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Guan H, Zhou P, Qi Y, Huang H, Wang J, Liu X. Cigarette smoke-induced trophoblast cell ferroptosis in rat placenta and the effects of L-arginine intervention. ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY 2022; 243:114015. [PMID: 36030684 DOI: 10.1016/j.ecoenv.2022.114015] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 05/26/2022] [Revised: 08/08/2022] [Accepted: 08/21/2022] [Indexed: 06/15/2023]
Abstract
Cigarette smoke (CS) disrupts placental development, and impairs fetal health and maternal fertility, thus resulting in low birth weight, premature delivery, and spontaneous abortion; however, the underlying mechanisms remain unclear. This study investigated the mechanism through which CS impairs placental trophoblast cell viability and function. An in vivo study in pregnant rats exposed to CS indicated that CS- exposure decreased antioxidant factors expression and blocked NRF2 activation in the placenta. Anti-ferroptosis regulators expression was downregulated, and pro-ferroptosis regulators expression was upregulated in placentas from CS-exposed rats. Further analysis revealed that cigarette smoke extract (CSE) led to peroxins downregulation and decreased the number of peroxisomes. An in vitro study in HTR-8/SVneo(HTR-8) cells showed that CSE led to free iron and ROS accumulation, and subsequently induced lipid peroxidation and cell death. Ferroptosis inhibitors and the antioxidant L-arginine (ARG) partially inhibited CSE-induced cell death. ARG partially alleviated the toxic effects of CSE by promoting antioxidant factors expression in placenta and suppressing HTR-8 cell ferroptosis. Knockdown of PEX14, a peroxisome biogenesis marker, led to the downregulation of multiple PEXs, thus increasing intracellular H2O2 levels and inducing HTR-8 cell ferroptosis. These findings demonstrated that ferroptosis is responsible for CSE-induced trophoblast cell death and suggest that peroxisome dysfunction is involved in CSE-induced ferroptosis. Therefore, CSE-induced ferroptosis may serve as a potential therapeutic target for preventing adverse pregnancy outcomes.
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Affiliation(s)
- Hongbo Guan
- Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang 110004, China
| | - Pei Zhou
- Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang 110004, China
| | - Ying Qi
- Virology Laboratory, Shengjing Hospital of China Medical University, Shenyang 110004, China
| | - Huan Huang
- Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang 110004, China
| | - Jun Wang
- Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang 110004, China
| | - Xiaomei Liu
- Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang 110004, China.
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Sampilvanjil A, Karasawa T, Yamada N, Komada T, Higashi T, Baatarjav C, Watanabe S, Kamata R, Ohno N, Takahashi M. Cigarette smoke extract induces ferroptosis in vascular smooth muscle cells. Am J Physiol Heart Circ Physiol 2020; 318:H508-H518. [PMID: 31975626 DOI: 10.1152/ajpheart.00559.2019] [Citation(s) in RCA: 114] [Impact Index Per Article: 22.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]
Abstract
Cigarette smoking is a major risk factor for aortic aneurysm and dissection; however, no causative link between smoking and these aortic disorders has been proven. In the present study, we investigated the mechanism by which cigarette smoke affects vascular wall cells and found that cigarette smoke extract (CSE) induced a novel form of regulated cell death termed ferroptosis in vascular smooth muscle cells (VSMCs). CSE markedly induced cell death in A7r5 cells and primary rat VSMCs, but not in endothelial cells, which was completely inhibited by specific ferroptosis inhibitors [ferrostatin-1 (Fer-1) and Liproxstatin-1] and an iron chelator (deferoxamine). CSE-induced VSMC death was partially inhibited by a GSH precursor (N-acetyl cysteine) and an NADPH oxidase inhibitor [diphenyleneiodonium chloride (DPI)], but not by inhibitors of pan-caspases (Z-VAD), caspase-1 (Z-YVAD), or necroptosis (necrostatin-1). CSE also upregulated IL-1β, IL-6, TNF-α, matrix metalloproteinase (MMP)-2, MMP-9, and TIMP-1 (tissue inhibitor of metalloproteinase)in A7r5 cells, which was inhibited by Fer-1. Furthermore, CSE induced the upregulation of Ptgs2 mRNA, lipid peroxidation, and intracellular GSH depletion, which are key features of ferroptosis. VSMC ferroptosis was induced by acrolein and methyl vinyl ketone, major constituents of CSE. Furthermore, CSE caused medial VSMC loss in ex vivo aortas. Electron microscopy analysis showed mitochondrial damage and fragmentation in medial VSMCs of CSE-treated aortas. All of these manifestations were partially restored by Fer-1. These findings demonstrate that ferroptosis is responsible for CSE-induced VSMC death and suggest that ferroptosis is a potential therapeutic target for preventing aortic aneurysm and dissection.NEW & NOTEWORTHY Cigarette smoke extract (CSE)-induced cell death in rat vascular smooth muscle cells (VSMCs) was completely inhibited by specific ferroptosis inhibitors and an iron chelator. CSE also induced the upregulation of Ptgs2 mRNA, lipid peroxidation, and intracellular GSH depletion, which are key features of ferroptosis. CSE caused medial VSMC loss in ex vivo aortas. These findings demonstrate that ferroptosis is responsible for CSE-induced VSMC death.
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Affiliation(s)
- Ariunaa Sampilvanjil
- Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan
| | - Tadayoshi Karasawa
- Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan
| | - Naoya Yamada
- Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan
| | - Takanori Komada
- Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan
| | - Tsunehito Higashi
- Department of Cellular Pharmacology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan
| | - Chintogtokh Baatarjav
- Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan
| | - Sachiko Watanabe
- Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan
| | - Ryo Kamata
- Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan
| | - Nobuhiko Ohno
- Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University, Tochigi, Japan.,Division of Ultrastructural Research, National Institute for Physiological Sciences, Aichi, Japan
| | - Masafumi Takahashi
- Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan
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Pedret A, Fernández-Castillejo S, Valls RM, Catalán Ú, Rubió L, Romeu M, Macià A, López de Las Hazas MC, Farràs M, Giralt M, Mosele JI, Martín-Peláez S, Remaley AT, Covas MI, Fitó M, Motilva MJ, Solà R. Cardiovascular Benefits of Phenol-Enriched Virgin Olive Oils: New Insights from the Virgin Olive Oil and HDL Functionality (VOHF) Study. Mol Nutr Food Res 2018; 62:e1800456. [PMID: 29956886 PMCID: PMC8456742 DOI: 10.1002/mnfr.201800456] [Citation(s) in RCA: 26] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/09/2018] [Indexed: 01/09/2023]
Abstract
SCOPE The main findings of the "Virgin Olive Oil and HDL Functionality" (VOHF) study and other related studies on the effect of phenol-enriched virgin olive oil (VOO) supplementation on cardiovascular disease are integrated in the present work. METHODS AND RESULTS VOHF assessed whether VOOs, enriched with their own phenolic compounds (FVOO) or with those from thyme (FVOOT), improve quantity and functionality of HDL. In this randomized, double-blind, crossover, and controlled trial, 33 hypercholesterolemic subjects received a control VOO (80 mg kg-1 ), FVOO (500 mg kg-1 ), and FVOOT (500 mg kg-1 ; 1:1) for 3 weeks. Both functional VOOs promoted cardioprotective changes, modulating HDL proteome, increasing fat-soluble antioxidants, improving HDL subclasses distribution, reducing the lipoprotein insulin resistance index, increasing endogenous antioxidant enzymes, protecting DNA from oxidation, ameliorating endothelial function, and increasing fecal microbial metabolic activity. Additional cardioprotective benefits were observed according to phenol source and content in the phenol-enriched VOOs. These insights support the beneficial effects of OO and PC from different sources. CONCLUSION Novel therapeutic strategies should increase HDL-cholesterol levels and enhance HDL functionality. The tailoring of phenol-enriched VOOs is an interesting and useful strategy for enhancing the functional quality of HDL, and thus, it can be used as a complementary tool for the management of hypercholesterolemic individuals.
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Affiliation(s)
- Anna Pedret
- Eurecat, Centre Tecnològic de Catalunya, Unitat de Nutrició i Salut, Functional Nutrition, Oxidation, and CVD Research Group (NFOC-Salut), 43204, Reus, Spain
- Facultat de Medicina i Ciències de la Salut, Functional Nutrition, Oxidation and Cardiovascular Diseases Group (NFOC-Salut), Universitat Rovira i Virgili, 43201, Reus, Spain
| | - Sara Fernández-Castillejo
- Facultat de Medicina i Ciències de la Salut, Functional Nutrition, Oxidation and Cardiovascular Diseases Group (NFOC-Salut), Universitat Rovira i Virgili, 43201, Reus, Spain
- Institut d'Investigació Sanitaria Pere Virgili, 43204, Reus, Spain
| | - Rosa-Maria Valls
- Facultat de Medicina i Ciències de la Salut, Functional Nutrition, Oxidation and Cardiovascular Diseases Group (NFOC-Salut), Universitat Rovira i Virgili, 43201, Reus, Spain
| | - Úrsula Catalán
- Facultat de Medicina i Ciències de la Salut, Functional Nutrition, Oxidation and Cardiovascular Diseases Group (NFOC-Salut), Universitat Rovira i Virgili, 43201, Reus, Spain
- Institut d'Investigació Sanitaria Pere Virgili, 43204, Reus, Spain
| | - Laura Rubió
- Facultat de Medicina i Ciències de la Salut, Functional Nutrition, Oxidation and Cardiovascular Diseases Group (NFOC-Salut), Universitat Rovira i Virgili, 43201, Reus, Spain
- Antioxidants Research Group, Food Technology Department, Universitat de Lleida-Agrotecnio Center, 25198, Lleida, Spain
| | - Marta Romeu
- Facultat de Medicina i Ciències de la Salut, Functional Nutrition, Oxidation and Cardiovascular Diseases Group (NFOC-Salut), Universitat Rovira i Virgili, 43201, Reus, Spain
| | - Alba Macià
- Antioxidants Research Group, Food Technology Department, Universitat de Lleida-Agrotecnio Center, 25198, Lleida, Spain
| | - Maria Carmen López de Las Hazas
- Antioxidants Research Group, Food Technology Department, Universitat de Lleida-Agrotecnio Center, 25198, Lleida, Spain
- Laboratory of Epigenetics of Lipid Metabolism, Instituto Madrileño de Estudios Avanzados-Alimentación, CEI UAM+CSIC, 28049, Madrid, Spain
| | - Marta Farràs
- Institut d'Investigacions Biomèdiques (IIB) Sant Pau, 08025, Barcelona, Spain
- Cardiovascular Risk and Nutrition Research Group, REGICOR Study Group, Hospital del Mar Research Institute (IMIM), 08003, Barcelona, Spain
| | - Montse Giralt
- Facultat de Medicina i Ciències de la Salut, Functional Nutrition, Oxidation and Cardiovascular Diseases Group (NFOC-Salut), Universitat Rovira i Virgili, 43201, Reus, Spain
| | - Juana I Mosele
- Antioxidants Research Group, Food Technology Department, Universitat de Lleida-Agrotecnio Center, 25198, Lleida, Spain
- Instituto de Bioquímica y Medicina Molecular (IBIMOL), CONICET - Universidad de Buenos Aires, 1053, Buenos Aires, Argentina
- Facultad de Farmacia y Bioquímica, Departamento de Química Analítica y Fisicoquímica, Cátedra de Fisicoquímica, Universidad de Buenos Aires, C1113AAD, Buenos Aires, Argentina
| | - Sandra Martín-Peláez
- Spanish Biomedical Research Networking Centre (CIBER), Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, 28029, Madrid, Spain
- Cardiovascular Risk and Nutrition Research Group, REGICOR Study Group, Hospital del Mar Research Institute (IMIM), 08003, Barcelona, Spain
| | - Alan T Remaley
- Department of Laboratory Medicine Clinical Center, National Institutes of Health, 20814, Bethesda, MD, USA
- Lipoprotein Metabolism Section Cardio-Pulmonary Branch National Heart, Lung and Blood Institute National Institutes of Health, 20814, Bethesda, MD, USA
| | - Maria-Isabel Covas
- Spanish Biomedical Research Networking Centre (CIBER), Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, 28029, Madrid, Spain
- Cardiovascular Risk and Nutrition Research Group, REGICOR Study Group, Hospital del Mar Research Institute (IMIM), 08003, Barcelona, Spain
- NUPROAS (Nutritional Project Assessment), Handesbolag (NUPROAS HB), 13100, Nacka, Sweden
| | - Montse Fitó
- Spanish Biomedical Research Networking Centre (CIBER), Physiopathology of Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, 28029, Madrid, Spain
- Cardiovascular Risk and Nutrition Research Group, REGICOR Study Group, Hospital del Mar Research Institute (IMIM), 08003, Barcelona, Spain
| | - Maria-José Motilva
- Antioxidants Research Group, Food Technology Department, Universitat de Lleida-Agrotecnio Center, 25198, Lleida, Spain
| | - Rosa Solà
- Facultat de Medicina i Ciències de la Salut, Functional Nutrition, Oxidation and Cardiovascular Diseases Group (NFOC-Salut), Universitat Rovira i Virgili, 43201, Reus, Spain
- Institut d'Investigació Sanitaria Pere Virgili, 43204, Reus, Spain
- Hospital Universitari Sant Joan de Reus, 43204, Reus, Spain
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Phenol-enriched olive oils improve HDL antioxidant content in hypercholesterolemic subjects. A randomized, double-blind, cross-over, controlled trial. J Nutr Biochem 2018; 51:99-104. [DOI: 10.1016/j.jnutbio.2017.09.010] [Citation(s) in RCA: 23] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/03/2016] [Revised: 08/22/2017] [Accepted: 09/11/2017] [Indexed: 11/23/2022]
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Hampl JS, Taylor CA, Booth CL. Differences in Dietary Patterns of Nonsmoking Adults Married to Smokers vs. Nonsmokers. Am J Health Promot 2016. [DOI: 10.4278/0890-1171-16.1.1] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/11/2023]
Abstract
Purpose. To compare dietary intakes of nonsmoking adults married to smokers or non-smokers. Design. Respondents to the U.S. Department of Agriculture's Continuing Survey of Food Intakes by Individuals (CSFII), 1994 to 1996 (response rate = 76.1% for 2 days of dietary intake). Nonsmoking adults aged 18 and older were grouped according to the smoking status of their spouse. Setting. In-home interviews in all 50 states and Washington, D.C. Subjects. The selected sample included 757 men and 754 women who were married to nonsmokers, and 197 men and 262 women who were married to smokers. Measures. Selected demographic variables, food group servings, food energy, and densities of selected nutrients were compared using χ2 and analysis of covariance. Results. Men and women married to smokers had greater (p ⩽ .025) energy-adjusted intakes of total and saturated fat but significantly lower (p ⩽ .05) energy-adjusted intakes of fiber and vitamin A. Men married to smokers consumed significantly more (p < .025) energy-adjusted cholesterol and ethanol but significantly less calcium (p = .026); women married to smokers consumed significantly less (p = .014) energy-adjusted folate. Men married to smokers consumed significantly more (p ⩽ .05) alcoholic beverages, coffee, and soft drinks; women married to smokers consumed significantly less water (p = .014) but more cheese and table sweeteners (p ⩽ .05). Conclusions. Nonsmoking men and women who were married to smokers had compromised dietary intakes. Nonsmoking men whose wives smoked, in particular, had unhealthy diets due to elevated intakes of fat and cholesterol and low intakes of vitamin A, calcium, and fiber. Health professionals should continue to provide tobacco cessation instruction and dietary guidance, but also be aware of at-risk patients' immediate family members who likely share an increased risk of disease because of poor diet quality and exposure to environmental tobacco smoke.
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Niklowitz P, Fischer A, Onur S, Paulussen M, Menke T, Döring F. Smoking habits and coenzyme Q10 status in healthy European adults. Arch Med Sci 2016; 12:715-20. [PMID: 27478450 PMCID: PMC4947618 DOI: 10.5114/aoms.2016.60953] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/21/2015] [Accepted: 09/14/2015] [Indexed: 12/04/2022] Open
Abstract
INTRODUCTION Coenzyme Q10 (CoQ10) is a lipophilic endogenously synthesised antioxidant that is present in nearly all human tissues and plays an important role in mitochondrial energy production. It has been postulated that smoking has a consumptive effect on CoQ10. MATERIAL AND METHODS To further define the relation between smoking and the serum CoQ10 status, 276 healthy volunteers aged 19 to 62 years were grouped into non-smokers (n = 113; 77 male, 36 female) and smokers (n = 163; 102 male, 61 female). Serum lipid profile was analysed by standard clinical chemistry. Coenzyme Q10 concentration and redox status were analysed by high-pressure liquid chromatography with electrochemical detection. RESULTS Male smokers showed higher serum CoQ10 levels than female smokers. This sex-related difference was accounted for when CoQ10 was related to low-density lipoprotein (LDL) cholesterol as the main carrier of CoQ10 in the circulation. Neither LDL-adjusted CoQ10 concentration nor redox status significantly differed when smokers and non-smokers were compared. Regarding the smoking history, the number of cigarettes consumed per day did not significantly affect the CoQ10 status. Interestingly, with increasing time of smoking habit we observed increasing levels of LDL-adjusted serum CoQ10 concentration (Spearman's p < 0.002) and of the reduced form of CoQ10 (Spearman's p < 0.0001). CONCLUSIONS As an adaptive response to oxidative stress in long-term smokers an increased demand for antioxidant capacity may be covered by increasing levels of LDL-adjusted CoQ10 serum concentrations and by a concomitantly increased availability of the reduced, active form of CoQ10, possibly by induction of enzymes that are involved in converting CoQ10ox to CoQ10red.
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Affiliation(s)
- Petra Niklowitz
- Children's Hospital of Datteln, Witten-Herdecke University, Datteln, Germany
| | - Alexandra Fischer
- Institute of Human Nutrition and Food Science, Division of Molecular Prevention, Christian Albrechts University of Kiel, Kiel, Germany
| | - Simone Onur
- Institute of Human Nutrition and Food Science, Division of Molecular Prevention, Christian Albrechts University of Kiel, Kiel, Germany
| | - Michael Paulussen
- Children's Hospital of Datteln, Witten-Herdecke University, Datteln, Germany
| | - Thomas Menke
- Children's Hospital of Datteln, Witten-Herdecke University, Datteln, Germany
| | - Frank Döring
- Institute of Human Nutrition and Food Science, Division of Molecular Prevention, Christian Albrechts University of Kiel, Kiel, Germany
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Cipollone F, Chiarelli F, Iezzi A, Fazia ML, Cuccurullo C, Pini B, De Cesare D, Torello M, Tumini S, Cuccurullo F, Mezzetti A. Relationship between Reduced BCL-2 Expression in Circulating Mononuclear Cells and Early Nephropathy in Type 1 Diabetes. Int J Immunopathol Pharmacol 2016; 18:625-35. [PMID: 16388709 DOI: 10.1177/039463200501800403] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
Microalbuminuria is the earliest clinical evidence of diabetic nephropathy, but the mechanisms linking hyperglycemia and kidney complications are not clear. The aim of this study was to evaluate whether enhanced oxidative stress in patients with microalbuminuria can contribute to diabetic nephropathy development through downregulation of the antiapoptotic gene Bcl-2 that promotes in turn a pro-inflammatory status. We studied 30 patients with type 1 diabetes (15 with and 15 without microalbuminuria) compared to 15 matched healthy controls. Plasma oxidant status, and expression of Bcl-2, activated NF-kB, inducible Nitric Oxide synthase (iNOS), and monocyte chemoattractant protein (MCP)-1 in circulating monocytes were evaluated at baseline and after 8-week oral vitamin E treatment (600 mg b.i.d.). Bcl-2 expression was significantly reduced in microalbuminuric diabetic patients as a consequence of increased oxidant burden secondary to persistent hyperglycemia. Bcl-2 down-regulation was associated with enhanced expression of NF-kB, iNOS and MCP-1, and showed a strong correlation with the albumin excretion rate. Low Bcl-2 expression and high inflammatory status were normalized by vitamin E both in vivo and in vitro. Our study showed that Bcl-2 down-regulation in diabetic patients with poor glycemic control results in the activation of the NF-kB pathway leading to the development of nephropathy. Vitamin E might provide a novel form of therapy for prevention of nephropathy in diabetic patients in which an acceptable glycemic control is difficult to achieve despite insulin therapy.
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Affiliation(s)
- F Cipollone
- Atherosclerosis Prevention Center, University of Chieti G D Annunzio School of Medicine, Chieti, Italy.
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Schmölz L, Birringer M, Lorkowski S, Wallert M. Complexity of vitamin E metabolism. World J Biol Chem 2016; 7:14-43. [PMID: 26981194 PMCID: PMC4768118 DOI: 10.4331/wjbc.v7.i1.14] [Citation(s) in RCA: 135] [Impact Index Per Article: 15.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/24/2015] [Revised: 11/25/2015] [Accepted: 01/19/2016] [Indexed: 02/05/2023] Open
Abstract
Bioavailability of vitamin E is influenced by several factors, most are highlighted in this review. While gender, age and genetic constitution influence vitamin E bioavailability but cannot be modified, life-style and intake of vitamin E can be. Numerous factors must be taken into account however, i.e., when vitamin E is orally administrated, the food matrix may contain competing nutrients. The complex metabolic processes comprise intestinal absorption, vascular transport, hepatic sorting by intracellular binding proteins, such as the significant α-tocopherol-transfer protein, and hepatic metabolism. The coordinated changes involved in the hepatic metabolism of vitamin E provide an effective physiological pathway to protect tissues against the excessive accumulation of, in particular, non-α-tocopherol forms. Metabolism of vitamin E begins with one cycle of CYP4F2/CYP3A4-dependent ω-hydroxylation followed by five cycles of subsequent β-oxidation, and forms the water-soluble end-product carboxyethylhydroxychroman. All known hepatic metabolites can be conjugated and are excreted, depending on the length of their side-chain, either via urine or feces. The physiological handling of vitamin E underlies kinetics which vary between the different vitamin E forms. Here, saturation of the side-chain and also substitution of the chromanol ring system are important. Most of the metabolic reactions and processes that are involved with vitamin E are also shared by other fat soluble vitamins. Influencing interactions with other nutrients such as vitamin K or pharmaceuticals are also covered by this review. All these processes modulate the formation of vitamin E metabolites and their concentrations in tissues and body fluids. Differences in metabolism might be responsible for the discrepancies that have been observed in studies performed in vivo and in vitro using vitamin E as a supplement or nutrient. To evaluate individual vitamin E status, the analytical procedures used for detecting and quantifying vitamin E and its metabolites are crucial. The latest methods in analytics are presented.
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Kanďár R. The ratio of oxidized and reduced forms of selected antioxidants as a possible marker of oxidative stress in humans. Biomed Chromatogr 2015; 30:13-28. [PMID: 26053056 DOI: 10.1002/bmc.3529] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/02/2014] [Revised: 05/20/2015] [Accepted: 05/29/2015] [Indexed: 02/04/2023]
Abstract
Oxidative stress is an imbalance between reactive oxygen species exposure and the ability of organisms to detoxify the reactive intermediates and to repair the oxidative damage of biologically important molecules. Many clinical studies of oxidative stress unfortunately provide conflicting and contradictory results. The ability of antioxidant systems to adequately respond to oxidative stress can be used in laboratory diagnostics. In the present review, methods using the ratio of reduced and oxidized forms of uric acid, ascorbic acid, glutathione and coenzyme Q10 as suitable indicators of oxidative stress are discussed. From the mentioned publications it is evident that suitable sample preparation prior to analysis is crucial.
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Affiliation(s)
- Roman Kanďár
- Department of Biological and Biochemical Sciences, Faculty of Chemical Technology, University of Pardubice, Pardubice, Czech Republic
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McClendon CJ, Gerald CL, Waterman JT. Farm animal models of organic dust exposure and toxicity: insights and implications for respiratory health. Curr Opin Allergy Clin Immunol 2015; 15:137-44. [PMID: 25636160 PMCID: PMC4783132 DOI: 10.1097/aci.0000000000000143] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
PURPOSE OF REVIEW Modern food animal production is a major contributor to the global economy, owing to advanced intensive indoor production facilities aimed at increasing market readiness and profit. Consequences of these advances are accumulation of dusts, gases, and microbial products that diminish air quality within production facilities. Chronic inhalation exposure contributes to onset and exacerbation of respiratory symptoms and diseases in animals and workers. This article reviews literature regarding constituents of farm animal production facility dusts, animal responses to production building and organic dust exposure, and the effect of chronic inhalation exposure on pulmonary oxidative stress and inflammation. RECENT FINDINGS Porcine models of production facility and organic dust exposures reveal striking similarities to observations of human cells, tissues, and clinical data. Oxidative stress plays a key role in mediating respiratory diseases in animals and humans, and enhancement of antioxidant levels through nutritional supplements can improve respiratory health. SUMMARY Pigs are well adapted to the exposures common to swine production buildings and thus serve as excellent models for facility workers. Insight for understanding mechanisms governing organic dust associated respiratory diseases may come from parallel comparisons between farmers and the animals they raise.
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Affiliation(s)
- Chakia J. McClendon
- Department of Animal Sciences, North Carolina Agricultural and Technical State University, Greensboro, NC
- Department of Energy and Environmental Systems, North Carolina Agricultural and Technical State University, Greensboro, NC
| | - Carresse L. Gerald
- Pulmonary and Critical Care Medicine, University of Nebraska Medical Center, Omaha, NE
| | - Jenora T. Waterman
- Department of Animal Sciences, North Carolina Agricultural and Technical State University, Greensboro, NC
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Cho MR, Han JH, Lee HJ, Park YK, Kang MH. Purple grape juice supplementation in smokers and antioxidant status according to different types of GST polymorphisms. J Clin Biochem Nutr 2015. [PMID: 25678751 DOI: 10.3164/jcbn.14.1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
Abstract
DNA damages and antioxidant status was assessed after 8 weeks of purple grape juice supplementation in male smokers depending on the glutathione S-transferase polymorphisms. Ninety-five smokers consumed 480 ml of purple grape juice for 8 weeks. The blood samples were collected before and after supplementation to measure lymphocyte DNA damages, plasma antioxidants, conjugated diene, and the erythrocyte antioxidant enzymes. The diastolic pressure, lymphocyte DNA damage, and plasma conjugated diene were significantly decreased but the plasma γ-tocopherol was increased in GSTM1-null genotype, while increased blood glutathione and decreased lymphocyte DNA damage were observed in GSTM1-present genotype. In case of GSTT1 on the other hand, the decrease in diastolic pressure and lymphocyte DNA damage was observed in both null types and present types, but the erythrocyte catalase activity was decreased in GSTT1-null type and the plasma vitamin C level was increased in GSTT1-present type, suggesting that, the antioxidant effect of grape juice was greater in GSTT1-present type compared to GSTT1-null type. The intakes of 8-week purple grape juice affected diastolic blood pressures, DNA damage reductions and antioxidant status in smokers, mainly greater in GSTM1-null type and GSTT1-present type.
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Affiliation(s)
- Mi-Ran Cho
- Department of Food & Nutrition, Daedeok Valley Campus, Hannam University, Daejeon 305-811, Korea
| | - Jeong-Hwa Han
- Department of Food & Nutrition, Daedeok Valley Campus, Hannam University, Daejeon 305-811, Korea
| | - Hye-Jin Lee
- Department of Food & Nutrition, Daedeok Valley Campus, Hannam University, Daejeon 305-811, Korea
| | - Yoo Kyoung Park
- Department of Medical Nutrition, Graduate School of East-West Medicine, Kyung Hee University, Yongin, 446-701, Korea
| | - Myung-Hee Kang
- Department of Food & Nutrition, Daedeok Valley Campus, Hannam University, Daejeon 305-811, Korea
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Cho MR, Han JH, Lee HJ, Park YK, Kang MH. Purple grape juice supplementation in smokers and antioxidant status according to different types of GST polymorphisms. J Clin Biochem Nutr 2014; 56:49-56. [PMID: 25678751 PMCID: PMC4306655 DOI: 10.3164/jcbn.14-1] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/07/2014] [Accepted: 05/07/2014] [Indexed: 11/22/2022] Open
Abstract
DNA damages and antioxidant status was assessed after 8 weeks of purple grape juice supplementation in male smokers depending on the glutathione S-transferase polymorphisms. Ninety-five smokers consumed 480 ml of purple grape juice for 8 weeks. The blood samples were collected before and after supplementation to measure lymphocyte DNA damages, plasma antioxidants, conjugated diene, and the erythrocyte antioxidant enzymes. The diastolic pressure, lymphocyte DNA damage, and plasma conjugated diene were significantly decreased but the plasma γ-tocopherol was increased in GSTM1-null genotype, while increased blood glutathione and decreased lymphocyte DNA damage were observed in GSTM1-present genotype. In case of GSTT1 on the other hand, the decrease in diastolic pressure and lymphocyte DNA damage was observed in both null types and present types, but the erythrocyte catalase activity was decreased in GSTT1-null type and the plasma vitamin C level was increased in GSTT1-present type, suggesting that, the antioxidant effect of grape juice was greater in GSTT1-present type compared to GSTT1-null type. The intakes of 8-week purple grape juice affected diastolic blood pressures, DNA damage reductions and antioxidant status in smokers, mainly greater in GSTM1-null type and GSTT1-present type.
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Affiliation(s)
- Mi-Ran Cho
- Department of Food & Nutrition, Daedeok Valley Campus, Hannam University, Daejeon 305-811, Korea
| | - Jeong-Hwa Han
- Department of Food & Nutrition, Daedeok Valley Campus, Hannam University, Daejeon 305-811, Korea
| | - Hye-Jin Lee
- Department of Food & Nutrition, Daedeok Valley Campus, Hannam University, Daejeon 305-811, Korea
| | - Yoo Kyoung Park
- Department of Medical Nutrition, Graduate School of East-West Medicine, Kyung Hee University, Yongin, 446-701, Korea
| | - Myung-Hee Kang
- Department of Food & Nutrition, Daedeok Valley Campus, Hannam University, Daejeon 305-811, Korea
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Yokus B, Mete N, Cakir U, Toprak G. Effects of Active and Passive Smoking on Antioxidant Enzymes and Antioxidant Micronutrients. BIOTECHNOL BIOTEC EQ 2014. [DOI: 10.1080/13102818.2005.10817238] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/25/2022] Open
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Wang Y, Chun OK, Song WO. Plasma and dietary antioxidant status as cardiovascular disease risk factors: a review of human studies. Nutrients 2013; 5:2969-3004. [PMID: 23912327 PMCID: PMC3775238 DOI: 10.3390/nu5082969] [Citation(s) in RCA: 121] [Impact Index Per Article: 10.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/13/2013] [Revised: 05/30/2013] [Accepted: 07/17/2013] [Indexed: 02/07/2023] Open
Abstract
Extensive evidence has demonstrated that many antioxidants such as vitamin C, vitamin E, carotenoids and polyphenols have protective effects in preventing cardiovascular disease (CVD), a chronic disease that is mediated by oxidative stress and inflammation. This review focuses on evidence from prospective cohort studies and clinical trials in regard to the associations between plasma/dietary antioxidants and cardiovascular events. Long-term, large-scale, population-based cohort studies have found that higher levels of serum albumin, bilirubin, glutathione, vitamin E, vitamin C, and carotenoids were associated with a lower risk of CVD. Evidence from the cohort studies in regard to dietary antioxidants also supported the protective effects of dietary vitamin E, vitamin C, carotenoids, and polyphenols on CVD risk. However, results from large randomized controlled trials did not support long-term use of single antioxidant supplements for CVD prevention due to their null or even adverse effects on major cardiovascular events or cancer. Diet quality indexes that consider overall diet quality rather than single nutrients have been drawing increasing attention. Cohort studies and intervention studies that focused on diet patterns such as high total antioxidant capacity have documented protective effects on CVD risk. This review provides a perspective for future studies that investigate antioxidant intake and risk of CVD.
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Affiliation(s)
- Ying Wang
- Epidemiology Research Program, American Cancer Society, Atlanta, GA 30303, USA; E-Mail:
| | - Ock K. Chun
- Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269, USA; E-Mail:
| | - Won O. Song
- Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI 48824, USA
- Author to whom correspondence should be addressed; E-Mail: ; Tel.: +1-517-355-8474 (ext. 109); Fax: +1-517-353-8963
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Smoking and age-related macular degeneration: biochemical mechanisms and patient support. Optom Vis Sci 2013; 89:1662-6. [PMID: 23034338 DOI: 10.1097/opx.0b013e31826c5df2] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/25/2023] Open
Abstract
A small percentage of the population associates smoking with ocular disease. Most optometrists do not stress the importance of smoking cessation to their patients, and the centrality of smoking regarding the risk for ocular disease is not emphasized in optometric education. Age-related macular degeneration has strong epidemiological associations with smoking, and so serves as an appropriate model for the adverse effects of cigarette smoke on the eye. This article aims to provide basic scientific information to optometrists and optometry students so that they can better understand the pathogenesis of age-related macular degeneration and provide education and support to their patients wishing to stop smoking.
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Fabian E, Pölöskey P, Kósa L, Elmadfa I, Réthy LA. Nutritional supplements and plasma antioxidants in childhood asthma. Wien Klin Wochenschr 2013; 125:309-15. [PMID: 23636616 DOI: 10.1007/s00508-013-0359-6] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/12/2012] [Accepted: 03/20/2013] [Indexed: 12/30/2022]
Abstract
OBJECTIVE This study investigated the relationship of plasma antioxidants to airway inflammation and systemic oxidative stress in children suffering from atopic asthma with consideration of the intake of nutritional supplements. SUBJECTS AND RESEARCH METHODS A total of 35 asthmatic children (AG) and 21 healthy controls (CG) participated in this study. Plasma levels of vitamins A and E, β-carotene, coenzyme Q10 and malondialdehyde (MDA) were analyzed with high-performance liquid chromatography (HPLC); the total antioxidant capacity (TAC) was measured photometrically, and selenium was determined by atomic absorption spectroscopy (AAS). The volume of fractionated exhaled nitric oxide (FeNO) was measured with the NIOX nitric oxide monitoring system. RESULTS The plasma antioxidants vitamins A and E, selenium, and coenzyme Q10 but not β-carotene were significantly (p < 0.05) lower in asthmatics than in controls. Further, asthmatic children had significantly reduced plasma concentrations of TAC (p < 0.01), significantly enhanced levels of MDA (p < 0.001), and exhaled a significantly (p < 0.001) higher mean volume of FENO than healthy children. Regular intake of supplements had a significant positive influence on plasma vitamin E (p < 0.01), selenium (p < 0.01), TAC (p < 0.05), MDA (p < 0.01), and FENO (p < 0.01) in asthmatics but not in controls. Additionally, significant negative associations of vitamin E and MDA (AG: p < 0.01; CG: p < 0.05), and vitamin E and FENO (AG: p < 0.05; CG: p > 0.05) were identified. CONCLUSION These results indicate that nutritional supplements beneficially modulate plasma antioxidants and thus might have a positive influence on systemic redox balance and subsequently, pulmonary inflammation in asthmatic children.
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Affiliation(s)
- Elisabeth Fabian
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria.
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17
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Assessment of the Bioactive Compounds, Color, and Mechanical Properties of Apricots as Affected by Drying Treatment. FOOD BIOPROCESS TECH 2012. [DOI: 10.1007/s11947-012-0988-1] [Citation(s) in RCA: 31] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/27/2022]
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18
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Szlagatys-Sidorkiewicz A, Zagierski M, Luczak G, Macur K, Bączek T, Kamińska B. Maternal smoking does not influence vitamin A and E concentrations in mature breastmilk. Breastfeed Med 2012; 7:285-9. [PMID: 22313392 DOI: 10.1089/bfm.2011.0058] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/14/2022]
Abstract
OBJECTIVES The aim of this study was to analyze the effects of maternal smoking on the total antioxidant status (TAS) and the concentrations of vitamins A and E in human breastmilk. METHODOLOGY The study group (n=20) comprised postpartum women who declared smoking more than five cigarettes per day (confirmed by urinalysis of the cotinine concentration). The control group included 25 nonsmoking postpartum women. Breastmilk samples were collected between day 30 and day 32 after delivery. TAS was determined by Rice-Evans and Miller method, whereas the amount of vitamins A and E was measured by high-performance liquid chromatography. RESULTS No significant differences were observed between breastmilk samples from smoking and nonsmoking mothers in terms of TAS and vitamin A and E concentrations. Additionally, no significant correlations were found between urinary cotinine and TAS (R=0.35, p=0.144) or vitamin A (R=0.14, p=0.571) and vitamin E (R=0.31, p=0.228) concentrations in breastmilk samples from smoking mothers. CONCLUSIONS Maternal smoking is not reflected by decreased TAS and vitamin A and E concentrations in mature milk.
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Reckziegel P, Boufleur N, Barcelos RCS, Benvegnú DM, Pase CS, Muller LG, Teixeira AM, Zanella R, Prado ACP, Fett R, Block JM, Burger ME. Oxidative stress and anxiety-like symptoms related to withdrawal of passive cigarette smoke in mice: beneficial effects of pecan nut shells extract, a by-product of the nut industry. ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY 2011; 74:1770-8. [PMID: 21531023 DOI: 10.1016/j.ecoenv.2011.04.022] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 04/10/2010] [Revised: 04/13/2011] [Accepted: 04/16/2011] [Indexed: 05/12/2023]
Abstract
The present study evaluated the role of pecan nut (Carya illinoensis) shells aqueous extract (AE) against oxidative damage induced by cigarette smoke exposure (CSE) and behavioral parameters of smoking withdrawal. Mice were passively exposed to cigarette smoke for 3 weeks (6, 10, and 14 cigarettes/day) and orally treated with AE (25 g/L). CSE induced lipid peroxidation in brain and red blood cells (RBC), increased catalase (CAT) activity in RBC, and decreased plasma ascorbic acid levels. AE prevented oxidative damage and increased antioxidant defenses of mice exposed to cigarette smoke. In addition, AE reduced the locomotor activity and anxiety symptoms induced by smoking withdrawal, and these behavioral parameters showed a positive correlation with RBC lipid peroxidation. Our results showed the beneficial effects of this by-product of the pecan industry, indicating its usefulness in smoking cessation.
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Affiliation(s)
- P Reckziegel
- Programa de Pós-Graduação em Farmacologia, Centro de Ciências da Saúde, Universidade Federal de Santa Maria (UFSM), RS, 97105-900, Brazil
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20
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Marino M, Masella R, Bulzomi P, Campesi I, Malorni W, Franconi F. Nutrition and human health from a sex-gender perspective. Mol Aspects Med 2011; 32:1-70. [PMID: 21356234 DOI: 10.1016/j.mam.2011.02.001] [Citation(s) in RCA: 84] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2010] [Revised: 01/25/2011] [Accepted: 02/18/2011] [Indexed: 02/07/2023]
Abstract
Nutrition exerts a life-long impact on human health, and the interaction between nutrition and health has been known for centuries. The recent literature has suggested that nutrition could differently influence the health of male and female individuals. Until the last decade of the 20th century, research on women has been neglected, and the results obtained in men have been directly translated to women in both the medicine and nutrition fields. Consequently, most modern guidelines are based on studies predominantly conducted on men. However, there are many sex-gender differences that are the result of multifactorial inputs, including gene repertoires, sex steroid hormones, and environmental factors (e.g., food components). The effects of these different inputs in male and female physiology will be different in different periods of ontogenetic development as well as during pregnancy and the ovarian cycle in females, which are also age dependent. As a result, different strategies have evolved to maintain male and female body homeostasis, which, in turn, implies that there are important differences in the bioavailability, metabolism, distribution, and elimination of foods and beverages in males and females. This article will review some of these differences underlying the impact of food components on the risk of developing diseases from a sex-gender perspective.
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Affiliation(s)
- Maria Marino
- Department of Biology, University Roma Tre, Viale Guglielmo Marconi 446, I-00146 Roma, Italy
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Usai P, Ibba I, Lai M, Boi MF, Savarese MF, Cuomo R, D'Alia G, Gemini S, Diaz G, Contu P. Cigarette smoking and appendectomy: effect on clinical course of diverticulosis. Dig Liver Dis 2011; 43:98-101. [PMID: 20579946 DOI: 10.1016/j.dld.2010.05.008] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/01/2010] [Revised: 04/09/2010] [Accepted: 05/09/2010] [Indexed: 12/11/2022]
Abstract
AIM To investigate the effect of appendectomy and cigarette smoking on the clinical course of diverticulosis. MATERIALS AND METHODS A retrospective case-control study of 207 consecutive patients (45.8% male mean age 64.0 years), 150 with asymptomatic diverticulosis, and 57 with acute diverticulitis. Diagnosis of diverticulosis was defined on the basis of clinical and colonoscopic criteria, diverticulitis was defined by means of clinical, colonoscopic and computerised tomography criteria. Logistic regression function was used to define the relationship between the dependent variable (diverticulitis) and several covariates: sex, age, body mass index, smoking habit, and history of appendectomy. RESULTS According to the final model, the risk of diverticulitis was 4.94-fold higher (95% confidence interval: 1.98-12.37) in patients with a history of appendectomy with emergency resection, compared to patients not submitted to appendectomy or with a history of elective resection (P < 0.001); and 2.79-fold higher (95% confidence interval: 1.30-5.96) in smokers than in non-smokers (P = 0.008). The effects of the two determinants were found to be independent, thus the cumulative risk of diverticulitis was 13.78-fold higher for smokers with a history of emergency surgical treatment. CONCLUSION Smoking and emergency appendectomy are important predictive factors for the clinical course of diverticulosis.
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Affiliation(s)
- Paolo Usai
- Department of Internal Medicine, Cagliari University, AOU Policlinico di Monserrato 09042, Monserrato, Italy.
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Wood LG, Wark PAB, Garg ML. Antioxidant and anti-inflammatory effects of resveratrol in airway disease. Antioxid Redox Signal 2010; 13:1535-48. [PMID: 20214495 DOI: 10.1089/ars.2009.3064] [Citation(s) in RCA: 102] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/08/2023]
Abstract
Respiratory diseases, such as asthma and chronic obstructive pulmonary disease (COPD), are a significant and increasing global health problem. These diseases are characterized by airway inflammation, which develops in response to various stimuli. In asthma, inflammation is driven by exposure to a variety of triggers, including allergens and viruses, which activate components of both the innate and acquired immune responses. In COPD, exposure to cigarette smoke is the primary stimulus of airway inflammation. Activation of airway inflammatory cells leads to the release of excessive quantities of reactive oxygen species (ROS), resulting in oxidative stress. Antioxidants provide protection against the damaging effects of oxidative stress and thus may be useful in the management of inflammatory airways disease. Resveratrol, a polyphenol that demonstrates both antioxidative and anti-inflammatory functions, has been shown to improve outcomes in a variety of diseases, in particular, in cancer. We review the evidence for a protective role of resveratrol in respiratory disease. Mechanisms of resveratrol action that may be relevant to respiratory disease are described. We conclude that resveratrol has potential as a therapeutic agent in respiratory disease, which should be further investigated.
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Affiliation(s)
- Lisa G Wood
- Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, John Hunter Hospital, Newcastle, NSW, Australia.
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Unverdorben M, von Holt K, Winkelmann BR. Smoking and atherosclerotic cardiovascular disease: part II: role of cigarette smoking in cardiovascular disease development. Biomark Med 2010; 3:617-53. [PMID: 20477529 DOI: 10.2217/bmm.09.51] [Citation(s) in RCA: 31] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022] Open
Abstract
Potential mechanisms and biomarkers of atherosclerosis related to cigarette smoking - a modifiable risk factor for that disease - are discussed in this article. These include smoking-associated inflammatory markers, such as leukocytes, high-sensitivity C-reactive protein, serum amyloid A, ICAM-1 and IL-6. Other reviewed markers are indicative for smoking-related impairment of arterial endothelial function (transcapillary leakage of albumin, inhibition of endogenous nitric oxide synthase activity and reduced endothelium-dependent vasodilation) or point to oxidative stress caused by various chemicals (cholesterol oxidation, autoantibodies to oxidized low-density lipoprotein, plasma levels of malondialdehyde and F(2)-isoprostanes and reduced antioxidant capacity). Smoking enhances platelet aggregability, increases blood viscosity and shifts the pro- and antithrombotic balance towards increased coagulability (e.g., fibrinogen, von Willebrand factor, ICAM-1 and P-selectin). Insulin resistance is higher in smokers compared with nonsmokers, and hemoglobin A1c is dose-dependently elevated, as is homocysteine. Smoke exposure may influence the kinetics of markers with different response to transient or chronic changes in cigarette smoking behavior.
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Affiliation(s)
- Martin Unverdorben
- Clinical Research Institute, Center for Cardiovascular Diseases, Heinz-Meise-Strasse 100, 36199 Rotenburg an der Fulda, Germany.
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Puchau B, Zulet MA, Hermsdorff HHM, Navarro-Blasco I, Martínez JA. Nail antioxidant trace elements are inversely associated with inflammatory markers in healthy young adults. Biol Trace Elem Res 2010; 133:304-12. [PMID: 19582378 DOI: 10.1007/s12011-009-8443-5] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/24/2009] [Accepted: 06/23/2009] [Indexed: 01/22/2023]
Abstract
Antioxidant intake may be linked to a reduction of the chronic low-grade inflammatory state related to obesity and several accompanying disorders such as insulin resistance, cardiovascular diseases, and metabolic syndrome. So, the aim of this study was to evaluate the potential associations between nail trace elements and several indicators in healthy young adults, emphasizing on the putative effect of antioxidant trace element intake on inflammation-related marker concentrations. This study enrolled 149 healthy young adults, whose anthropometrical and blood pressure values as well as lifestyle features were analyzed. Fasting blood samples were collected for the biochemical and inflammation-related measurements (C-reactive protein, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-18, and homocysteine). Nail samples were collected for the analysis of selenium, zinc, and copper concentrations. Our results showed that nail selenium was negatively associated with IL-18; nail zinc concentrations were inversely related to circulating IL-6, IL-18, and TNF-alpha, whereas nail copper (Cu) and Cu/selenium values were negatively correlated with homocysteine levels and the Cu/zinc ratio was unaffected. In conclusion, nail content on some trace elements related to antioxidant defense mechanisms seems to be associated with several inflammation-related markers linked to chronic diseases in apparently healthy young adults, which is of interest to understand the role of antioxidant intake.
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Affiliation(s)
- Blanca Puchau
- Department of Nutrition and Food Science, Physiology and Toxicology, University of Navarra, Calle Irunlarrea 1, 31008, Pamplona, Spain
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25
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Lee SH, Kang HJ, Lee HJ, Kang MH, Park YK. Six-week supplementation with Chlorella has favorable impact on antioxidant status in Korean male smokers. Nutrition 2010; 26:175-83. [DOI: 10.1016/j.nut.2009.03.010] [Citation(s) in RCA: 51] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/22/2008] [Revised: 03/27/2009] [Accepted: 03/27/2009] [Indexed: 11/25/2022]
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Comhair SAA, Erzurum SC. Redox control of asthma: molecular mechanisms and therapeutic opportunities. Antioxid Redox Signal 2010; 12:93-124. [PMID: 19634987 PMCID: PMC2824520 DOI: 10.1089/ars.2008.2425] [Citation(s) in RCA: 169] [Impact Index Per Article: 11.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
An imbalance in reducing and oxidizing (redox) systems favoring a more oxidative environment is present in asthma and linked to the pathophysiology of the defining symptoms and signs including airflow limitation, hyper-reactivity, and airway remodeling. High levels of hydrogen peroxide, nitric oxide ((*)NO), and 15-F(2t)-isoprostane in exhaled breath, and excessive oxidative protein products in lung epithelial lining fluid, peripheral blood, and urine provide abundant evidence for pathologic oxidizing processes in asthma. Parallel studies document loss of reducing potential by nonenzymatic and enzymatic antioxidants. The essential first line antioxidant enzymes superoxide dismutases (SOD) and catalase are reduced in asthma as compared to healthy individuals, with lowest levels in those patients with the most severe asthma. Loss of SOD and catalase activity is related to oxidative modifications of the enzymes, while other antioxidant gene polymorphisms are linked to susceptibility to develop asthma. Monitoring of exhaled (*)NO has entered clinical practice because it is useful to optimize asthma care, and a wide array of other biochemical oxidative and nitrative biomarkers are currently being evaluated for asthma monitoring and phenotyping. Novel therapeutic strategies that target correction of redox abnormalities show promise for the treatment of asthma.
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Affiliation(s)
- Suzy A A Comhair
- Pathobiology, Lerner Research Institute, and the Respiratory Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA.
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NAZZARO F, CALIENDO G, ARNESI G, VERONESI A, SARZI P, FRATIANNI F. COMPARATIVE CONTENT OF SOME BIOACTIVE COMPOUNDS IN TWO VARIETIES OF CAPSICUM ANNUUM L. SWEET PEPPER AND EVALUATION OF THEIR ANTIMICROBIAL AND MUTAGENIC ACTIVITIES. J Food Biochem 2009. [DOI: 10.1111/j.1745-4514.2009.00259.x] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/28/2022]
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Matos C, Moutinho C, Balcão V, Almeida C, Ribeiro M, Marques AF, Guerra A. Total antioxidant activity and trace elements in human milk: the first 4 months of breast-feeding. Eur Food Res Technol 2009. [DOI: 10.1007/s00217-009-1157-2] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022]
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Chiu YW, Chuang HY, Huang MC, Wu MT, Liu HW, Huang CT. Comparison of Plasma Antioxidant Levels and Related Metabolic Parameters Between Smokers and Non-smokers. Kaohsiung J Med Sci 2009; 25:423-30. [DOI: 10.1016/s1607-551x(09)70537-6] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/03/2023] Open
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30
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Kamışlı F, Karatas F. Effects of sulphurisation on vitamins (A, C and E) and malondialdehyde in apricots. Int J Food Sci Technol 2009. [DOI: 10.1111/j.1365-2621.2008.01803.x] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022]
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Farhat N, Thorin-Trescases N, Voghel G, Villeneuve L, Mamarbachi M, Perrault LP, Carrier M, Thorin E. Stress-induced senescence predominates in endothelial cells isolated from atherosclerotic chronic smokers. Can J Physiol Pharmacol 2009; 86:761-9. [PMID: 19011671 DOI: 10.1139/y08-082] [Citation(s) in RCA: 72] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
Age-associated telomere shortening leads to replicative senescence of human endothelial cells (EC). Risk factors for cardiovascular disease (CVD) accelerate ageing, while there is a concomitant rise in oxidative stress known to promote stress-induced senescence (SIS) in vitro. Of all risk factors for CVD, smoking is most associated with the development of inflammation and accelerated atherosclerosis due to a prooxidant-antioxidant imbalance. We tested the hypothesis that SIS predominates in EC isolated from chronic smokers with premature atherosclerosis undergoing coronary artery bypass graft surgery (CABG). We isolated and cultured EC from segments of internal mammary arteries from smoker, former smoker, and nonsmoker coronary patients. Senescence of EC was induced by serial passage and quantified by the measurement of telomere length and senescence-associated beta-galactosidase activity. Compared with nonsmokers, smoker patients were 10 years younger at the time of CABG, evidence of premature atherosclerosis. Cellular senescence was independent of telomere length and directly related to oxidative damage. EC exhibited higher expression levels of markers of oxidative stress (lipid peroxydation level and caveolin-1 mRNA), inflammation (angiopoietin-like 2 mRNA), hypoxia (vascular endothelial growth factor (VEGF)-A mRNA), and cell damage (p53 mRNA). In conclusion, a high oxidative stress environment in EC isolated from atherosclerotic chronic smokers predisposes to SIS rather than replicative senescence.
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Affiliation(s)
- Nada Farhat
- Department of Surgery and Research Center, Institut de Cardiologie de Montreal, Universite de Montreal, 5000, rue Belanger, Montreal, QC H1T1C8, Canada
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Abstract
Chronic obstructive pulmonary disease (COPD) is associated with a high incidence of morbidity and mortality. Cigarette smoke-induced oxidative stress is intimately associated with the progression and exacerbation of COPD and therefore targeting oxidative stress with antioxidants or boosting the endogenous levels of antioxidants is likely to have beneficial outcome in the treatment of COPD. Among the various antioxidants tried so far, thiol antioxidants and mucolytic agents, such as glutathione, N-acetyl-L-cysteine, N-acystelyn, erdosteine, fudosteine and carbocysteine; Nrf2 activators; and dietary polyphenols (curcumin, resveratrol, and green tea catechins/quercetin) have been reported to increase intracellular thiol status along with induction of GSH biosynthesis. Such an elevation in the thiol status in turn leads to detoxification of free radicals and oxidants as well as inhibition of ongoing inflammatory responses. In addition, specific spin traps, such as alpha-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (ECSOD mimetic), porphyrins (AEOL 10150 and AEOL 10113), and a SOD mimetic M40419 have also been reported to inhibit cigarette smoke-induced inflammatory responses in vivo in the lung. Since a variety of oxidants, free radicals and aldehydes are implicated in the pathogenesis of COPD, it is possible that therapeutic administration of multiple antioxidants and mucolytics will be effective in management of COPD. However, a successful outcome will critically depend upon the choice of antioxidant therapy for a particular clinical phenotype of COPD, whose pathophysiology should be first properly understood. This article will review the various approaches adopted to enhance lung antioxidant levels, antioxidant therapeutic advances and recent past clinical trials of antioxidant compounds in COPD.
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Affiliation(s)
- Irfan Rahman
- Department of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, NY, USA.
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Abstract
Vitamin E is an important nutrient with antioxidant and non-antioxidant functions, and certain evidence suggests that it has a cardiovascular protective role. It is therefore important to maintain an optimal vitamin E status. In the present paper, a number of MS applications to monitor vitamin E status and its interactions, including the use of stable-isotope-labelled vitamin E and metabonomics, are highlighted. Specifically, stable-isotope studies have been used to monitor vitamin E absorption, hepatic processing and lipoprotein transport. As oxidative stress may influence vitamin E status, a number of studies comparing vitamin E biokinetics and metabolism in cigarette smokers and non-smokers have been able to show differences in vitamin E processing in smokers. Metabonomics represents a method to identify changes to metabolite profiles, offering the potential to investigate interactions between vitamin E and metabolic pathways. These applications represent innovative approaches to investigate the role of vitamin E in health and disease.
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Abstract
CVD is a major cause of mortality and morbidity in the Western world. In recent years its importance has expanded internationally and it is believed that by 2020 it will be the biggest cause of mortality in the world, emphasising the importance to prevent or minimise this increase. A beneficial role for vitamins in CVD has long been explored but the data are still inconsistent. While being supported by observational studies, randomised controlled trials have not yet supported a role for vitamins in primary or secondary prevention of CVD and have in some cases even indicated increased mortality in those with pre-existing late-stage atherosclerosis. The superiority of combination therapy over single supplementation has been suggested but this has not been confirmed in trials. Studies have indicated that beta-carotene mediates pro-oxidant effects and it has been suggested that its negative effects may diminish the beneficial effects mediated by the other vitamins in the supplementation cocktail. The trials that used a combination of vitamins that include beta-carotene have been disappointing. However, vitamin E and vitamin C have in combination shown long-term anti-atherogenic effects but their combined effect on clinical endpoints has been inconsistent. Studies also suggest that vitamins would be beneficial to individuals who are antioxidant-deficient or exposed to increased levels of oxidative stress, for example, smokers, diabetics and elderly patients, emphasising the importance of subgroup targeting. Through defining the right population group and the optimal vitamin combination we could potentially find a future role for vitamins in CVD.
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A comparison of oxidative stress in smokers and non-smokers: an in vivo human quantitative study of n-3 lipid peroxidation. BMC Psychiatry 2008; 8 Suppl 1:S4. [PMID: 18433514 PMCID: PMC2330079 DOI: 10.1186/1471-244x-8-s1-s4] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/10/2022] Open
Abstract
BACKGROUND Cigarette smoking is believed to cause oxidative stress by several mechanisms, including direct damage by radical species and the inflammatory response induced by smoking, and would therefore be expected to cause increased lipid peroxidation. The aim was to carry out the first study of the relationship of smoking in humans to the level of n-3 lipid peroxidation indexed by the level of ethane in exhaled breath. METHODS Samples of alveolar air were obtained from 11 smokers and 18 non-smokers. The air samples were analyzed for ethane using mass spectrometry. RESULTS The two groups of subjects were matched with respect to age and gender. The mean cumulative smoking status of the smokers was 11.8 (standard error 2.5) pack-years. The mean level of ethane in the alveolar breath of the group of smokers (2.53 (0.55) ppb) was not significantly different from that of the group of non-smokers (2.59 (0.29) ppb; p = 0.92). With all 29 subjects included, the Spearman rank correlation coefficient between ethane levels and cumulative smoking status was -0.11 (p = 0.58), while an analysis including only the smokers yielded a corresponding correlation coefficient of 0.11 (p = 0.75). CONCLUSION Our results show no evidence that cigarette smoking is related to increased n-3 lipid peroxidation as measured by expired ethane.
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Abstract
Oxidative stress is an important feature in the pathogenesis of COPD. Targeting oxidative stress with antioxidants or boosting the endogenous levels of antioxidants is likely to be beneficial in the treatment of COPD. Antioxidant agents such as thiol molecules (glutathione and mucolytic drugs, such as N-acetyl-L-cysteine and N-acystelyn), dietary polyphenols (curcumin, resveratrol, green tea, catechins/quercetin), erdosteine, and carbocysteine lysine salt, all have been reported to control nuclear factor-kappaB (NF-κ B) activation, regulation of glutathione biosynthesis genes, chromatin remodeling, and hence inflammatory gene expression. Specific spin traps such as α-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (ECSOD mimetic), porphyrins (AEOL 10150 and AEOL 10113), and a superoxide dismutase mimetic M40419 have also been reported to inhibit cigarette smoke-induced inflammatory responses in vivo. Since a variety of oxidants, free radicals, and aldehydes are implicated in the pathogenesis of COPD, it is possible that therapeutic administration of multiple antioxidants will be effective in the treatment of COPD. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in COPD are discussed.
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Affiliation(s)
- Irfan Rahman
- Department of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, 601 Elmwood Ave, Box 850, Rochester, NY 14642, USA.
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Thaiparambil JT, Vadhanam MV, Srinivasan C, Gairola CG, Gupta RC. Time-dependent formation of 8-oxo-deoxyguanosine in the lungs of mice exposed to cigarette smoke. Chem Res Toxicol 2007; 20:1737-40. [PMID: 18031018 DOI: 10.1021/tx700289g] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/23/2023]
Abstract
Active and passive smoking are major risk factors for lung cancer. Pro-oxidants in tobacco smoke have been implicated in smoking-associated disease development due to their potential role in inducing oxidative stress. Previous studies have failed to associate increased levels of oxidative damage to DNA with the formation of the potentially mutagenic lesion, 8-oxo-2-deoxyguanosine (8-oxodG), probably due to repair of this lesion. However, no systematic studies have been performed to assess the dose- and time-dependent formation and removal of this lesion by cigarette smoke exposure. In the present study, female A/J mice were exposed to side-stream cigarette smoke in a whole body exposure chamber for 6 h a day, 5 days a week for up to 6 weeks. Age-matched controls were maintained in filtered ambient air. Lung tissues were harvested from 2, 4, and 6 weeks smoke-exposed mice after 1, 3, 6, and 20 h, following the cessation of smoking. A significant increase in the levels of 8-oxodG in lung DNA was observed in 10 day smoke-exposed mice at 1 (11.5+/-1.1/10(6) nucleotides), 3 (20.2+/-2.7/10(6) nucleotides; p=0.0008), and 6 h (17.2+/-1.0/10(6) nucleotides; p<0.005) postcessation, as compared with age-matched sham treatment (8.8+/-2.3/10(6) nucleotides) (mean+/-SD). The levels significantly declined 20 h after the cessation of smoke exposure (14.0+/-1.6/10(6) nucleotides), although they were still higher than the control. Our results strongly suggest that there is a significant increase in the 8-oxodG levels immediately after the cessation of smoking, which is repaired over time. This initial increase in 8-oxodG levels may lead to gene mutations, and accumulation of such mutations over time can eventually lead to malignant transformation of the cells.
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Affiliation(s)
- Jose T Thaiparambil
- James Graham Brown Cancer Center and Department of Pharmacology and Toxicology, University of Louisville, 580 South Preston Street, Louisville, Kentucky 40202, USA
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Faustino J, Barroca M, Guiné R. Study of the Drying Kinetics of Green Bell Pepper and Chemical Characterization. FOOD AND BIOPRODUCTS PROCESSING 2007. [DOI: 10.1205/fbp07009] [Citation(s) in RCA: 49] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/19/2022]
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Nicita-Mauro V, Lo Balbo C, Mento A, Nicita-Mauro C, Maltese G, Basile G. Smoking, aging and the centenarians. Exp Gerontol 2007; 43:95-101. [PMID: 17686596 DOI: 10.1016/j.exger.2007.06.011] [Citation(s) in RCA: 48] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/04/2006] [Revised: 12/29/2006] [Accepted: 06/26/2007] [Indexed: 11/19/2022]
Abstract
The smoke of cigarettes represents an important accelerator of the aging process, both directly through complex mechanisms mediated prevalently by excessive formation of free radicals, and indirectly by favoring the appearance of various pathologies in which smoke is a recognized risk factor. This means that smoke compromises not only life expectancy, but also the quality of the life, favoring the occurrence of non-autosufficiency. Smoking is an important risk factor for many diseases, such as cancer, cardiovascular and respiratory diseases. These are also the main causes of death in the industrialized Countries, where the habit of smoking is also largely diffused. Non-smokers have a much higher life expectancy than smokers, and the suspension of smoking is accompanied, even in the elderly, by an increase in the survival time due to the reduction of smoke-induced biological damage. Therefore, cigarette smoking is opposing the longevity, particularly the extreme one, as it is confirmed by the observations obtained on centenarians. Among them, smoking is extremely rare, and even when it occurs among them, it is correlated almost exclusively to bad health conditions and non-autosufficiency, indicating that it compromises health status and the quality of life even in extremely long living subjects. Considering the demonstrated beneficial effects of suspension of smoking, all practitioners and geriatricians in particular, should promote the abstinence from smoking as a behavioral norm for a correct life style. Non-smokers can delay the appearance of diseases and of the aging process, thus attaining longevity; further, non-smoking habit allows genetically predisposed subjects to reach the extreme longevity and maintain an acceptable health status and autosufficiency.
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Affiliation(s)
- V Nicita-Mauro
- Cattedra di Geriatria e Gerontologia, Scuola di Specializzazione in Geriatria, Università degli Studi di Messina, Azienda Ospedaliera Universitaria Policlinico G. Martino, I-98125 Messina, Italy.
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Lykkesfeldt J, Viscovich M, Poulsen HE. Plasma malondialdehyde is induced by smoking: a study with balanced antioxidant profiles. Br J Nutr 2007; 92:203-6. [PMID: 15333149 DOI: 10.1079/bjn20041191] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022]
Abstract
It has been reported that smokers have higher plasma malondialdehyde concentrations compared with non-smokers. However, smokers have also consistently been shown to have a lower intake of fruits and vegetables as well as lower plasma antioxidant concentrations. Since both the latter issues may well influence the malondialdehyde concentration, we wanted to investigate if the observed difference between smokers and non-smokers was a result of differences in antioxidant status or if a more direct effect of smoking could also be isolated. In the present study, the plasma malondialdehyde and antioxidant profiles of a cohort of smokers (n48) and non-smokers (n32) were compared. While there was no significant difference in the major plasma antioxidants measured, i.e. ascorbic acid, α- and γ-tocopherol and uric acid, we found a significant effect of smoking on plasma malondialdehyde (P=0·0003). Consequently, the present study suggests that lipid peroxidation as measured by plasma malondialdehyde is induced by smokingper se. While poor antioxidant status presumably also affects lipid peroxidation, it is only partly responsible for the increased level found in smokers in general.
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Affiliation(s)
- Jens Lykkesfeldt
- Section of Pharmacology, Department of Veterinary Pathobiology, Royal Veterinary and Agricultural University, 9 Ridebanevej, DK-1870 Frederiksberg C, Copenhagen, Denmark.
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Nthenge AK, Weese JS, Carter M, Wei CI, Huang TS. Efficacy of gamma radiation and aqueous chlorine on Escherichia coli O157:H7 in hydroponically grown lettuce plants. J Food Prot 2007; 70:748-52. [PMID: 17388070 DOI: 10.4315/0362-028x-70.3.748] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022]
Abstract
Interaction of Escherichia coli O157:H7/pGFP with hydroponically grown lettuce plants was evaluated in this study. Lettuce seedlings were planted in contaminated Hoagland's nutrient solution and thereafter subjected to gamma radiation at 0.25, 0.5, and 0.75 kGy, and aqueous chlorine at 200 ppm. There was no trace of E. coli O157:H7/pGFP in lettuce leaves harvested from noncontaminated nutrient solution (control); however, for plants grown in contaminated nutrient solution, the pathogen was recovered from the leaves disinfected with 80% ethanol and 0.1% mercuric chloride. Most of the lettuce seedlings grown in contaminated nutrient solution tested negative for E. coli O157:H7/pGFP under controlled conditions. Gamma radiation at 0.25 and 0.5 kGy, and aqueous chlorine at 200 ppm failed to eliminate E. coli O157:H7/pGFP in lettuce tissue completely; however, the bacteria were not detected in 0.75-kGy treated plants. The presence of E. coli O157:H7/pGFP in lettuce leaves is an indication that the pathogen migrated from the contaminated hydroponic system through the roots to the internal locations of lettuce tissue. Due to inaccessibility and limited penetrating power, aqueous chlorine could not eliminate the bacteria localized in the internal tissue. Findings from this study suggest that gamma irradiation was more efficacious than was aqueous chlorine to control internal contamination in hydroponically grown lettuce. Gamma irradiation is a process that processors can use to inactivate E. coli O157:H7 and therefore, consumers benefit from a safer food product [corrected]
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Onol FF, Demir A, Temiz Y, Yüksel M, Eren F, Türkeri LN. The inhibitory effect of vitamin E on cigarette smoke-induced oxidative damage to the rat urothelium: can it prevent transitional cell carcinoma? Urol Int 2007; 78:150-4. [PMID: 17293656 DOI: 10.1159/000098074] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/02/2006] [Accepted: 07/21/2006] [Indexed: 11/19/2022]
Abstract
INTRODUCTION We aimed to detect reactive oxygen species (ROS) and assess subsequent carcinogenesis in terms of cellular proliferation in the bladder and kidney epithelial tissues of rats exposed to cigarette smoke (CS), and to investigate the changes following vitamin E treatment. MATERIALS AND METHODS Twenty-four male Sprague-Dawley rats were divided into 3 groups: group 1 was kept intact; group 2 was subjected to CS exposure for 8 weeks, and group 3 received intraperitoneal vitamin E injections (200 mg/kg/week) for 8 weeks in addition to CS exposure. Histological examination and Ki67 antigen expression measurements were made from bladder and renal pelvic tissue sections. Luminol-amplified chemiluminescence was used to measure ROS levels. All results were compared using a one-way ANOVA test. RESULTS In CS-exposed rats, light microscopy of renal and bladder tissues revealed nonspecific epithelial changes; however, Ki67 expression was significantly increased in bladder tissues compared to other groups (17.5 +/- 4.7, 35 +/- 2.9 and 18.7 +/- 5.1% in groups 1, 2 and 3, respectively, p < 0.05). Chemiluminescence levels in bladder and renal tissues were also significantly higher in the CS-exposed animals (78.1 +/- 11.4, 148 +/- 13.3, 97.8 +/- 6.1 rlu/mg for the bladder, and 99.8 +/- 12.2, 176.1 +/- 27.9, 67.1 +/- 9 rlu/mg, for renal pelvic tissues, respectively, p < 0.05). CONCLUSIONS Vitamin E can alleviate CS-induced oxidative damage in rat bladder and kidney epithelium suggesting a potential role for vitamin E in the prevention of CS-mediated carcinogenesis.
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Affiliation(s)
- Fikret Fatih Onol
- Department of Urology, Marmara University School of Medicine, Istanbul, Turkey.
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Karatas F, Kamışlı F. Variations of vitamins (A, C and E) and MDA in apricots dried in IR and microwave. J FOOD ENG 2007. [DOI: 10.1016/j.jfoodeng.2005.10.040] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/29/2022]
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Gabriel HE, Liu Z, Crott JW, Choi SW, Song BC, Mason JB, Johnson EJ. A comparison of carotenoids, retinoids, and tocopherols in the serum and buccal mucosa of chronic cigarette smokers versus nonsmokers. Cancer Epidemiol Biomarkers Prev 2006; 15:993-9. [PMID: 16702382 DOI: 10.1158/1055-9965.epi-05-0664] [Citation(s) in RCA: 33] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
BACKGROUND Cigarette smoking, a major risk factor for oropharyngeal cancer, is reported to alter oral levels of carotenoids and tocopherols. Such effects may be important because these nutrients, as well as retinoids, are putative chemoprotective agents. OBJECTIVES To determine whether chronic smoking is associated with altered concentrations of these nutrients in serum and buccal mucosa; to distinguish whether such effects are ascribable to diet; and to determine whether oral concentrations of these nutrients correlate with a putative biomarker of oral cancer risk. METHODS Serum and buccal mucosal cells (BMC) were analyzed for these nutrients and for BMC micronuclei in smokers (n = 35) and nonsmokers (n = 21). RESULTS General linear regression with adjustments for dietary intake showed that smokers possess lower serum concentrations of beta- and alpha-carotene, cryptoxanthin, lutein, and zeaxanthin (P </= 0.01) and a significantly higher serum gamma-tocopherol (P = 0.03). In BMCs, smokers had significantly lower concentrations of beta- and alpha-carotene, lycopene, and alpha-tocopherol (P < 0.05) but significantly higher gamma-tocopherol (P < 0.01). Among nonsmokers, many serum carotenoid concentrations correlated with concentrations of the corresponding nutrient in BMCs whereas no such correlations existed among smokers. BMC micronuclei did not correlate with the oral concentration of any micronutrient. CONCLUSIONS Chronic cigarette smokers have lower concentrations of many dietary antioxidants in serum and BMCs compared with nonsmokers, an effect which is not entirely ascribable to diet. Nevertheless, the lack of concordance between oral concentrations of these nutrients and genetic damage in the BMCs of smokers does not support a protective role for these nutrients in oral carcinogenesis.
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Affiliation(s)
- Helen E Gabriel
- Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111, USA.
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Abstract
Vitamin E is comprised of four tocopherols and four tocotrienols, and functions as a lipophilic chain-breaking antioxidant that prevents lipid peroxidation. Although it is well recognized that cigarette smoke is source of oxidative stress, relatively little is known regarding how oxidative stress alters vitamin E utilization in humans. Therefore, this review will highlight the recent knowledge regarding how cigarette smoking alters vitamin E (as alpha- and gamma-tocopherols) utilization in humans. Specifically, we will discuss the mechanisms by which cigarette smoking increases the turnover of plasma vitamin E, decreases the P450-mediated metabolism of vitamin E, and increases the nitration of gamma-tocopherol to result in the formation of 5-nitro-gamma-tocopherol. In addition, the interrelationship between oxidative stress and vitamin C will also be emphasized as it relates to vitamin E utilization.
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Affiliation(s)
- Richard S Bruno
- Department of Nutritional Sciences, University of Connecticut, Storrs, CT, United States
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Proteggente AR, Rota C, Majewicz J, Rimbach G, Minihane AM, Kraemer K, Lodge JK. Cigarette smokers differ in their handling of natural (RRR) and synthetic (all rac) alpha-tocopherol: a biokinetic study in apoE4 male subjects. Free Radic Biol Med 2006; 40:2080-91. [PMID: 16785022 DOI: 10.1016/j.freeradbiomed.2006.02.006] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/14/2005] [Revised: 01/20/2006] [Accepted: 02/07/2006] [Indexed: 10/25/2022]
Abstract
We have compared the biokinetics of deuterated natural (RRR) and synthetic (all rac) alpha-tocopherol in male apoE4-carrying smokers and nonsmokers. In a randomized, crossover study subjects underwent two 4-week treatments (400 mg/day) with undeuterated RRR- and all rac-alpha-tocopheryl acetate around a 12-week washout. Before and after each supplementation period subjects underwent a biokinetic protocol (48 h) with 150 mg deuterated RRR- or all rac-alpha-tocopheryl acetate. During the biokinetic protocols, the elimination of endogenous plasma alpha-tocopherol was significantly faster in smokers (P < 0.05). However, smokers had a lower uptake of deuterated RRR than nonsmokers, but there was no difference in uptake of deuterated all rac. The supplementation regimes significantly raised plasma alpha-tocopherol (P < 0.001) with no differences in response between smokers and nonsmokers or between alpha-tocopherol forms. Smokers had significantly lower excretion of alpha-carboxyethyl-hydroxychroman than nonsmokers following supplementation (P < 0.05). Nonsmokers excreted more alpha-carboxyethyl-hydroxychroman following RRR than all rac; however, smokers did not differ in excretion between forms. At baseline, smokers had significantly lower ascorbate (P < 0.01) and higher F(2)-isoprostanes (P < 0.05). F(2)-isoprostanes in smokers remained unchanged during the study, but increased in nonsmokers following alpha-tocopherol supplementation. These data suggest that apoE4-carrying smokers and nonsmokers differ in their handling of natural and synthetic alpha-tocopherol.
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Affiliation(s)
- Anna R Proteggente
- Centre for Nutrition and Food Safety, School of Biomedical and Molecular Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK
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Qin F, Yan C, Patel R, Liu W, Dong E. Vitamins C and E attenuate apoptosis, beta-adrenergic receptor desensitization, and sarcoplasmic reticular Ca2+ ATPase downregulation after myocardial infarction. Free Radic Biol Med 2006; 40:1827-42. [PMID: 16678021 DOI: 10.1016/j.freeradbiomed.2006.01.019] [Citation(s) in RCA: 43] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/19/2005] [Revised: 01/12/2006] [Accepted: 01/19/2006] [Indexed: 02/07/2023]
Abstract
Oxidative stress plays an important role in mediating ventricular remodeling and dysfunction in heart failure (HF), but its mechanism of action has not been fully elucidated. In this study we determined whether a combination of antioxidant vitamins reduced myocyte apoptosis, beta-adrenergic receptor desensitization, and sarcoplasmic reticular (SR) Ca2+ ATPase downregulation in HF after myocardial infarction (MI) and whether these effects were associated with amelioration of left ventricular (LV) remodeling and dysfunction. Vitamins (vitamin C 300 mg and vitamin E 300 mg) were administered to rabbits 1 week after MI or sham operation for 11 weeks. The results showed that MI rabbits exhibited cardiac dilation and LV dysfunction measured by fractional shortening and the maximal rate of pressure rise (dP/dt), an index of contractility. These changes were associated with elevation of oxidative stress, decreases of mitochondrial Bcl-2 and cytochrome c proteins, increases of cytosolic Bax and cytochrome c proteins, caspase 9 and caspase 3 activities and myocyte apoptosis, and downregulation of beta-adrenergic receptor sensitivity and SR Ca2+ ATPase. Combined treatment with vitamins C and E diminished oxidative stress, increased mitochondrial Bcl-2 protein, decreased cytosolic Bax, prevented cytochrome c release from mitochondria to cytosol, reduced caspase 9 and caspase 3 activities and myocyte apoptosis, blocked beta-adrenergic receptor desensitization and SR Ca2+ ATPase downregulation, and attenuated LV dilation and dysfunction in HF after MI. The results suggest that antioxidant therapy may be beneficial in HF.
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Affiliation(s)
- Fuzhong Qin
- Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
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Kelly FJ. Vitamins and respiratory disease: antioxidant micronutrients in pulmonary health and disease. Proc Nutr Soc 2006; 64:510-26. [PMID: 16313695 DOI: 10.1079/pns2005457] [Citation(s) in RCA: 37] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]
Abstract
The lungs are continually exposed to relatively-high O(2) tensions, and as such, in comparison with other organs, they represent a unique tissue for the damaging effects of oxidant attack. At particular times during a lifetime this every day challenge may increase exponentially. The first oxidative insult occurs at birth, when cells are exposed to a sudden 5-fold increase in O(2) concentration. Thereafter, the human lung, from infancy through to old age, can be subjected to deleterious oxidative events as a consequence of inhaling environmental pollutants or irritants, succumbing to several pulmonary diseases (including infant and adult respiratory distress syndromes, asthma, chronic obstructive pulmonary disease, cystic fibrosis and cancer) and receiving treatment for these diseases. The present paper will review the concept that consumption of a healthy diet and the consequent ability to establish and then maintain adequate micronutrient antioxidant concentrations in the lung throughout life, and following various oxidative insults, could prevent or reduce the incidence of oxidant-mediated respiratory diseases. Furthermore, the rationale, practicalities and complexities of boosting the antioxidant pool of the respiratory-tract lining fluid in diseases in which oxidative stress is actively involved, by direct application to the lung v. dietary modification, in order to achieve a therapeutic effect will be discussed.
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Affiliation(s)
- Frank J Kelly
- Lung Biology, School of Health & Life Sciences, King's College, London, UK.
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Bruno RS, Leonard SW, Atkinson J, Montine TJ, Ramakrishnan R, Bray TM, Traber MG. Faster plasma vitamin E disappearance in smokers is normalized by vitamin C supplementation. Free Radic Biol Med 2006; 40:689-97. [PMID: 16458200 DOI: 10.1016/j.freeradbiomed.2005.10.051] [Citation(s) in RCA: 134] [Impact Index Per Article: 7.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/12/2005] [Revised: 10/11/2005] [Accepted: 10/18/2005] [Indexed: 11/19/2022]
Abstract
Vitamin E disappearance is accelerated in cigarette smokers due to their increased oxidative stress and is inversely correlated with plasma vitamin C concentrations. Therefore, we hypothesized that ascorbic acid supplementation (500 mg, twice daily; 2 weeks) would normalize smokers' plasma alpha- and gamma-tocopherol disappearance rates and conducted a double-blind, placebo-controlled, randomized crossover investigation in smokers (n=11) and nonsmokers (n=13) given a single dose of deuterium-labeled alpha- and gamma-tocopherols (50 mg each d6-RRR-alpha and d2-RRR-gamma-tocopheryl acetate). During the placebo trial, smokers, compared with nonsmokers, had significantly (P<0.05) greater alpha- and gamma-tocopherol fractional disappearance rates and shorter half-lives. Ascorbic acid supplementation doubled (P<0.0001) plasma ascorbic acid concentrations in both groups and attenuated smokers', but not nonsmokers', plasma alpha- and gamma-tocopherol (P<0.05) fractional disappearance rates by 25% and 45%, respectively. Likewise, smokers' plasma deuterium-labeled alpha- and gamma-tocopherol concentrations were significantly higher (P<0.05) at 72 h during ascorbic acid supplementation compared with placebo. Ascorbic acid supplementation did not significantly change (P>0.05) time of maximal or maximal-labeled alpha- and gamma-tocopherol concentrations. Smokers' plasma F2alpha-isoprostanes were approximately 26% higher than nonsmokers (P>0.05) and were not affected by ascorbic acid supplementation in either group (P>0.05). In summary, cigarette smoking increased plasma alpha- and gamma-tocopherol fractional disappearance rates, suggesting that the oxidative stress from smoking oxidizes tocopherols and that plasma ascorbic acid reduces alpha- and gamma-tocopheroxyl radicals to nonoxidized forms, thereby decreasing vitamin E disappearance in humans.
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Affiliation(s)
- Richard S Bruno
- Linus Pauling Institute, 571 Weniger Hall, Oregon State University, Corvallis, OR 97331, USA
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Kirkham P, Rahman I. Oxidative stress in asthma and COPD: antioxidants as a therapeutic strategy. Pharmacol Ther 2006; 111:476-94. [PMID: 16458359 DOI: 10.1016/j.pharmthera.2005.10.015] [Citation(s) in RCA: 313] [Impact Index Per Article: 16.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/25/2005] [Accepted: 10/25/2005] [Indexed: 01/10/2023]
Abstract
Asthma and chronic obstructive pulmonary disease (COPD) are inflammatory lung diseases that are characterized by systemic and chronic localized inflammation and oxidative stress. Sources of oxidative stress arise from the increased burden of inhaled oxidants, as well as elevated amounts of reactive oxygen species (ROS) released from inflammatory cells. Increased levels of ROS, either directly or via the formation of lipid peroxidation products, may play a role in enhancing the inflammatory response in both asthma and COPD. Moreover, in COPD it is now recognized as the main pathogenic factor for driving disease progression and increasing severity. ROS and lipid peroxidation products can influence the inflammatory response at many levels through its impact on signal transduction mechanisms, activation of redox-sensitive transcriptions factors, and chromatin regulation resulting in pro-inflammatory gene expression. It is this impact of ROS on chromatin regulation by reducing the activity of the transcriptional co-repressor, histone deacetylase-2 (HDAC-2), that leads to the poor efficacy of corticosteroids in COPD, severe asthma, and smoking asthmatics. Thus, the presence of oxidative stress has important consequences for the pathogenesis, severity, and treatment of asthma and COPD. However, for ROS to have such an impact, it must first overcome a variety of antioxidant defenses. It is likely, therefore, that a combination of antioxidants may be effective in the treatment of asthma and COPD. Various approaches to enhance the lung antioxidant screen and clinical trials of antioxidant compounds are discussed.
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Affiliation(s)
- Paul Kirkham
- Respiratory Diseases, Novartis Institutes for Biomedical Research, Horsham, West Sussex, RH12 5AB, UK.
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