
- Department of Biological Sciences, North Carolina State University, Raleigh, NC, USA
| | - Thomas C. Wiegers
- Department of Biological Sciences, North Carolina State University, Raleigh, NC, USA
| | - Daniela Sciaky
- Department of Biological Sciences, North Carolina State University, Raleigh, NC, USA
| | - Robin J. Johnson
- Department of Biological Sciences, North Carolina State University, Raleigh, NC, USA
| | - Carolyn J. Mattingly
- Department of Biological Sciences, North Carolina State University, Raleigh, NC, USA
- Center for Human Health and the Environment, North Carolina State University, Raleigh, NC, USA
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Bold KW, Krishnan-Sarin S, Stoney CM. E-cigarette use as a potential cardiovascular disease risk behavior. ACTA ACUST UNITED AC 2019; 73:955-967. [PMID: 30394775 DOI: 10.1037/amp0000231] [Citation(s) in RCA: 24] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
Electronic cigarette (e-cigarette) use is rapidly increasing among youth and adults despite limited information regarding the long-term risks or benefits. The potential impact of e-cigarette use on public health is complex. E-cigarettes are sometimes considered as smoking cessation aids and, to the extent that they are successful in this regard, could have a net population benefit for adult smokers. However, limited knowledge exists about the long-term health effects of e-cigarette use, and research has suggested these novel tobacco products may lead to initiation and continued use among vulnerable populations, including youth. The current review aimed to summarize trends and available scientific information about e-cigarette use, focusing on the potential cardiovascular health risks and benefits, characteristics associated with e-cigarette use, and critical areas for future investigation to inform the research and clinical work of psychologists. Psychologists have a leadership role in mitigating health risks from smoking behavior, and there is a need for rigorous research assessing the impact of e-cigarette use on population health. In addition, psychologists are uniquely qualified to understand the underlying processes regarding decision-making and behaviors around e-cigarette use. Collectively, the research of psychologists in this area can have a substantial impact on patient education, policies, and the development of prevention and intervention programs to promote public health. (PsycINFO Database Record (c) 2018 APA, all rights reserved).
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Affiliation(s)
- Krysten W Bold
- Department of Psychiatry, Yale University School of Medicine
| | | | - Catherine M Stoney
- Clinical Applications and Prevention Branch, National Heart, Lung, and Blood Institute, National Institutes of Health
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11
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Luan Z, Liu B, Shi L. Angiotensin II-induced micro RNA-21 culprit for non-small-cell lung adenocarcinoma. Drug Dev Res 2019; 80:1031-1039. [PMID: 31823412 DOI: 10.1002/ddr.21597] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/13/2019] [Revised: 08/01/2019] [Accepted: 08/19/2019] [Indexed: 12/19/2022]
Abstract
Lung cancer is among the most complicated cancers, with an estimated 1.6 million deaths each year for both men and women. However, the proportion of lung cancer patients in developing nations has increased from 31% to 49.9% in the last two decades. There are two main subtypes of lung cancer, small-cell lung carcinoma and non-small-cell lung carcinoma (NSCLC), accounting for 15% and 85% of all lung cancer, respectively. Adenocarcinoma is the most common type of lung cancer in smokers and nonsmokers in men and women regardless of their age. Chemicals in cigarette smoke and nicotine enter our bloodstream and can then affect the entire body and finally lead to the activation of several important, pro-survival signaling pathways. The biologically active peptide of RAAS on overstimulation enhance Ang II mediates cell proliferation, fibrosis and inflammatory effects via AT1 receptor. Very few studies highlight the diagnostic and therapeutic potential of miRNAs with the EGFR-regulated miRNA-21.
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Affiliation(s)
- Zhaoji Luan
- Department of Respiratory and Critical Care Medicine, ZiBo First Hospital, Zibo, Shandong Province, China
| | - Baoliang Liu
- Department of Respiratory and Critical Care Medicine, ZiBo First Hospital, Zibo, Shandong Province, China
| | - Lina Shi
- Department of Hematology, ZiBo First Hospital, Boshan District, Zibo, Shandong Province, China
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12
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Babic M, Schuchardt M, Tölle M, van der Giet M. In times of tobacco-free nicotine consumption: The influence of nicotine on vascular calcification. Eur J Clin Invest 2019; 49:e13077. [PMID: 30721530 DOI: 10.1111/eci.13077] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/02/2018] [Revised: 01/11/2019] [Accepted: 02/01/2019] [Indexed: 12/12/2022]
Abstract
BACKGROUND Smoking remains the most important avoidable cause of global mortality. Even though the number of cigarette smokers declines in first world countries, the uses of alternative nicotine delivery products increase and may even surpass the sells of cigarettes. In this light, the explicit role of nicotine in the development of cardiovascular diseases should be elucidated. OBJECTIVES This narrative review attempts to connect current literature about possible effects of nicotine on the environment of the vasculature to the pathogenesis of vascular calcification, focusing on the tunica media of the vessel wall. METHODS For this review, papers found on Pubmed and Medline until December 2018 by searching for the keywords nicotine, vascular calcification, oxidative stress, osteoblastic transdifferentiation and matrix degradation were considered. RESULTS Nicotine creates an environment that probably facilitates and maybe even induces osteogenic transdifferentiation of VSMC by inflammation, endothelial dysfunction and reactive oxygen species. This process is believed to be a key event in calcification of the tunica media of the vessel wall. Furthermore, nicotine could lead to the formation of nucleation sites for hydroxyapatite by facilitating matrix vesicles and extracellular matrix degradation. CONCLUSIONS There is a growing body of evidence implicating that nicotine alone could impair vascular function and lead to vascular calcification. Further research is necessary to elucidate the explicit influence of nicotine on arteriosclerosis.
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Affiliation(s)
- Milen Babic
- Department of Nephrology, Charité - Universitaetsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
| | - Mirjam Schuchardt
- Department of Nephrology, Charité - Universitaetsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
| | - Markus Tölle
- Department of Nephrology, Charité - Universitaetsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
| | - Markus van der Giet
- Department of Nephrology, Charité - Universitaetsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
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13
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Liang X, Su S, Hao G, Snieder H, Treiber F, Kapuku G, Wang X. Determinants of pulse wave velocity trajectories from youth to young adulthood: the Georgia Stress and Heart Study. J Hypertens 2019; 37:563-571. [PMID: 30234784 PMCID: PMC6355367 DOI: 10.1097/hjh.0000000000001933] [Citation(s) in RCA: 22] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
OBJECTIVE Increased arterial stiffness measured by pulse wave velocity (PWV) has been shown to be an important parameter of cardiovascular risk. Longitudinal development of PWV from youth to early adulthood and its possible sociodemographic, anthropometric, hemodynamic and behavioral moderators will be illustrated. METHODS Individual growth curves of carotid-distal PWV across age were created for 559 African American and European American men and women with a maximum of five assessments over an average of 7-year follow-up (mean age at participants' first assessment, 22.3 ± 3.4). RESULTS African Americans and men had significantly higher PWV than did European Americans and women (Ps < 0.01), respectively. A three-way interaction (P < 0.001) between age, sex and ethnicity was observed with African American men displaying a larger rate of increase in PWV with age than the other three ethnic and sex groups. The ethnicity and sex effects on PWV persisted when controlling for other moderators. Waist circumference was the strongest anthropometric predictor but its effect on PWV was only significant in women. Mean arterial pressure was the strongest hemodynamic predictor, marital status of parents was the strongest socioeconomic predictor and marijuana use was the strongest behavioral predictor of PWV. The best-fitting full model explained in total 59.4% of the between-subject variance in PWV with ethnicity, sex and age explaining 25.6%. CONCLUSION We observed significant ethnic and sex differences in longitudinal trajectories of PWV in youth and young adults. In addition, individual differences in PWV growth can largely be explained by mean arterial pressure, waist, marital status of parents and marijuana use.
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Affiliation(s)
- Xiaohua Liang
- Children’s Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, China International Science and Technology Cooperation Center of Child Development and Critical Disorders, Chongqing, China,
- Georgia Prevention Institute, Medical College of Georgia, Augusta University, Augusta, Georgia, USA,
| | - Shaoyong Su
- Georgia Prevention Institute, Medical College of Georgia, Augusta University, Augusta, Georgia, USA,
| | - Guang Hao
- Georgia Prevention Institute, Medical College of Georgia, Augusta University, Augusta, Georgia, USA,
| | - Harold Snieder
- Department of Epidemiology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands
| | - Frank Treiber
- College of Nursing, Medical University of South Carolina, Charleston, USA
| | - Gaston Kapuku
- Georgia Prevention Institute, Medical College of Georgia, Augusta University, Augusta, Georgia, USA,
| | - Xiaoling Wang
- Georgia Prevention Institute, Medical College of Georgia, Augusta University, Augusta, Georgia, USA,
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14
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Fouda MA, El-Gowelli HM, El-Gowilly SM, El-Mas MM. Hemin blunts the depressant effect of chronic nicotine on reflex tachycardia via activation of central NOS/PI3K pathway in female rats. Pharmacol Rep 2018; 70:455-462. [DOI: 10.1016/j.pharep.2017.09.008] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/10/2017] [Revised: 09/08/2017] [Accepted: 09/29/2017] [Indexed: 12/25/2022]
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15
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Li C, Sun H, Xu G, McCarter KD, Li J, Mayhan WG. Mito-Tempo prevents nicotine-induced exacerbation of ischemic brain damage. J Appl Physiol (1985) 2018; 125:49-57. [PMID: 29420160 DOI: 10.1152/japplphysiol.01084.2017] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/17/2023] Open
Abstract
Nicotine may contribute to the pathogenesis of cerebrovascular disease via the generation of reactive oxygen species (ROS). Overproduction of ROS leads to brain damage by intensifying postischemic inflammation. Our goal was to determine the effect of Mito-Tempo, a mitochondria-targeted antioxidant, on ischemic brain damage and postischemic inflammation during chronic exposure to nicotine. Male Sprague-Dawley rats were divided into four groups: control, nicotine, Mito-Tempo-treated control, and Mito-Tempo-treated nicotine. Nicotine (2 mg·kg-1·day-1) was administered via an osmotic minipump for 4 wk. Mito-Tempo (0.7 mg·kg-1·day-1 ip) was given for 7 days before cerebral ischemia. Transient focal cerebral ischemia was induced by occlusion of the middle cerebral artery for 2 h. Brain damage and inflammation were evaluated after 24 h of reperfusion by measuring infarct volume, expression of adhesion molecules, activity of matrix metalloproteinase, brain edema, microglial activation, and neutrophil infiltration. Nicotine exacerbated infarct volume and worsened neurological deficits. Nicotine did not alter baseline ICAM-1 expression, matrix metallopeptidase-2 activity, microglia activation, or neutrophil infiltration but increased these parameters after cerebral ischemia. Mito-Tempo did not have an effect in control rats but prevented the chronic nicotine-induced augmentation of ischemic brain damage and postischemic inflammation. We suggest that nicotine increases brain damage following cerebral ischemia via an increase in mitochondrial oxidative stress, which, in turn, contributes to postischemic inflammation. NEW & NOTEWORTHY Our findings have important implications for the understanding of mechanisms contributing to increased susceptibility of the brain to damage in smokers and users of nicotine-containing tobacco products.
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Affiliation(s)
- Chun Li
- Department of Cellular Biology and Anatomy, Center for Cardiovascular Diseases and Sciences, Louisiana State University Health Sciences Center-Shreveport , Shreveport, Louisiana
| | - Hong Sun
- Department of Cellular Biology and Anatomy, Center for Cardiovascular Diseases and Sciences, Louisiana State University Health Sciences Center-Shreveport , Shreveport, Louisiana
| | - Guodong Xu
- Department of Cellular Biology and Anatomy, Center for Cardiovascular Diseases and Sciences, Louisiana State University Health Sciences Center-Shreveport , Shreveport, Louisiana.,Department of Neurology, Hebei General Hospital , Shijiazhuang, Hebei , China
| | - Kimberly D McCarter
- Department of Cellular Biology and Anatomy, Center for Cardiovascular Diseases and Sciences, Louisiana State University Health Sciences Center-Shreveport , Shreveport, Louisiana
| | - Jiyu Li
- Department of Cellular Biology and Anatomy, Center for Cardiovascular Diseases and Sciences, Louisiana State University Health Sciences Center-Shreveport , Shreveport, Louisiana
| | - William G Mayhan
- Division of Basic Biomedical Sciences, Sanford School of Medicine, The University of South Dakota, Vermillion, South Dakota
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Safety Assessment of Electronic Cigarettes and Their Relationship with Cardiovascular Disease. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2018; 15:ijerph15010075. [PMID: 29304018 PMCID: PMC5800174 DOI: 10.3390/ijerph15010075] [Citation(s) in RCA: 24] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 10/09/2017] [Revised: 12/14/2017] [Accepted: 01/02/2018] [Indexed: 12/31/2022]
Abstract
Smoking leads to the occurrence and development of a variety of diseases. Most importantly, it is an independent risk factor of cardiovascular atherosclerosis. In recent years, electronic cigarettes have become a popular alternative to traditional cigarettes, since modern micro-electronic techniques provide the possibility of simulating the process of traditional smoking. Additionally, it is convenient and fashionable. Nevertheless, comments about the safety of electronic cigarettes remain controversial. Although the research about electronic cigarettes increased exponentially, there has been no systematic study of its safety. The aim of the current study is to review the literature reports about the safety of electronic cigarettes, and to understand their hazards and disadvantages. It was found that most of the current research about electronic cigarettes comprises short-term and in vitro studies. There are few reports of in vivo and long-term studies. Notably, the level of harmful components such as volatile organic compounds, tobacco-specific nitrosamines and heavy metals in electronic cigarettes are even higher than in traditional cigarettes. Therefore, the harm of electronic cigarettes should not be underestimated. In conclusion, the question of whether electronic cigarettes are a safe and sufficient substitute for traditional smoking needs further investigation.
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Ahmad S, Hassan A, Abbasi WM, Rehman T. Phytochemistry and pharmacological potential of Cassia absus - a review. ACTA ACUST UNITED AC 2017; 70:27-41. [PMID: 28872683 DOI: 10.1111/jphp.12816] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/24/2017] [Accepted: 08/04/2017] [Indexed: 01/12/2023]
Abstract
OBJECTIVES Cassia absus is a plant of the family fabaceae with Ayurvedic ethnomedical records. It is used in traditional medicine for the treatment of bronchitis, asthma, cough, conjunctivitis, leucoderma, renal and hepatic diseases, constipation, tumors, venereal ulcer, headache, hemorrhoids and wound healing. Preliminary in vitro and in vivo studies have provided valuable scientific evidence for its use. This review aims to summarize reported pharmacognosy, traditional uses, phytochemistry and pharmacological potential of C. absus while identifying potential areas of further research of plant. KEY FINDINGS The review comprises literature pertaining to the evidence base therapeutic potential, pharmacognosy and phytochemistry of C. absus spanning from 1935 to 2016 using published articles in peer-reviewed journals, ethno botanical text books, and worldwide accepted scientific databases via electronic search (Elsevier, Google Scholar, PubMed, Scopus, Springer, Web of Science, Wiley online library). Kew Botanical Garden databases and the Plant List were used to authenticate the scientific names. Different pharmacological experiments in many in-vitro and in-vivo models have proved the potential of C. absus with antihypertensive, antifertility, antifungal, anti-inflammatory, anti-hyperglycemic, anti-glycation, antibacterial activity, α- amylase inhibitory activity, antioxidant and reducing activitity etc. chaksine, iso-chaksine, saturated and unsaturated fatty acids, chrysophanol, aloe-emodin and a wide range of chemical compounds have also been reported. Toxicity studies reveal the nontoxic nature of C. absus at a dose of 2000 mg/kg, however, plant possess reproductive toxicity and can be used as birth control or abortifacient. SUMMARY Reported activities suggest that there is sufficient pharmacological potential for developing C. absus as a drug for hypertension, infections, diabetes and its complications. However, heterogeneity in study protocol and conflicting results mask the ability to replicate these studies. So, future studies should be replicated in line with best practices. More toxicological studies would aid the progress to clinical trial studies. Various ethno medical uses of C. absus have not been evaluated yet.
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Affiliation(s)
- Saeed Ahmad
- Department of Pharmacy, Faculty of Pharmacy and Alternative Medicine, The Islamia University of Bahawalpur, Bahawalpur, Pakistan.,Faculty of Pharmacy and Alternative Medicine, University College of Conventional Medicine, The Islamia University of Bahawalpur, Bahawalpur, Pakistan
| | - Ayesha Hassan
- Department of Pharmacy, Faculty of Pharmacy and Alternative Medicine, The Islamia University of Bahawalpur, Bahawalpur, Pakistan
| | - Waheed Mumtaz Abbasi
- Faculty of Pharmacy and Alternative Medicine, University College of Conventional Medicine, The Islamia University of Bahawalpur, Bahawalpur, Pakistan
| | - Tayyeba Rehman
- Faculty of Pharmacy and Alternative Medicine, University College of Conventional Medicine, The Islamia University of Bahawalpur, Bahawalpur, Pakistan
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Júnior EPN, Ribeiro ÍJ, Freire IV, da Silva Passos R, Casotti CA, Pereira R. The smoking habit negatively influences autonomic heart control in community-dwelling elderly adults. Hellenic J Cardiol 2017; 58:283-288. [DOI: 10.1016/j.hjc.2016.12.004] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/20/2016] [Revised: 12/03/2016] [Accepted: 12/05/2016] [Indexed: 01/03/2023] Open
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19
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Kim HJ, Park KK, Chung WY, Lee SK, Kim KR. Protective Effect of White-fleshed Peach ( Prunus persica (L.) Batsch) on Chronic Nicotine-induced Toxicity. J Cancer Prev 2017; 22:22-32. [PMID: 28382283 PMCID: PMC5380186 DOI: 10.15430/jcp.2017.22.1.22] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/22/2016] [Revised: 02/28/2017] [Accepted: 03/01/2017] [Indexed: 11/04/2022] Open
Abstract
Background Nicotine is a major toxic component of tobacco smoke and has been recognized as a risk factor to induce oxidative tissue damage, which is a precursor to cardiovascular diseases, lung-related diseases, and cancers. Peaches (Prunus persica) have been used for the treatment of degenerative disorders, such as hypermenorrhea, dysmenorrhea, and infertility in Asian countries. In this study, we investigated the effects of white-fleshed peach on the excretion of nicotine metabolites and 1-hydroxypyrene in smokers and chronic nicotine-induced tissue damages in mice. Methods The concentrations of cotinine and 1-hydroxypyrene were measured in urine of smokers before or after intake of white-fleshed peaches. In addition, ICR mice were injected with nicotine (5 mg/kg body weight) and then orally administered with white-fleshed peach extracts (WFPE) (250 or 500 mg/kg body weight) for 36 days. The oxidative stress parameters and the activities of antioxidant enzymes were measured in liver and kidney tissues. Also, histological changes and nitrotyrosine expression were assessed. Results Intake of white-fleshed peaches increased the urinary concentration of nicotine metabolites and 1-hydroxypyrene in 91.67% and 83.33% of smokers, respectively. WFPE decreased the malondialdehyde levels and recovered the activities of antioxidant enzymes in nicotine-injected mice. In addition, WFPE inhibited nitrotyrosine expression and inflammatory responses in the liver, kidney, and lung tissues of nicotine-treated mice. Conclusions White-fleshed peaches may increase the metabolism of toxic components in tobacco smoke in smokers and protect normal tissues against nicotine toxicity in mice. Therefore, supplementation of white-fleshed peaches might be beneficial to smokers.
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Affiliation(s)
- Hyun-Jeong Kim
- Department of Oral Biology and Oral Cancer Research Institute, BK21 PLUS Project, Yonsei University College of Dentistry, Seoul, Korea
| | - Kwang-Kyun Park
- Department of Oral Biology and Oral Cancer Research Institute, BK21 PLUS Project, Yonsei University College of Dentistry, Seoul, Korea; Department of Applied Life Science, The Graduate School, Yonsei University, Seoul, Korea
| | - Won-Yoon Chung
- Department of Oral Biology and Oral Cancer Research Institute, BK21 PLUS Project, Yonsei University College of Dentistry, Seoul, Korea; Department of Applied Life Science, The Graduate School, Yonsei University, Seoul, Korea
| | - Sun Kyoung Lee
- Department of Oral Biology and Oral Cancer Research Institute, BK21 PLUS Project, Yonsei University College of Dentistry, Seoul, Korea
| | - Ki-Rim Kim
- Department of Dental Hygiene, Kyungpook National University, Sangju, Korea
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20
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Nicotine facilitates VSMC dysfunction through a miR-200b/RhoGDIA/cytoskeleton module. Sci Rep 2017; 7:43798. [PMID: 28252009 PMCID: PMC5333142 DOI: 10.1038/srep43798] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/07/2016] [Accepted: 01/30/2017] [Indexed: 12/27/2022] Open
Abstract
Nicotine can induce the abnormal migration and proliferation of vascular smooth muscle cells (VSMCs). We have previously shown that cytoskeletal proteins and RhoGDIA, a negative regulator of the Rho GTPase pathway, are involved in the nicotine-induced dysfunction of VSMCs. Here, we found that nicotine can activate the Rho GTPase pathway and induce the synthesis of the cytoskeletal proteins in VSMCs through the activation of intracellular downstream signaling pathways, including targets such as MYPT1, PAK1 and PI3K/AKT. Upon nicotine treatment, the mRNA level of RhoGDIA is increased but protein level is decreased both in vitro and in vivo, which suggested a mechanism of post-translational regulation. By the dual luciferase reporter assay, we identified the microRNA-200b (miR-200b) as a modulator of the behavioural changes of VSMCs in response to nicotine through targeting RhoGDIA directly. Introducing miR-200b inhibitors into cultured VSMCs significantly attenuated cell proliferation and migration. Additionally, we found that hypomethylation in the CpG island shore region of miR-200b was responsible for the nicotine-induced miR-200b up-regulation in VSMCs. The study demonstrates that nicotine facilitates VSMC dysfunction through a miR-200b/RhoGDIA/cytoskeleton module through the hypomethylation of miR-200b promoter and suggests that epigenetic modifications may play an important role in the pathological progression.
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Dupont P, Benyamina A, Aubin HJ. Sécurité d’emploi de la nicotine au long cours : le débat n’est pas clos. Rev Mal Respir 2016; 33:892-898. [DOI: 10.1016/j.rmr.2016.05.002] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/29/2015] [Accepted: 11/07/2015] [Indexed: 02/02/2023]
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22
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Fouda MA, El-Gowelli HM, El-Gowilly SM, El-Mas MM. The estrogen-dependent baroreflex dysfunction caused by nicotine in female rats is mediated via NOS/HO inhibition: Role of sGC/PI3K/MAPKERK. Toxicol Appl Pharmacol 2015; 289:466-73. [DOI: 10.1016/j.taap.2015.10.014] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/04/2015] [Revised: 10/07/2015] [Accepted: 10/22/2015] [Indexed: 12/31/2022]
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Manzella F, Maloney SE, Taylor GT. Smoking in schizophrenic patients: A critique of the self-medication hypothesis. World J Psychiatry 2015; 5:35-46. [PMID: 25815253 PMCID: PMC4369547 DOI: 10.5498/wjp.v5.i1.35] [Citation(s) in RCA: 54] [Impact Index Per Article: 5.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/29/2014] [Revised: 11/27/2014] [Accepted: 01/12/2015] [Indexed: 02/05/2023] Open
Abstract
A common remark among laypeople, and notably also among mental health workers, is that individuals with mental illnesses use drugs as self-medication to allay clinical symptoms and the side effects of drug treatments. Roots of the self-medication concept in psychiatry date back at least to the 1980s. Observations that rates of smokers in schizophrenic patients are multiple times the rates for regular smoking in the general population, as well as those with other disorders, proved particularly tempting for a self-medication explanation. Additional evidence came from experiments with animal models exposed to nicotine and the identification of neurobiological mechanisms suggesting self-medication with smoking is a plausible idea. More recently, results from studies comparing smoking and non-smoking schizophrenic patients have led to the questioning of the self-medication hypothesis. Closer examination of the literature points to the possibility that smoking is less beneficial on schizophrenic symptomology than generally assumed while clearly increasing the risk of cancer and other smoking-related diseases responsible for early mortality. It is a good time to examine the evidence for the self-medication concept as it relates to smoking. Our approach is to focus on data addressing direct or implied predictions of the hypothesis in schizophrenic smokers.
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Barreto GE, Iarkov A, Moran VE. Beneficial effects of nicotine, cotinine and its metabolites as potential agents for Parkinson's disease. Front Aging Neurosci 2015; 6:340. [PMID: 25620929 PMCID: PMC4288130 DOI: 10.3389/fnagi.2014.00340] [Citation(s) in RCA: 72] [Impact Index Per Article: 7.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/31/2014] [Accepted: 12/04/2014] [Indexed: 01/10/2023] Open
Abstract
Parkinson’s disease (PD) is a progressive neurodegenerative disorder, which is characterized by neuroinflammation, dopaminergic neuronal cell death and motor dysfunction, and for which there are no proven effective treatments. The negative correlation between tobacco consumption and PD suggests that tobacco-derived compounds can be beneficial against PD. Nicotine, the more studied alkaloid derived from tobacco, is considered to be responsible for the beneficial behavioral and neurological effects of tobacco use in PD. However, several metabolites of nicotine, such as cotinine, also increase in the brain after nicotine administration. The effect of nicotine and some of its derivatives on dopaminergic neurons viability, neuroinflammation, and motor and memory functions, have been investigated using cellular and rodent models of PD. Current evidence shows that nicotine, and some of its derivatives diminish oxidative stress and neuroinflammation in the brain and improve synaptic plasticity and neuronal survival of dopaminergic neurons. In vivo these effects resulted in improvements in mood, motor skills and memory in subjects suffering from PD pathology. In this review, we discuss the potential benefits of nicotine and its derivatives for treating PD.
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Affiliation(s)
- George E Barreto
- Department of Nutrition and Biochemistry, Pontificia Universidad Javeriana Bogotá, D. C., Colombia
| | - Alexander Iarkov
- Center of Research in Biomedical Sciences, Universidad Autónoma de Chile Santiago, Chile ; Research & Development Service, Bay Pines VA Healthcare System Bay Pines, FL, USA
| | - Valentina Echeverria Moran
- Center of Research in Biomedical Sciences, Universidad Autónoma de Chile Santiago, Chile ; Research & Development Service, Bay Pines VA Healthcare System Bay Pines, FL, USA ; Research Service, James A Haley Veterans' Hospital Tampa, FL, USA ; Department of Molecular Medicine, Morsani College of Medicine, University of South Tampa, FL, USA
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Abstract
Cardiovascular disease remains the most prevalent cause of human morbidity and mortality in ageing Western societies. Basic and translational scientific efforts have focused on the development and improvement of diagnostic and therapeutic strategies to limit the burden of associated diseases, such as stroke and myocardial infarction, and diabetes mellitus and arterial hypertension. Progress in molecular medicine and biology has unravelled a complex epigenetic and post-transcriptional gene-regulating machinery in humans which may limit disease development. An increasing number of attractive molecular strategies, which use the potential of modulating noncoding RNAs, have surfaced over the last decade. Currently, the most extensively studied gene-regulating RNA subspecies are microRNAs, which have been shown to adjust the translational output of coding transcripts by enforcing their degradation and inhibiting their translation into protein. Key findings indicate that microRNAs act as crucial regulators in the majority of human pathologies. Thus, recent research has focused on detecting and modulating microRNAs for therapeutic and biomarker purposes. This review focuses on main and repeated discoveries regarding the role and the therapeutic and biomarker feasibility of microRNAs during cardiovascular disease development and exacerbation.
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Affiliation(s)
- L Maegdefessel
- Department of Medicine, Karolinska Institutet, Stockholm, Sweden
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Yu M, Li Z, Shu Z, Liu Q, Sun J, Tan X. Nicotine promotes late endothelial progenitor cells functional activity in a PI 3-kinase-dependent manner. Cell Biochem Biophys 2014; 70:1023-8. [PMID: 24817640 DOI: 10.1007/s12013-014-0013-6] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Recent studies have shown that endothelial progenitor cells (EPCs) participated in angiogenic effects of nicotine and nicotine dose dependently increased the functional activity of early EPCs. The effects of nicotine on late EPCs remain to be determined. Therefore, we investigated whether nicotine had influences on the functional activity of late EPCs. Late EPCs were isolated from human umbilical cord blood and characterized. Late EPCs of 3-5 passages were treated for 32 h with either vehicle or nicotine. The proliferative, migratory, and in vitro vasculogenesis activities of late EPCs were assayed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, modified Boyden chamber assay, and in matrigel, respectively. Late EPCs adhesion assay was performed by replating cells on fibronectin-coated dishes, and then adherent cells were counted. Nicotine enhanced proliferative, migratory, adhesive, and in vitro vasculogenesis capacities of late EPCs. These effects were significantly reduced in the presence of phosphatidylinositol (PI) 3-kinase inhibitor.
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Affiliation(s)
- Min Yu
- Department of Cardiology, The First Affiliated Hospital, Shantou University Medical College, Shantou, 515041, Guangdong, China
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Bhatnagar A, Whitsel LP, Ribisl KM, Bullen C, Chaloupka F, Piano MR, Robertson RM, McAuley T, Goff D, Benowitz N. Electronic cigarettes: a policy statement from the American Heart Association. Circulation 2014; 130:1418-36. [PMID: 25156991 DOI: 10.1161/cir.0000000000000107] [Citation(s) in RCA: 307] [Impact Index Per Article: 27.9] [Reference Citation Analysis] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]
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Grizzell JA, Iarkov A, Holmes R, Mori T, Echeverria V. Cotinine reduces depressive-like behavior, working memory deficits, and synaptic loss associated with chronic stress in mice. Behav Brain Res 2014; 268:55-65. [DOI: 10.1016/j.bbr.2014.03.047] [Citation(s) in RCA: 45] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/21/2014] [Revised: 03/28/2014] [Accepted: 03/31/2014] [Indexed: 12/21/2022]
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Fouda MA, El-Gowelli HM, El-Gowilly SM, Rashed L, El-Mas MM. Impairment of nitric oxide synthase but not heme oxygenase accounts for baroreflex dysfunction caused by chronic nicotine in female rats. PLoS One 2014; 9:e98681. [PMID: 24870610 PMCID: PMC4037226 DOI: 10.1371/journal.pone.0098681] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/28/2013] [Accepted: 05/07/2014] [Indexed: 12/31/2022] Open
Abstract
We recently reported that chronic nicotine impairs reflex chronotropic activity in female rats. Here, we sought evidence to implicate nitric oxide synthase (NOS) and/or heme oxygenase (HO) in the nicotine-baroreflex interaction. Baroreflex curves relating changes in heart rate to increases (phenylephrine) or decreases (sodium nitroprusside) in blood pressure were generated in conscious female rats treated with nicotine or saline in absence and presence of pharmacological modulators of NOS or HO activity. Compared with saline-treated rats, nicotine (2 mg/kg/day i.p., for 14 days) significantly reduced the slopes of baroreflex curves, a measure of baroreflex sensitivity (BRS). Findings that favor the involvement of NOS inhibition in the nicotine effect were (i) NOS inhibition (Nω-Nitro-L-arginine methyl ester, L-NAME) reduced BRS in control rats but failed to do so in nicotine-treated rats, (ii) L-arginine, NO donor, reversed the BRS inhibitory effect of nicotine. Alternatively, HO inhibition (zinc protoporphyrin IX, ZnPP) had no effect on BRS in nicotine- or control rats and failed to reverse the beneficial effect of L-arginine on nicotine-BRS interaction. Similar to female rats, BRS was reduced by L-NAME, but not ZnPP, in male rats and the L-NAME effect was not accentuated after concomitant administration of nicotine. Baroreflex dysfunction caused by nicotine in female rats was blunted after supplementation with hemin (HO inducer) but not tricarbonyldichlororuthenium(II) dimer (CORM-2), a carbon monoxide (CO) releasing molecule, or bilirubin, the breakdown product of heme catabolism. The facilitatory effect of hemin was abolished upon simultaneous treatment with L-NAME or 1H-[1], [2], [4] oxadiazolo[4,3-a] quinoxalin-1-one (inhibitor of soluble guanylate cyclase, sGC). The activities of HO and NOS in brainstem tissues were also significantly increased by hemin. Thus, the inhibition of NOS, but not HO, accounts for the baroreflex depressant of chronic nicotine. Further, hemin alleviates the nicotine effect through a mechanism that is NOS/sGC but not CO or bilirubin-dependent.
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Affiliation(s)
- Mohamed A. Fouda
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Alexandria, Egypt
| | - Hanan M. El-Gowelli
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Alexandria, Egypt
| | - Sahar M. El-Gowilly
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Alexandria, Egypt
| | - Laila Rashed
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Alexandria, Egypt
| | - Mahmoud M. El-Mas
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Alexandria, Egypt
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Favero G, Paganelli C, Buffoli B, Rodella LF, Rezzani R. Endothelium and its alterations in cardiovascular diseases: life style intervention. BIOMED RESEARCH INTERNATIONAL 2014; 2014:801896. [PMID: 24719887 PMCID: PMC3955677 DOI: 10.1155/2014/801896] [Citation(s) in RCA: 159] [Impact Index Per Article: 14.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/15/2013] [Accepted: 01/11/2014] [Indexed: 01/07/2023]
Abstract
The endothelium, which forms the inner cellular lining of blood vessels and lymphatics, is a highly metabolically active organ that is involved in many physiopathological processes, including the control of vasomotor tone, barrier function, leukocyte adhesion, and trafficking and inflammation. In this review, we summarized and described the following: (i) endothelial cell function in physiological conditions and (ii) endothelial cell activation and dysfunction in the main cardiovascular diseases (such as atherosclerosis, and hypertension) and to diabetes, cigarette smoking, and aging physiological process. Finally, we presented the currently available evidence that supports the beneficial effects of physical activity and various dietary compounds on endothelial functions.
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Affiliation(s)
- Gaia Favero
- Section of Anatomy and Physiopathology, Department of Clinical and Experimental Sciences, University of Brescia, Viale Europa 11, 25123 Brescia, Italy
| | - Corrado Paganelli
- Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Viale Europa 11, 25123 Brescia, Italy
| | - Barbara Buffoli
- Section of Anatomy and Physiopathology, Department of Clinical and Experimental Sciences, University of Brescia, Viale Europa 11, 25123 Brescia, Italy
| | - Luigi Fabrizio Rodella
- Section of Anatomy and Physiopathology, Department of Clinical and Experimental Sciences, University of Brescia, Viale Europa 11, 25123 Brescia, Italy
| | - Rita Rezzani
- Section of Anatomy and Physiopathology, Department of Clinical and Experimental Sciences, University of Brescia, Viale Europa 11, 25123 Brescia, Italy
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Kudo M, Matsuda K, Sugawara K, Iki Y, Kogure N, Saito-Ito T, Shimizu K, Sato I, Yoshikawa T, Uruno A, Ito R, Yokoyama A, Saito-Hakoda A, Ito S, Sugawara A. ARB affects nicotine-induced gene expression profile in human coronary artery endothelial cells. World J Hypertens 2014; 4:7-14. [DOI: 10.5494/wjh.v4.i1.7] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/10/2013] [Revised: 12/12/2013] [Accepted: 01/16/2014] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate the effects of nicotine and nicotine plus angiotensin II receptor blocker (ARB) on the gene expression profile of human coronary artery endothelial cells (HCAECs).
METHODS: The changes in gene expression profiles in HCAECs treated with nicotine and nicotine plus ARB olmesartan were analyzed by DNA microarray. In nicotine-treated HCAECs, 432 genes selected by P < 0.01 were greater than 1.5-fold compared with the untreated cells. Data were analyzed using IPA (Ingenuity® Systems, www.ingenuity.com).
RESULTS: The gene expression levels of tumor necrosis factor-α, collagen type 1, matrix metalloproteinase-10, and disintegrin and metalloprotease domain 8, which are related to “cardiovascular function and disease”, were significantly increased. In canonical pathway analyses using IPA, “atherosclerosis signaling” was strongly affected by nicotine treatment and this effect was reduced by co-incubation with ARB olmesartan. These data indicate that the deleterious cardiovascular consequences of cigarette smoking may, at least in part, be due to the nicotine-induced gene expression profile related to “atherosclerosis signaling”.
CONCLUSION: The inhibitory effect of ARB against the nicotine-induced gene expression profile may possibly induce anti-atherosclerotic effects that are independent of those from lowering the blood pressure.
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Rollema H, Russ C, Lee TC, Hurst RS, Bertrand D. Functional interactions of varenicline and nicotine with nAChR subtypes implicated in cardiovascular control. Nicotine Tob Res 2014; 16:733-42. [PMID: 24406270 DOI: 10.1093/ntr/ntt208] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
INTRODUCTION It has been suggested that varenicline-induced activation of nicotinic acetylcholine receptors (nAChRs) could play a role in the cardiovascular (CV) safety of varenicline. However, since preclinical studies showed that therapeutic varenicline concentrations have no effect in models of CV function, this study examined in vitro profiles of varenicline and nicotine at nAChR subtypes possibly involved in CV control. METHODS Concentration-dependent functional effects of varenicline and nicotine at human α3β4, α3α5β4, α7, and α4β2 nAChRs expressed in oocytes were determined by electrophysiology. The proportion of nAChRs predicted to be activated and inhibited by concentrations of varenicline (1mg b.i.d.) and of nicotine in smokers was derived from activation-inhibition curves for each nAChR subtype. RESULTS Human varenicline and nicotine concentrations can desensitize and inhibit nAChRs but cause only low-level activation of α3β4, α4β2 (<2%), α7 (<0.05%), and α3α5β4 (<0.01%) nAChRs, which is consistent with literature data. Nicotine concentrations in smokers are predicted to inhibit larger fractions of α3β4 (48%) and α3α5β4 (10%) nAChRs than therapeutic varenicline concentrations (11% and 0.6%, respectively) and to inhibit comparable fractions of α4β2 nAChRs (42%-56%) and α7 nAChRs (16%) as varenicline. CONCLUSIONS Nicotine and varenicline concentrations in patients and smokers are predicted to cause minimal activation of ganglionic α3β4* nAChRs, while their functional profiles at α3β4, α3α5β4, α7, and α4β2 nAChRs cannot explain that substituting nicotine from tobacco with varenicline would cause CV adverse events in smokers who try to quit. Other pharmacological properties that could mediate varenicline-induced CV effects have not been identified.
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Palmina NP, Maltseva EL, Chasovskaya TE, Kasparov VV, Bogdanova NG, Menshov VA, Trofimov AV. Effects of Different Phases of Cigarette Smoke on Lipid Peroxidation and Membrane Structure in Liposomes. Aust J Chem 2014. [DOI: 10.1071/ch13663] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/23/2022]
Abstract
This paper discloses for the first time the effects of the gas phase (GP) and the tar of cigarette smoke on lipid peroxidation (LPO) and on the structure of different lipid regions in liposomes. The LPO development was analysed in terms of the total unsaturation of lipids (double-bond, DB, content) and the formation of dienic conjugates (DC), ketodienes (KD), and malonic dialdehyde (MDA). As expected, the exposure of liposomes to either the GP or the tar led to a significant decrease in the DB content. However, the formation of oxidation products revealed different dynamics: MDA generation was inhibited, while the formation of DC and KD increased during the first few hours of the LPO development followed by its inhibition. The smoke constituents exhibited opposite effects on the structure of the lipid bilayer of liposomes: the GP markedly enhanced the microviscosity of liposomal membranes, whereas the tar caused a drastic lowering of microviscosity.
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DePalma RG, Zacharski LR, Chow BK, Shamayeva G, Hayes VW. Reduction of iron stores and clinical outcomes in peripheral arterial disease: outcome comparisons in smokers and non-smokers. Vascular 2013; 21:233-41. [DOI: 10.1177/1708538113478776] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
A prospective randomized trial suggested that iron (ferritin) reduction improved outcomes in smokers. The present study reanalyzed the trial results in smokers compared with non-smokers. Randomization of 1262 men with peripheral arterial disease (540 smokers and 722 non-smokers) to iron reduction (phlebotomy) or control groups permitted analysis of the effects of iron reduction and smoking on primary (all-cause mortality) and secondary (death plus non-fatal myocardial infarction or stroke) endpoints. Iron reduction resulted in significant improvement in the primary (hazard ratio [HR] 0.661, 95% confidence interval [CI] 0.45, 0.97; P = 0.036) and secondary (HR 0.64, 95% CI 0.46, 0.88; P = 0.006) endpoints compared with controls in smokers but not in non-smokers. Smokers required removal of a greater volume of blood to attain targeted ferritin reduction as compared with non-smokers ( P = 0.003) and also exhibited differing characteristics from non-smokers, including significantly less statin use. Phlebotomy-related outcomes favored smokers over non-smokers. Biological linkages responsible for this unique effect offer promising lines for future iron reduction studies (ClinicalTrial.Gov Identifier: NCT00032357).
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Affiliation(s)
| | - Leo R Zacharski
- VA New England Health Care System, White River Junction, VT 05009
| | - Bruce K Chow
- VA Palo Alto Health Care System, Menlo Park, CA 94025
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Valenti VE, Vanderlei LCM, Ferreira C, Fonseca FLA, Oliveira FR, Sousa FH, Rodrigues LM, Monteiro CBM, Adami F, Wajnsztejn R, de Abreu LC. Sidestream cigarette smoke and cardiac autonomic regulation. Int Arch Med 2013; 6:11. [PMID: 23497654 PMCID: PMC3599979 DOI: 10.1186/1755-7682-6-11] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/26/2013] [Accepted: 03/04/2013] [Indexed: 11/10/2022] Open
Abstract
BACKGROUND The literature has already demonstrated that cigarette influences the cardiovascular system. In this study, we performed a literature review in order to investigate the relationship between sidestream cigarette smoke (SSCS) and cardiac autonomic regulation. METHODS Searches were performed on Medline, SciELO, Lilacs and Cochrane databases using the crossing between the key-words: "cigarette smoking", "autonomic nervous system", "air pollution" and "heart rate variability". RESULTS The selected studies indicated that SSCS exposure affects the sympathetic and parasympathetic responses to changes in arterial blood pressure. Moreover, heart rate responses to environmental tobacco smoke are increased in smokers compared to non-smokers. The mechanism involved on this process suggest increased oxidative stress in brainstem areas that regulate the cardiovascular system. CONCLUSION Further studies are necessary to add new elements in the literature to improve new therapies to treat cardiovascular disorders in subjects exposed to sidestream cigarette smoke.
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Affiliation(s)
- Vitor E Valenti
- Department of Speech Language and Hearing therapy, Faculty of Philosophy and Sciences, UNESP, Av, Higyno Muzzi Filho, 737, Marilia, SP 17,525-900, Brazil.
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Kathuria S, Mahadevan N, Balakumar P. Possible involvement of PPARγ-associated eNOS signaling activation in rosuvastatin-mediated prevention of nicotine-induced experimental vascular endothelial abnormalities. Mol Cell Biochem 2013; 374:61-72. [PMID: 23149826 DOI: 10.1007/s11010-012-1505-6] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/02/2012] [Accepted: 10/25/2012] [Indexed: 12/30/2022]
Abstract
Nicotine exposure via cigarette smoking and tobacco chewing is associated with vascular complications. The present study investigated the effect of rosuvastatin in nicotine (2 mg/kg/day, i.p., 4 weeks)-induced vascular endothelial dysfunction (VED) in rats. The development of VED was assessed by employing isolated aortic ring preparation and estimating aortic and serum nitrite/nitrate concentration. Further, scanning electron microscopy and hematoxylin-eosin staining of thoracic aorta were performed to assess the vascular endothelial integrity. Moreover, oxidative stress was assessed by estimating aortic superoxide anion generation and serum thiobarbituric acid-reactive substances. The nicotine administration produced VED by markedly reducing acetylcholine-induced endothelium-dependent relaxation, impairing the integrity of vascular endothelium, decreasing aortic and serum nitrite/nitrate concentration, increasing oxidative stress, and inducing lipid alteration. However, treatment with rosuvastatin (10 mg/kg/day, i.p., 4 weeks) markedly attenuated nicotine-induced vascular endothelial abnormalities, oxidative stress, and lipid alteration. Interestingly, the co-administration of peroxisome proliferator-activated receptor γ (PPARγ) antagonist, GW9662 (1 mg/kg/day, i.p., 2 weeks) submaximally, significantly prevented rosuvastatin-induced improvement in vascular endothelial integrity, endothelium-dependent relaxation, and nitrite/nitrate concentration in rats administered nicotine. However, GW9662 co-administration did not affect rosuvastatin-associated vascular anti-oxidant and lipid-lowering effects. The incubation of aortic ring, isolated from rosuvastatin-treated nicotine-administered rats, with L-NAME (100 μM), an inhibitor of nitric oxide synthase (NOS), significantly attenuated rosuvastatin-induced improvement in acetylcholine-induced endothelium-dependent relaxation. Rosuvastatin prevents nicotine-induced vascular endothelial abnormalities by activating PPARγ and endothelial NOS signaling pathways. Moreover, the PPARγ-independent anti-oxidant and lipid-lowering effects of rosuvastatin might additionally play a role in the improvement of vascular endothelial function.
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Affiliation(s)
- Sonam Kathuria
- Cardiovascular Pharmacology Division, Department of Pharmacology, Rajendra Institute of Technology and Sciences, Sirsa, 125 055, India
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NF-κB pathway mediates vascular smooth muscle response to nicotine. Int J Biochem Cell Biol 2013; 45:375-83. [DOI: 10.1016/j.biocel.2012.10.016] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/15/2012] [Revised: 10/29/2012] [Accepted: 10/30/2012] [Indexed: 01/11/2023]
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Gu Z, Fonseca V, Hai CM. Nicotinic acetylcholine receptor mediates nicotine-induced actin cytoskeletal remodeling and extracellular matrix degradation by vascular smooth muscle cells. Vascul Pharmacol 2013; 58:87-97. [PMID: 22940282 PMCID: PMC3530635 DOI: 10.1016/j.vph.2012.08.003] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/19/2012] [Revised: 08/13/2012] [Accepted: 08/16/2012] [Indexed: 01/21/2023]
Abstract
Cigarette smoking is a significant risk factor for atherosclerosis, which involves the invasion of vascular smooth muscle cells (VSMCs) from the media to intima. A hallmark of many invasive cells is actin cytoskeletal remodeling in the form of podosomes, accompanied by extracellular matrix (ECM) degradation. A7r5 VSMCs form podosomes in response to PKC activation. In this study, we found that cigarette smoke extract, nicotine, and the cholinergic agonist, carbachol, were similarly effective in inducing the formation of podosome rosettes in A7r5 VSMCs. α-Bungarotoxin and atropine experiments confirmed the involvement of nicotinic acetylcholine receptors (nAChRs). Western blotting and immunofluorescence experiments revealed the aggregation of nAChRs at podosome rosettes. Cycloheximide experiments and media exchange experiments suggested that autocrine factor(s) and intracellular phenotypic modulation are putative mechanisms. In situ zymography experiments indicated that, in response to PKC activation, nicotine-treated cells degraded ECM near podosome rosettes, and possibly endocytose ECM fragments to intracellular compartments. Invasion assay of human aortic smooth muscle cells indicated that nicotine and PKC activation individually and synergistically enhanced cell invasion through ECM. Results from this study suggest that nicotine enhances the ability of VSMCs to degrade and invade ECM. nAChR activation, actin cytoskeletal remodeling and phenotypic modulation are possible mechanisms.
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MESH Headings
- Actin Cytoskeleton/drug effects
- Actin Cytoskeleton/metabolism
- Animals
- Aorta/cytology
- Aorta/drug effects
- Aorta/metabolism
- Blotting, Western
- Carbachol/pharmacology
- Cells, Cultured
- Extracellular Matrix/drug effects
- Extracellular Matrix/metabolism
- Fluorescent Antibody Technique
- Humans
- Muscle, Smooth, Vascular/cytology
- Muscle, Smooth, Vascular/drug effects
- Muscle, Smooth, Vascular/metabolism
- Myocytes, Smooth Muscle/drug effects
- Myocytes, Smooth Muscle/metabolism
- Nicotine/toxicity
- Protein Kinase C/metabolism
- Rats
- Receptors, Nicotinic/metabolism
- Smoke/adverse effects
- Smoking/adverse effects
- Nicotiana/chemistry
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Affiliation(s)
- Zhizhan Gu
- Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115
| | - Vera Fonseca
- Department of Molecular Pharmacology, Physiology & Biotechnology, Brown University, Providence, RI 02912, USA
| | - Chi-Ming Hai
- Department of Molecular Pharmacology, Physiology & Biotechnology, Brown University, Providence, RI 02912, USA
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Chellan G, Srikumar S, Varma AK, Mangalanandan TS, Sundaram KR, Jayakumar RV, Bal A, Kumar H. Foot care practice - the key to prevent diabetic foot ulcers in India. Foot (Edinb) 2012; 22:298-302. [PMID: 22999359 DOI: 10.1016/j.foot.2012.08.007] [Citation(s) in RCA: 34] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/18/2012] [Revised: 08/20/2012] [Accepted: 08/21/2012] [Indexed: 02/04/2023]
Abstract
BACKGROUND The magnitude of diabetic foot ulcers (DFUs) and the amputation rates due to DFUs remain high even in developing and developed countries. Yet, the influence of knowledge, attitude, and practice (KAP) of diabetic foot care (DFC) on DFU incidence is not studied much. OBJECTIVE To study causal relationship between knowledge, attitude and practice (KAP) on DFC between diabetic patients with and without DFUs; and the risk factors associated with DFUs. METHODS A consecutive of 203 diabetic patients (103 with DFU and 100 without DFU) were included in the study. Their demographic details, medical history, and personal habits were recorded. KAP on DFC was assessed using a questionnaire. Responses were recorded, scored, and analyzed. RESULTS Of the cohort, 67.5% were males, mean age: 59.9 ± 11.4 years. Patients without DFU had good knowledge on DFC compared to those with DFU (86% versus 69.9%) (p<0.001). Incidence of DFU was 9% and 39.8% (p<0.001) among patients who practiced and not practiced DFC respectively. 88% patients with and without DFUs; showed favorable attitude toward adopting DFC. Risk factors - diabetic peripheral neuropathy, peripheral vascular disease, retinopathy, nephropathy, smoking, tobacco chewing and alcohol consumption were significantly (p<0.001) associated with DFUs. CONCLUSIONS An inverse relationship between DFU and foot care knowledge as well as practice was observed. Apart from tight glycemic control, diabetic patients must be educated and motivated on proper foot care practice and life style modifications for preventing DFUs.
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Affiliation(s)
- Gopi Chellan
- Department of Endocrinology, Diabetes and Podiatric Surgery, School of Medicine, Amrita Institute of Medical Sciences and Research Center, Kerala, India.
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Balakumar P, Kathuria S. Submaximal PPARγ activation and endothelial dysfunction: new perspectives for the management of cardiovascular disorders. Br J Pharmacol 2012; 166:1981-92. [PMID: 22404217 DOI: 10.1111/j.1476-5381.2012.01938.x] [Citation(s) in RCA: 61] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022] Open
Abstract
PPARγ activation plays an important role in glucose metabolism by enhancing insulin sensitization. PPARγ is a primary target for thiazolidinedione-structured insulin sensitizers like pioglitazone and rosiglitazone employed for the treatment of type 2 diabetes mellitus. Additionally, PPARγ activation inhibits adhesion cascades and detrimental vascular inflammatory events. Importantly, activation of PPARγ plays a distinctive role in regulating the physiology and expression of endothelial nitric oxide synthase (eNOS) in the endothelium, resulting in enhanced generation of vascular nitric oxide. The PPARγ activation-mediated vascular anti-inflammatory and direct endothelial functional regulatory actions could, therefore, be beneficial in improving the vascular function in patients with atherosclerosis and hypertension with or without diabetes mellitus. Despite the disappointing cardiac side effect profile of rosiglitazone-like PPARγ full agonists, the therapeutic potential of novel pharmacological agents targeting PPARγ submaximally cannot be ruled out. This review discusses the potential regulatory role of PPARγ on eNOS expression and activation in improving the function of vascular endothelium. We argue that partial/submaximal activation of PPARγ could be a major target for vascular endothelial functional improvement. Interestingly, newly synthesized partial agonists of PPARγ such as balaglitazone, MBX-102, MK-0533, PAR-1622, PAM-1616, KR-62776 and SPPARγM5 are devoid of or have a reduced tendency to cause the adverse effects associated with full agonists of PPARγ. We propose that the vascular protective properties of pharmacological agents, which submaximally activate PPARγ, should be investigated. Moreover, the therapeutic opportunities of agents that submaximally activate PPARγ in preventing vascular endothelial dysfunction (VED) and VED-associated cardiovascular disorders are discussed.
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Affiliation(s)
- Pitchai Balakumar
- Cardiovascular Pharmacology Division, Department of Pharmacology, Institute of Pharmacy, Rajendra Institute of Technology and Sciences-RITS, Sirsa, India.
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Abstract
AIMS To provide an initial abuse liability assessment of an electronic cigarette (EC) in current tobacco cigarette smokers. DESIGN The first of four within-subject sessions was an EC sampling session that involved six, 10-puff bouts (30 seconds inter-puff interval), each bout separated by 30 minutes. In the remaining three sessions participants made choices between 10 EC puffs and varying amounts of money, 10 EC puffs and a varying number of own brand cigarette (OB) puffs, or 10 OB puffs and varying amounts of money using the multiple-choice procedure (MCP). The MCP was completed six times at 30-minute intervals, and one choice was reinforced randomly at each trial. SETTING Clinical laboratory. PARTICIPANTS Twenty current tobacco cigarette smokers. MEASUREMENTS Sampling session outcome measures included plasma nicotine, cardiovascular response and subjective effects. Choice session outcome was the cross-over value on the MCP. FINDINGS EC use resulted in significant nicotine delivery, tobacco abstinence symptom suppression and increased product acceptability ratings. On the MCP, participants chose to receive 10 EC puffs over an average of $1.06 or three OB puffs and chose 10 OB puffs over an average of $1.50 (P < 0.003). CONCLUSIONS Electronic cigarettes can deliver clinically significant amounts of nicotine and reduce cigarette abstinence symptoms and appear to have lower potential for abuse relative to traditional tobacco cigarettes, at least under certain laboratory conditions.
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Affiliation(s)
- Andrea R Vansickel
- Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA
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El-Mas MM, El-Gowelli HM, El-Gowilly SM, Fouda MA, Helmy MM. Estrogen provokes the depressant effect of chronic nicotine on vagally mediated reflex chronotropism in female rats. J Pharmacol Exp Ther 2012; 342:568-75. [PMID: 22619254 DOI: 10.1124/jpet.112.191940] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 03/08/2025] Open
Abstract
We recently reported that acute nicotine impairs reflex tachycardic activity in estrogen-depleted, but not estrogen-repleted, female rats, suggesting a restraining influence for estrogen against the nicotine effect. In this study, we tested whether the baroreflex-protective effect of estrogen can be replicated when nicotine was administered chronically. We also report on the dose dependence and autonomic modulation of the nicotine-baroreflex interaction. The effects of nicotine (0.5, 1, or 2 mg/kg/day for 14 days) on baroreflex curves relating changes in heart rate to increases [phenylephrine (PE)] or decreases [sodium nitroprusside (SNP)] in blood pressure were evaluated in sham-operated (SO), ovariectomized (OVX), and estrogen-replaced OVX (OVXE(2)) rats. Slopes of the curves were taken as a measure of baroreflex sensitivity (BRS(PE) and BRS(SNP)). In SO rats, both reflex bradycardic and tachycardic responses were attenuated by nicotine in a dose-related fashion. In nicotine-treated rats, blockade of β-adrenergic (propranolol), but not muscarinic (atropine), receptors caused additional reductions in reflex chronotropic responses, implying that nicotine selectively impairs reflex vagal activity. OVX selectively decreased BRS(PE) but not BRS(SNP) and abolished the nicotine-induced impairment of either response. These effects of OVX were reversed after treatment with estrogen or the estrogen receptor modulator raloxifene. In atropine-treated rats, comparable BRS values were demonstrated in all rat preparations regardless of the estrogen or nicotine milieu. Collectively, the inhibition of vagal activity accounts for the depressant effect of chronic nicotine on baroreflex activity. Furthermore, contrary to nicotine's acute effects, the baroreflex-attenuating effect of chronic nicotine is exacerbated by estrogen.
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Affiliation(s)
- Mahmoud M El-Mas
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Alexandria, Egypt.
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Vinader-Caerols C, Monleón S, Carrasco C, Parra A. Effects of Alcohol, Coffee, and Tobacco, Alone or in Combination, on Physiological Parameters and Anxiety in a Young Population. JOURNAL OF CAFFEINE RESEARCH 2012; 2:70-76. [PMID: 24761267 DOI: 10.1089/jcr.2012.0018] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/12/2022]
Abstract
OBJECTIVE The objective was to evaluate the effects of a single dose of alcohol, caffeine, and nicotine, alone or in combination, on physiological parameters (systolic and diastolic blood pressure [SBP and DBP] and heart rate [HR]) and state-trait anxiety in healthy young volunteers. METHOD The procedure reproduces the conditions under which the subjects (n=76) usually ingest alcohol (through an alcoholic beverage), caffeine (through a cup of coffee), and nicotine (by smoking a cigarette), separately or in combination, according to their consumption habits of each individual. SBP and DBP, HR, and state anxiety (SA) were registered before (phase 1) and after (phase 2) treatment. RESULTS Intake of alcohol or alcohol-nicotine reduced DBP. Comparisons between control and combined treatment (coffee-alcohol-nicotine) groups revealed a decrease in HR in the former group but not in the latter. The coffee consumers alone exhibited a tendency toward an increase in SA, while the control group showed a tendency toward a decrease in this measure. When Phase 1 and Phase 2 were compared, a decrease was observed in SBP (alcohol and coffee-alcohol groups), DBP (alcohol and alcohol-nicotine groups), HR (all groups, except coffee-alcohol and coffee-alcohol-nicotine groups), and SA (coffee-alcohol-nicotine group). CONCLUSIONS (i) A low dose of alcohol, either alone or in combination with a cigarette, decreases DBP but not SBP; (ii) the polyconsumption of coffee, alcohol, and nicotine blocks the adaptation response (the reduction in HR in control subjects in the second phase); (iii) an increase of SA is observed after consuming coffee, while the opposite occurs in control subjects (a decrease of SA).
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Affiliation(s)
| | - Santiago Monleón
- Department of Psychobiology, University of Valencia , Valencia, Spain
| | - Carmen Carrasco
- Department of Psychobiology, University of Valencia , Valencia, Spain
| | - Andres Parra
- Department of Psychobiology, University of Valencia , Valencia, Spain
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Kuhn J, Vollmer T, Martin C, Hendig D, Knabbe C. Fast and sample cleanup-free measurement of nicotine and cotinine by stable isotope dilution ultra-performance liquid chromatography-tandem mass spectrometry. J Pharm Biomed Anal 2012; 67-68:137-43. [PMID: 22608097 DOI: 10.1016/j.jpba.2012.04.036] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/14/2012] [Revised: 04/24/2012] [Accepted: 04/25/2012] [Indexed: 11/24/2022]
Abstract
We developed a stable isotope dilution ultra-performance liquid chromatography-electrospray ionization tandem mass spectrometry assay to measure nicotine and cotinine, the major oxidative and pharmacologically less active metabolite of nicotine, in human urine. A simple dilution step was used as sample preparation and the measurement of nicotine and cotinine was performed during a 1.5-min run-time using nicotine-D₄ and cotinine-D₄ as internal standards. Multiple calibration curves for the analysis of both nicotine and cotinine exhibited a consistent excellent linearity and reproducibility in the range of 5-35,000 μg/L (r>0.999). Limits of Detection were 0.7 μg/L for nicotine and 0.4 μg/L for cotinine, and Lower Limits of Quantification were 1.7 μg/L for nicotine and 1.1 μg/L for cotinine. The intraassay coefficients of variation (CVs) for nicotine and cotinine were <4% and <2%, respectively, the interassay CVs were <6% for nicotine and <4% for cotinine. The inaccuracy was <6% for both substances. The mean recovery was 103.2% (range 96.8-105.1%) for nicotine and 97.4% (range 94.3-99.2%) for cotinine. A method comparison showed that the values of nicotine metabolites in human urine samples (n=98) measured by a commercially available chemiluminescent immunoassay tested on analyzer IMMULITE 2000 were much higher than the cotinine concentration in the same urine samples measured by our UPLC-MS/MS assay. The Passing-Bablok regression line was: immunoassay=4.62 (UPLC-MS/MS)+3.64 [μg/L]; r=0.75. This robust, sensitive and interference-free UPLC-MS/MS assay permits rapid and accurate determination of nicotine and cotinine in human urine.
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Affiliation(s)
- Joachim Kuhn
- Institut für Laboratoriums- und Transfusionsmedizin, Herz- und Diabeteszentrum Nordrhein-Westfalen, Universitätsklinik der Ruhr-Universität Bochum, 32545 Bad Oeynhausen, Germany.
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45
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Pathogenesis of abdominal aortic aneurysms: role of nicotine and nicotinic acetylcholine receptors. Mediators Inflamm 2012; 2012:103120. [PMID: 22529515 PMCID: PMC3317239 DOI: 10.1155/2012/103120] [Citation(s) in RCA: 32] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/30/2011] [Revised: 01/11/2012] [Accepted: 01/11/2012] [Indexed: 11/18/2022] Open
Abstract
Inflammation, proteolysis, smooth muscle cell apoptosis, and angiogenesis have been implicated in the pathogenesis of abdominal aortic aneurysms (AAAs), although the well-defined initiating mechanism is not fully understood. Matrix metalloproteinases (MMPs) such as MMP-2 and -9 and other proteinases degrading elastin and extracellular matrix are the critical pathogenesis of AAAs. Among the risk factors of AAAs, cigarette smoking is an irrefutable one. Cigarette smoke is practically involved in various aspects of the AAA pathogenesis. Nicotine, a major alkaloid in tobacco leaves and a primary component in cigarette smoke, can stimulate the MMPs expression by vascular SMCs, endothelial cells, and inflammatory cells in vascular wall and induce angiogenesis in the aneurysmal tissues. However, for the inflammatory and apoptotic processes in the pathogenesis of AAAs, nicotine seems to be moving in just the opposite direction. Additionally, the effects of nicotine are probably dose dependent or associated with the exposure duration and may be partly exerted by its receptors—nicotinic acetylcholine receptors (nAChRs). In this paper, we will mainly discuss the pathogenesis of AAAs involving inflammation, proteolysis, smooth muscle cell apoptosis and angiogenesis, and the roles of nicotine and nAChRs.
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El-Mas MM, Fouda MA, El-gowilly SM, Saad EI. Central estrogenic pathways protect against the depressant action of acute nicotine on reflex tachycardia in female rats. Toxicol Appl Pharmacol 2012; 258:410-7. [DOI: 10.1016/j.taap.2011.12.011] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/18/2011] [Revised: 12/07/2011] [Accepted: 12/09/2011] [Indexed: 11/24/2022]
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Huttunen T, Riihinen A, Pukkala E, von und zu Fraunberg M, Koivisto T, Ronkainen A, Rinne J, Hernesniemi J, Sankila R, Jääskeläinen JE. Increased Relative Risk of Lung Cancer in 2,904 Patients with Saccular Intracranial Aneurysm Disease in Eastern Finland. Neuroepidemiology 2012; 38:93-9. [DOI: 10.1159/000335041] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/11/2011] [Accepted: 11/14/2011] [Indexed: 12/31/2022] Open
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Weil J, Stritzke J, Schunkert H. [Risk factor "smoking" : smoking cessation in patients with cardiovascular diseases]. Internist (Berl) 2011; 53:45-50. [PMID: 22146935 DOI: 10.1007/s00108-011-2892-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/14/2022]
Abstract
Smoking is the most frequent cause of avoidable premature death. Annually, almost 6 million people die due to nicotine consumption. Comparing modifiable cardiovascular risk factors, smoking has the strongest impact on cardiovascular mortality. More than 50% of all premature myocardial infarctions are related to nicotine consumption. Even in patients with known coronary disease receiving optimal medical therapy, there is a remarkable additional preventive effect of smoking cessation detectable. Therefore, smoking cessation is an essential component of primary and secondary prevention strategies. Smoking cessation programs applying a combination of behavior therapy and supporting medical treatment have been demonstrated to be the most effective.
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Affiliation(s)
- J Weil
- Medizinische Klinik 2, Universitätsklinik Schleswig-Holstein, Campus Lübeck, Lübeck, Deutschland.
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El-Seweidy MM, Mohamed HE, Asker ME, Atteia HH. Nicotine and vascular endothelial dysfunction in female ovariectomized rats: role of estrogen replacement therapy. J Pharm Pharmacol 2011; 64:108-19. [PMID: 22150678 DOI: 10.1111/j.2042-7158.2011.01377.x] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
OBJECTIVES The protective effects of estrogen replacement therapy (ERT) against oxidative injury and endothelial dysfunction in the aortic tissues induced with nicotine in ovariectomized (OVX) rats were investigated. METHODS Female rats were divided into a sham-operated group (n = 8) and four groups in which OVX rats received either vehicle (0.1 ml sesame oil, i.m., n = 8), or nicotine (0.1 mg/kg, s.c., n = 8), or estradiol benzoate (0.1 mg/kg, i.m., n = 8), or both nicotine and estradiol benzoate (n = 8) starting at week 5 after the surgery and continuing for the following 6 weeks. KEY FINDINGS ERT was effective in preventing the rise in plasma lipid profile, atherogenic index and the level of induced endothelin-1 (ET-1) in nicotine-treated OVX rats. It also reduced aortic malondialdehyde, hydroxyproline levels, calcium content and caspase-3 expression induced in nicotine-treated OVX rats. ERT increased serum estradiol, high-density lipoprotein cholesterol and nitric oxide levels in nicotine-treated OVX rats. Furthermore, ERT was effective in restoring reduced glutathione and cyclic guanosine monophosphate contents and endothelial nitric oxide synthase expression in aortic tissues of nicotine-treated OVX rats. CONCLUSIONS Short-term ERT could be a promising therapeutic strategy to minimize nicotine-induced oxidative stress and vascular endothelial dysfunction in menopausal women subjected to environmental smoke.
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Affiliation(s)
- Mohamed M El-Seweidy
- Department of Biochemistry, Faculty of Pharmacy, University of Zagazig, Zagazig, Egypt
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Ferrari MFR, Coelho EF, Farizatto KLG, Chadi G, Fior-Chadi DR. Modulation of tyrosine hydroxylase, neuropeptide y, glutamate, and substance p in Ganglia and brain areas involved in cardiovascular control after chronic exposure to nicotine. Int J Hypertens 2011; 2011:216464. [PMID: 21822476 PMCID: PMC3147125 DOI: 10.4061/2011/216464] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/11/2011] [Revised: 06/03/2011] [Accepted: 06/14/2011] [Indexed: 11/20/2022] Open
Abstract
Considering that nicotine instantly interacts with central and peripheral nervous systems promoting cardiovascular effects after tobacco smoking, we evaluated the modulation of glutamate, tyrosine hydroxylase (TH), neuropeptide Y (NPY), and substance P (SP) in nodose/petrosal and superior cervical ganglia, as well as TH and NPY in nucleus tractus solitarii (NTS) and hypothalamic paraventricular nucleus (PVN) of normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR) after 8 weeks of nicotine exposure. Immunohistochemical and in situ hybridization data demonstrated increased expression of TH in brain and ganglia related to blood pressure control, preferentially in SHR, after nicotine exposure. The alkaloid also increased NPY immunoreactivity in ganglia, NTS, and PVN of SHR, in spite of decreasing its receptor (NPY1R) binding in NTS of both strains. Nicotine increased SP and glutamate in ganglia. In summary, nicotine positively modulated the studied variables in ganglia while its central effects were mainly constrained to SHR.
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Affiliation(s)
- Merari F R Ferrari
- Departamento de Genetica e Biologia Evolutiva, Instituto de Biociencias, Universidade de São Paulo, Rua do Matao 277, 05508-090 São Paulo, SP, Brazil
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