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Ghasempour Dabaghi G, Rabiee Rad M, Mohammad-Zamani M, Karimi Shervedani A, Bahrami-Samani F, Heshmat-Ghahdarijani K. The role of coenzyme Q10 as a preventive and therapeutic agent for the treatment of cancers. Curr Probl Cancer 2024; 48:101063. [PMID: 38330781 DOI: 10.1016/j.currproblcancer.2024.101063] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/02/2023] [Revised: 01/08/2024] [Accepted: 01/23/2024] [Indexed: 02/10/2024]
Abstract
Currently, several options are available for the prevention and treatment of cancers; however, many limitations remain with these approaches. Recently, antioxidants have become important preventive and therapeutic alternatives with few adverse events and minimum cost. Coenzyme Q10 (CoQ10) is a naturally occurring component that performs an anticancer function by reducing oxidative stress. CoQ10 supplementation as an adjuvant therapy offers more progress in the elimination and development of cancers. This review aimed to critically assess and summarize the implication of CoQ10 in cancers, highlighting possible mechanisms, and future directions of research for the standardization of the current regimen for cancer prevention and treatment.
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Affiliation(s)
| | - Mehrdad Rabiee Rad
- School of Medicine, Isfahan University of Medical Science, Isfahan, Iran
| | | | | | | | - Kiyan Heshmat-Ghahdarijani
- Heart Failure Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Shahid Rahmani Alley, Moshtagh Sevom St., Isfahan, Iran.
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2
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Nagase M, Sakamoto M, Amekura S, Akiba S, Kashiba M, Yokoyama K, Yamamoto Y, Fujisawa A. Riboflavin compounds show NAD(P)H dependent quinone oxidoreductase-like quinone reducing activity. J Clin Biochem Nutr 2023; 73:52-60. [PMID: 37534093 PMCID: PMC10390810 DOI: 10.3164/jcbn.22-140] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/12/2022] [Accepted: 02/01/2023] [Indexed: 08/04/2023] Open
Abstract
NAD(P)H-dependent quinone oxidoreductase (NQO) is an essential enzyme in living organisms and cells protecting them from oxidative stress. NQO reduces coenzyme Q (CoQ) using NAD(P)H as an electron donor. In the present study, we searched for coenzyme Q10 reducing activity from fractions of gel filtration-fractionated rat liver homogenate. In addition to the large-molecular-weight fraction containing NQO, CoQ10 reducing activity was also detected in a low-molecular-weight fraction. Furthermore, dicumarol, a conventional inhibitor of NQO1 (DT diaphorase), did not inhibit the reduction but quercetin did, suggesting that the activity was not due to NQO1. After further purification, the NADH-dependent CoQ10-reducing compound was identified as riboflavin. Riboflavin is an active substituent of other flavin compounds such as FAD and FMN. These flavin compounds also reduced not only CoQ homologues but also vitamin K homologues in the presence of NADH. The mechanism was speculated to work as follows: NADH reduces flavin compounds to the corresponding reduced forms, and subsequently, the reduced flavin compounds immediately reduce bio-quinones. Furthermore, the flavin-NADH system reduces CoQ10 bound with saposin B, which is believed to function as a CoQ transfer protein in vivo. This flavin-dependent CoQ10 reduction, therefore, may function in aqueous phases such as the cell cytosol and bodily fluids.
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Affiliation(s)
- Midori Nagase
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Miku Sakamoto
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Sakiko Amekura
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Sayaka Akiba
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Misato Kashiba
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Kenji Yokoyama
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Yorihiro Yamamoto
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Akio Fujisawa
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
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Orlando P, Sabbatinelli J, Silvestri S, Marcheggiani F, Cirilli I, Dludla PV, Molardi A, Nicolini F, Tiano L. Ubiquinol supplementation in elderly patients undergoing aortic valve replacement: biochemical and clinical aspects. Aging (Albany NY) 2020; 12:15514-15531. [PMID: 32741773 PMCID: PMC7467386 DOI: 10.18632/aging.103742] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/06/2020] [Accepted: 07/07/2020] [Indexed: 12/24/2022]
Abstract
Epidemiological data show a rise in the mean age of patients affected by heart disease undergoing cardiac surgery. Senescent myocardium reduces the tolerance to ischemic stress and there are indications about age-associated deficit in post-operative cardiac performance. Coenzyme Q10 (CoQ10), and more specifically its reduced form ubiquinol (QH), improve several conditions related to bioenergetic deficit or increased exposure to oxidative stress. This trial (Eudra-CT 2009-015826-13) evaluated the clinical and biochemical effects of ubiquinol in 50 elderly patients affected by severe aortic stenosis undergoing aortic valve replacement and randomized to either placebo or 400 mg/day ubiquinol from 7 days before to 5 days after surgery. Plasma and cardiac tissue CoQ10 levels and oxidative status, circulating troponin I, CK-MB (primary endpoints), IL-6 and S100B were assessed. Moreover, main cardiac adverse effects, NYHA class, contractility and myocardial hypertrophy (secondary endpoints) were evaluated during a 6-month follow-up visit. Ubiquinol treatment counteracted the post-operative plasma CoQ10 decline (p<0.0001) and oxidation (p=0.038) and curbed the post-operative increase in troponin I (QH, 1.90 [1.47-2.48] ng/dL; placebo, 4.03 [2.45-6.63] ng/dL; p=0.007) related to cardiac surgery. Moreover, ubiquinol prevented the adverse outcomes that might have been associated with defective left ventricular ejection fraction recovery in elderly patients.
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Affiliation(s)
- Patrick Orlando
- Department of Life and Environmental Sciences, Università Politecnica delle Marche, Via Brecce Bianche, Ancona 60100, Italy
| | - Jacopo Sabbatinelli
- Department of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona 60100, Italy
| | - Sonia Silvestri
- Department of Life and Environmental Sciences, Università Politecnica delle Marche, Via Brecce Bianche, Ancona 60100, Italy
| | - Fabio Marcheggiani
- Department of Life and Environmental Sciences, Università Politecnica delle Marche, Via Brecce Bianche, Ancona 60100, Italy
| | - Ilenia Cirilli
- Department of Life and Environmental Sciences, Università Politecnica delle Marche, Via Brecce Bianche, Ancona 60100, Italy
| | - Phiwayinkosi Vusi Dludla
- Department of Life and Environmental Sciences, Università Politecnica delle Marche, Via Brecce Bianche, Ancona 60100, Italy.,Biomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg 7505, South Africa
| | - Alberto Molardi
- Cardiac Surgery Department, Parma University Hospital, Parma 43126, Italy
| | - Francesco Nicolini
- Cardiac Surgery Department, Parma University Hospital, Parma 43126, Italy
| | - Luca Tiano
- Department of Life and Environmental Sciences, Università Politecnica delle Marche, Via Brecce Bianche, Ancona 60100, Italy
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Miso Soup Consumption Enhances the Bioavailability of the Reduced Form of Supplemental Coenzyme Q 10. J Nutr Metab 2020; 2020:5349086. [PMID: 31998536 PMCID: PMC6969983 DOI: 10.1155/2020/5349086] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/31/2019] [Accepted: 11/25/2019] [Indexed: 12/22/2022] Open
Abstract
Coenzyme Q10 (CoQ10) is an essential compound that is involved in energy production and is a lipid-soluble antioxidant. Although it has been proposed as an antiaging and a health-supporting supplement, its low bioavailability remains a significant issue. Concurrent food intake enhances the absorption of orally administered CoQ10, but it has not been fully established whether specific food substances affect intestinal CoQ10 absorption. Therefore, to determine whether the bioavailability of supplemental CoQ10 is affected by diet, P30, a granulated and reduced form of CoQ10, was dispersed in four different foods, clear soup, miso soup, milk soup, and raw egg sauce. Those foods which contained CoQ10 were consumed on different occasions at intervals of 6–14 weeks by the same participants. Thirteen participants were recruited in the single-dose and repeated clinical study. When miso soup containing P30 was provided, the serum CoQ10 concentration increased faster than when participants consumed other P30-containing soups or a P30-containing raw egg sauce. The area under the curve for serum CoQ10 during the first 5 h after consumption of the P30-containing miso soup was approximately 1.5 times larger than those after the consumption of other P30-containing meals. These data imply that the absorption of CoQ10 supplements can be enhanced by consuming them with food and in particular with specific food substances, such as miso soup.
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Kloer HU, Belardinelli R, Ruchong O, Rosenfeldt F. Combining Ubiquinol With a Statin May Benefit Hypercholesterolaemic Patients With Chronic Heart Failure. Heart Lung Circ 2019; 29:188-195. [PMID: 31668616 DOI: 10.1016/j.hlc.2019.08.017] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/19/2017] [Revised: 07/01/2019] [Accepted: 08/16/2019] [Indexed: 12/17/2022]
Abstract
Heart failure (HF) is one of the most common causes of death in Western society. Recent results underscore the utility of coenzyme Q10 (CoQ10) addition to standard medications in order to reduce mortality and to improve quality of life and functional capacity in chronic heart failure (CHF). The rationale for CoQ10 supplementation in CHF is two-fold. One is the well-known role of CoQ10 in myocardial bioenergetics, and the second is its antioxidant property. Redox balance is also improved by oral supplementation of CoQ10, and this effect contributes to enhanced endothelium-dependent relaxation. Previous reports have shown that CoQ10 concentration is decreased in myocardial tissue in CHF and by statin therapy, and the greater the CoQ10 deficiency the more severe is the cardiocirculatory impairment. In patients with CHF and hypercholesterolaemia being treated with statins, the combination of CoQ10 with a statin may be useful for two reasons: decreasing skeletal muscle injury and improving myocardial function. Ubiquinol, the active reduced form of CoQ10, presents higher bioavailability than the oxidised form ubiquinone, and should be the preferred form to be added to a statin. The combination ezetimibe/simvastatin may have advantages over single statins. Since ezetimibe reduces absorption of cholesterol and does not affect CoQ10 synthesis in the liver, the impact of this combination on CoQ10 tissue levels will be much less than that of high dose statin monotherapy at any target low density lipoprotein-cholesterol (LDL-C) level to be reached. This consideration makes the ezetimibe/statin combination the ideal LDL-lowering agent to be combined with ubiquinol in CHF patients. However, particular caution is advisable with the use of strategies of extreme lowering of cholesterol that may negatively impact on myocardial function. All in all there is a strong case for considering co-administration of ubiquinol with statin therapy in patients with depressed or borderline myocardial function.
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Affiliation(s)
- Hans-Ulrich Kloer
- Emer, Third Medical Department, UKGM, University of Giessen, Germany
| | | | - Ou Ruchong
- Baker Heart and Diabetes Institute, Melbourne, Vic, Australia; Faculty of Health, Arts and Design, Swinburne University of Technology, Melbourne, Vic, Australia
| | - Franklin Rosenfeldt
- Baker Heart and Diabetes Institute, Melbourne, Vic, Australia; Faculty of Health, Arts and Design, Swinburne University of Technology, Melbourne, Vic, Australia.
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Iida S, Yamamoto Y, Susa C, Tsukui K, Fujisawa A. 5- N-Carboxyimino-6- N-chloroaminopyrimidine-2,4(3 H)-dione as a hypochlorite-specific oxidation product of uric acid. J Clin Biochem Nutr 2018; 63:85-89. [PMID: 30279617 PMCID: PMC6160727 DOI: 10.3164/jcbn.18-6] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/11/2018] [Accepted: 01/31/2018] [Indexed: 01/11/2023] Open
Abstract
Although uric acid is known to react with many reactive oxygen species, its specific oxidation products have not been fully characterized. We now report that 5-N-carboxyimino-6-N-chloroaminopyrimidine-2,4(3H)-dione (CCPD) is a hypochlorite (ClO-)-specific oxidation product of uric acid. The yield of CCPD was 40-70% regardless of the rate of mixing of ClO- with uric acid. A previously reported product, allantoin (AL), was a minor product. Its yield (0-20%) decreased with decreasing rate of mixing of ClO- with uric acid, indicating that allantoin is less important in vivo. Kinetic studies revealed that the formation of CCPD required two molecules of ClO- per uric acid reacted. The identity of CCPD was determined from its molecular formula (C5H3ClN4O4) measured by LC/time-of-flight mass spectrometry and a plausible reaction mechanism. This assumption was verified by the fact that all mass fragments (m/z -173, -138, -113, and -110) fit with the chemical structure of CCPD and its tautomers. Isolated CCPD was stable at pH 6.0-8.0 at 37°C for at least 6 h. The above results and the fact that uric acid is widely distributed in the human body at relatively high concentrations indicate that CCPD is a good marker of ClO- generation in vivo.
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Affiliation(s)
- Sayaka Iida
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Yorihiro Yamamoto
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Chisato Susa
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Kana Tsukui
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Akio Fujisawa
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
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Iida S, Ohkubo Y, Yamamoto Y, Fujisawa A. Parabanic acid is the singlet oxygen specific oxidation product of uric acid. J Clin Biochem Nutr 2017; 61:169-175. [PMID: 29203957 PMCID: PMC5703782 DOI: 10.3164/jcbn.17-24] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/08/2017] [Accepted: 05/16/2017] [Indexed: 12/26/2022] Open
Abstract
Uric acid quenches singlet oxygen physically or reacts with it, but the oxidation product has not been previously characterized. The present study determined that the product is parabanic acid, which was confirmed by LC/TOFMS analysis. Parabanic acid was stable at acidic pH (<5.0), but hydrolyzed to oxaluric acid at neutral or alkaline pH. The total yields of parabanic acid and oxaluric acid based on consumed uric acid were ~100% in clean singlet oxygen production systems such as UVA irradiation of Rose Bengal and thermal decomposition of 3-(1,4-dihydro-1,4-epidioxy-4-methyl-1-naphthyl)propionic acid. However, the ratio of the amount of uric acid consumed to the total amount of singlet oxygen generated was less than 1/180, indicating that most of the singlet oxygen was physically quenched. The total yields of parabanic acid and oxaluric acid were high in the uric acid oxidation systems with hydrogen peroxide plus hypochlorite or peroxynitrite. They became less than a few percent in peroxyl radical-, hypochlorite- or peroxynitrite-induced oxidation of uric acid. These results suggest that parabanic acid could be an in vivo probe of singlet oxygen formation because of the wide distribution of uric acid in human tissues and extracellular spaces. In fact, sunlight exposure significantly increased human skin levels of parabanic acid.
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Affiliation(s)
- Sayaka Iida
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Yuki Ohkubo
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Yorihiro Yamamoto
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
| | - Akio Fujisawa
- School of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakura-cho, Hachioji, Tokyo 192-0982, Japan
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Tabassum H, Parvez S, Raisuddin S. Melatonin abrogates nonylphenol-induced testicular dysfunction in Wistar rats. Andrologia 2016; 49. [DOI: 10.1111/and.12648] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 04/20/2016] [Indexed: 12/24/2022] Open
Affiliation(s)
- H. Tabassum
- Department of Medical Elementology and Toxicology; Jamia Hamdard (Hamdard University); New Delhi India
- Department of Biochemistry; Jamia Hamdard (Hamdard University); New Delhi India
| | - S. Parvez
- Department of Medical Elementology and Toxicology; Jamia Hamdard (Hamdard University); New Delhi India
| | - S. Raisuddin
- Department of Medical Elementology and Toxicology; Jamia Hamdard (Hamdard University); New Delhi India
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Langsjoen PH, Langsjoen AM. Comparison study of plasma coenzyme Q10 levels in healthy subjects supplemented with ubiquinol versus ubiquinone. Clin Pharmacol Drug Dev 2013; 3:13-7. [PMID: 27128225 DOI: 10.1002/cpdd.73] [Citation(s) in RCA: 41] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/25/2012] [Accepted: 05/31/2013] [Indexed: 12/21/2022]
Abstract
The bioavailability of the reduced form of coenzyme Q10 (ubiquinol) was compared to oxidized coenzyme Q10 (ubiquinone) with identical soft gel capsule excipients by measuring steady state plasma coenzyme Q10 (CoQ10 ) levels in 12 healthy volunteers. After baseline levels of ubiquinol, ubiquinone, total CoQ10 , α-tocopherol, and total cholesterol were obtained, follow-up lab work was performed after 4 weeks of 200 mg/day of ubiquinone, after 4 weeks washout, and after 4 weeks of 200 mg/day of ubiquinol. Plasma total CoQ10 increased from 0.9 to 2.5 µg/mL (P < 0.001) after 4 weeks of ubiquinone and increased from 0.9 to 4.3 µg/mL (P < 0.001) after 4 weeks of ubiquinol. Total CoQ10 /cholesterol ratio increased from 0.2 to 0.7 µmol/mmol after 4 weeks of ubiquinone and increased from 0.2 to 1.2 µmol/mmol after 4 weeks of ubiquinol. Both the increase in plasma CoQ10 and the increase in CoQ10 /cholesterol ratio were significantly better after ubiquinol (P < 0.005 and P < 0.001, respectively) than after ubiquinone indicating superior bioavailability. Plasma ubiquinol/total CoQ10 ratio increased from baseline during ubiquinol supplementation (P < 0.005) and remained unchanged after ubiquinone supplementation. No side effects were noted in this study.
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Yuan B, Liu C, Xu P, Lin L, Pan C, Wang L, Xu H. Validated HPLC method for the quantitative determination of CoQ10 in dog plasma and its application to a pharmacokinetic study. Biomed Chromatogr 2010; 25:1038-44. [DOI: 10.1002/bmc.1567] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/14/2010] [Revised: 09/29/2010] [Accepted: 09/30/2010] [Indexed: 11/08/2022]
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Renal preservation effect of ubiquinol, the reduced form of coenzyme Q10. Clin Exp Nephrol 2010; 15:30-3. [PMID: 20878200 DOI: 10.1007/s10157-010-0350-8] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/21/2010] [Accepted: 08/29/2010] [Indexed: 10/19/2022]
Abstract
BACKGROUND The aim of this study was to evaluate the renal preservation effect of ubiquinol, the reduced form of coenzyme Q10 (CoQ10). METHODS Three-week-old heminephrectomized male Sprague-Dawley rats were divided into three groups (10 animals each): diet with normal (0.3%) salt, high (8%) salt, and high salt plus 600 mg/kg body weight/day of ubiquinol, for 4 weeks. Systolic blood pressure (SBP), urinary albumin (u-alb), superoxide anion generation (lucigenin chemiluminescence) and ubiquinol levels in renal tissues were examined. RESULTS Salt loading increased SBP (111.0 ± 3.6 vs. 169.4 ± 14.3 mmHg, p < 0.01) and u-alb (43.8 ± 28.0 vs. 2528.7 ± 1379.0 µg/day, p < 0.02). These changes were associated with stimulation of superoxide generation in the kidney (866.3 ± 102.8 vs. 2721.4 ± 973.3 RLU/g kidney, p < 0.01). However, ubiquinol decreased SBP (143.9 ± 29.0 mmHg, p < 0.05), u-alb (256.1 ± 122.1 µg/day, p < 0.02), and renal superoxide production (877.8 ± 195.6 RLU/g kidney, p < 0.01), associated with an increase in renal ubiquinol levels. CONCLUSION Ubiquinol, the reduced form of CoQ10, effectively ameliorates renal function, probably due to its antioxidant effect. Thus, ubiquinol may be a candidate for the treatment of patients with kidney disease.
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Miles MV, Miles L, Tang PH, Horn PS, Steele PE, DeGrauw AJ, Wong BL, Bove KE. Systematic evaluation of muscle coenzyme Q10 content in children with mitochondrial respiratory chain enzyme deficiencies. Mitochondrion 2008; 8:170-80. [DOI: 10.1016/j.mito.2008.01.003] [Citation(s) in RCA: 33] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/30/2007] [Revised: 12/19/2007] [Accepted: 01/18/2008] [Indexed: 10/22/2022]
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Tasci I, Mas MR, Vural SA, Deveci S, Comert B, Alcigir G, Mas N, Akay C, Bozdayi M, Yurdaydin C, Bozkaya H, Uzunalimoglu O, Isik AT, Said HM. Pegylated interferon-alpha plus taurine in treatment of rat liver fibrosis. World J Gastroenterol 2007; 13:3237-3244. [PMID: 17589904 PMCID: PMC4436611 DOI: 10.3748/wjg.v13.i23.3237] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/07/2006] [Revised: 02/02/2007] [Accepted: 02/08/2007] [Indexed: 02/06/2023] Open
Abstract
AIM To investigate the antifibrotic effects of peginterferon-alpha 2b and taurine on oxidative stress markers and hepatocellular apoptosis. METHODS Sixty rats with CCl4-induced liver fibrosis were divided into 4 groups (n=15). Group 1 was left for spontaneous recovery (SR). Groups 2-4 received peginterferon-alpha 2b, taurine, and their combination, respectively, for four weeks. Histological fibrosis scores, histomorphometric analysis, tissue hydroxyproline, tissue MDA, GPx and SOD activities were determined. Activated stellate cells and hepatocellular apoptosis were also evaluated. RESULTS The degree of fibrosis decreased in all treatment groups compared to spontaneous recovery group. Taurine alone and in combination with peginterferon-alpha 2b reduced oxidative stress markers, but peginterferon-alpha 2b alone did not. Apoptotic hepatocytes and activated stellate cells were higher in groups 2-4 than in group 1. Combined taurine and peginterferon-alpha 2b further reduced fibrosis and increased activated stellate cell apoptosis, but could not improve oxidative stress more than taurine alone. CONCLUSION Peginterferon-alpha 2b exerts anti-fibrotic effects on rat liver fibrosis. It seems ineffective against oxidative stress in vivo. Peginterferon-alpha 2b in combination with taurine seems to be an antifibrotic strategy.
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Affiliation(s)
- Ilker Tasci
- Department of Internal Medicine, Gulhane School of Medicine Etlik 06018 Ankara, Turkey.
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Oudshoorn JH, Lecluse AL, van den Berg R, Vaes WHJ, van der Laag J, Houwen RHJ. Decreased coenzyme Q10 concentration in plasma of children with cystic fibrosis. J Pediatr Gastroenterol Nutr 2006; 43:646-50. [PMID: 17130743 DOI: 10.1097/01.mpg.0000233193.77521.66] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/10/2022]
Abstract
OBJECTIVES Coenzyme Q10 (CoQ10) is an effective lipophilic antioxidant and protects against lipid peroxidation by scavenging radicals. Patients with cystic fibrosis generally have fat malabsorption; thus, we hypothesized that overall plasma CoQ10 concentration in pediatric patients with cystic fibrosis might be diminished. Because these patients have increased oxidative stress due to chronic pulmonary inflammation, we also assumed that the oxidized form of CoQ10 might be relatively increased. PATIENTS AND METHODS The total plasma CoQ10 levels and the oxidized and reduced form were measured by high-performance liquid chromatography in 30 children with cystic fibrosis (mean FEV1 % predicted = 88.5% +/- 18.7%) and 30 age-matched controls. RESULTS Total plasma CoQ10 levels were significantly lower in the cystic fibrosis group as compared with the control group (0.87 +/- 0.42 micromol/L and 1.35 +/- 0.39 micromol/L, respectively; P < 0.001). When correcting for the lower serum cholesterol level in patients with cystic fibrosis, this difference remained significant: the CoQ10/cholesterol ratio (micromol/mol) was 268.8 +/- 136.7 and 334.0 +/- 102.9 in patients and controls, respectively (P < 0.05). However, the CoQ10 redox status was identical in patients and controls (86.4% +/- 7.1% and 85.4% +/- 7.3%, respectively). CONCLUSIONS We found that the overall plasma CoQ10 concentration is lower in patients with cystic fibrosis, probably because of fat malabsorption. The CoQ10 redox status was not disturbed, indicating that CoQ10 could still be adequately regenerated in this group of patients with cystic fibrosis with mild-to-moderate pulmonary disease.
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Affiliation(s)
- Johanna H Oudshoorn
- Department of Pediatric Gastroenterology, Wilhelmina Children's Hospital, UMC Utrecht, The Netherlands.
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Manna P, Sinha M, Sil PC. Aqueous extract of Terminalia arjuna prevents carbon tetrachloride induced hepatic and renal disorders. BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE 2006; 6:33. [PMID: 17010209 PMCID: PMC1599753 DOI: 10.1186/1472-6882-6-33] [Citation(s) in RCA: 113] [Impact Index Per Article: 5.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 06/12/2006] [Accepted: 09/30/2006] [Indexed: 12/15/2022]
Abstract
BACKGROUND Carbon tetrachloride (CCl4) is a well-known hepatotoxin and exposure to this chemical is known to induce oxidative stress and causes liver injury by the formation of free radicals. Acute and chronic renal damage are also very common pathophysiologic disturbances caused by CCl4. The present study has been conducted to evaluate the protective role of the aqueous extract of the bark of Termnalia arjuna (TA), an important Indian medicinal plant widely used in the preparation of ayurvedic formulations, on CCl4 induced oxidative stress and resultant dysfunction in the livers and kidneys of mice. METHODS Animals were pretreated with the aqueous extract of TA (50 mg/kg body weight) for one week and then challenged with CCl4 (1 ml/kg body weight) in liquid paraffin (1:1, v/v) for 2 days. Serum marker enzymes, namely, glutamate pyruvate transaminase (GPT) and alkaline phosphatase (ALP) were estimated in the sera of all study groups. Antioxidant status in both the liver and kidney tissues were estimated by determining the activities of the antioxidative enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST); as well as by determining the levels of thiobarbutaric acid reactive substances (TBARS) and reduced glutathione (GSH). In addition, free radical scavenging activity of the extract was determined from its DPPH radical quenching ability. RESULTS Results showed that CCl4 caused a marked rise in serum levels of GPT and ALP. TBARS level was also increased significantly whereas GSH, SOD, CAT and GST levels were decreased in the liver and kidney tissue homogenates of CCl4 treated mice. Aqueous extract of TA successfully prevented the alterations of these effects in the experimental animals. Data also showed that the extract possessed strong free radical scavenging activity comparable to that of vitamin C. CONCLUSION Our study demonstrated that the aqueous extract of the bark of TA could protect the liver and kidney tissues against CCl4-induced oxidative stress probably by increasing antioxidative defense activities.
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Affiliation(s)
- Prasenjit Manna
- Department of Chemistry, Bose Institute, 93/1, Acharya Prafulla Chandra Road, Kolkata-700009, India
| | - Mahua Sinha
- Department of Chemistry, Bose Institute, 93/1, Acharya Prafulla Chandra Road, Kolkata-700009, India
| | - Parames C Sil
- Department of Chemistry, Bose Institute, 93/1, Acharya Prafulla Chandra Road, Kolkata-700009, India
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Wada H, Hagiwara SI, Saitoh E, Ieki R, Okamura T, Ota T, Iguchi M, Yuasa K, Kodaka T, Koishi T, Yamamoto Y, Goto H. Increased oxidative stress in patients with chronic obstructive pulmonary disease (COPD) as measured by redox status of plasma coenzyme Q10. PATHOPHYSIOLOGY 2006; 13:29-33. [PMID: 16289557 DOI: 10.1016/j.pathophys.2005.09.014] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/01/2005] [Revised: 07/19/2005] [Accepted: 09/23/2005] [Indexed: 11/18/2022] Open
Abstract
STUDY OBJECTIVES The percentage of oxidized coenzyme Q10 in total coenzyme Q10 (%CoQ-10) has been shown to indicate the degree of systemic oxidative stress. Chronic obstructive pulmonary disease (COPD) is regarded as a systemic disease that is linked to oxidative stress in its pathogenesis. In this study, the plasma %CoQ-10 levels in COPD patients were determined and assessed. In addition, the effect of oxygen supplementation on plasma %CoQ-10 was also evaluated. MATERIAL AND METHODS Thirteen COPD patients who had not received oxygen supplementation (COPD-Pt), five COPD patients who had received oxygen supplementation (COPD + O2) and 20 age-matched control subjects (CONTROL) were enrolled. We have also enrolled 83 young healthy non/slight smokers (smoking index <20 pack-year) and 24 young healthy smokers (smoking index > or = 20 pack-year) in order to assess the effect of smoking history on %CoQ-10 level. Their plasma was collected and plasma %CoQ-10 levels were determined and compared. RESULTS AND CONCLUSION The plasma %CoQ-10 of COPD-Pt was 6.3 +/- 2.3, significantly higher than that of CONTROL, 4.7 +/- 1.6 (p < 0.05), indicating an increased oxidative stress in the patients. In contrast, no significant difference in %CoQ-10 was observed between young healthy non/slight smokers (%CoQ-10 = 3.2 +/- 0.9) and young healthy smokers (%CoQ-10 = 3.7 +/- 1.3). Our observation of five COPD patients who received an oxygen supplementation revealed that their %CoQ-10 values (4.0 +/- 1.5) were significantly lower than those in COPD-Pt subjects (p < 0.05), suggesting that oxygen supplementation ameliorates the oxidative stress. In contrast, our study showed that no significant difference was observed among the three groups in plasma levels of Vitamin C or E. In conclusion, plasma %CoQ-10 levels are increased in COPD patients and oxygen supplementation attenuates this increasing effect by COPD. This implies that %CoQ-10 might be used practically to assess the COPD patients systemically.
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Affiliation(s)
- Hiroo Wada
- The First Department of Internal Medicine, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka City, Tokyo 181-8611, Japan
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Belardinelli R, Muçaj A, Lacalaprice F, Solenghi M, Principi F, Tiano L, Littarru GP. Coenzyme Q10 improves contractility of dysfunctional myocardium in chronic heart failure. Biofactors 2005; 25:137-45. [PMID: 16873938 DOI: 10.1002/biof.5520250115] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/07/2022]
Abstract
BACKGROUND There is evidence that plasma CoQ(10) levels decrease in patients with advanced chronic heart failure (CHF). OBJECTIVE To investigate whether oral CoQ(10) supplementation could improve cardiocirculatory efficiency in patients with CHF. METHODS We studied 21 patients in NYHA class II and III (18M, 3W, mean age 59 +/- 9 years) with stable CHF secondary to ischemic heart disease (ejection fraction 37 +/- 7%), using a double-blind, placebo-controlled cross-over design. Patients were assigned to oral CoQ(10) (100 mg tid) and to placebo for 4 weeks, respectively. RESULTS CoQ(10) supplementation resulted in a threefold increase in plasma CoQ(10) level (P < 0.0001 vs placebo). Systolic wall thickening score index (SWTI) was improved both at rest and peak dobutamine stress echo after CoQ(10) supplementation (+12.1 and 15.6%, respectively, P < 0.05 vs placebo). Left ventricular ejection fraction improved significantly also at peak dobutamine (15% from study entry P < 0.0001) in relation to a decrease in LV end-systolic volume index (from 57 +/- 7 mL/m(2) to 45 mL/m(2), P < 0.001). Improvement in the contractile response was more evident among initially akinetic (+33%) and hypokinetic (+25%) segments than dyskinetic ones (+6%). Improvement in SWTI was correlated with changes in plasma CoQ(10) levels (r = -0.52, P < 0.005). Peak VO(2) was also improved after CoQ(10) as compared with placebo (+13%, <0.005). No side effects were reported with CoQ(10). CONCLUSIONS Oral CoQ(10) improves LV contractility in CHF without any side effects. This improvement is associated with an enhanced functional capacity.
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Affiliation(s)
- Romualdo Belardinelli
- Lancisi Heart Institute, Department of Cardiology and Cardiac Surgery, Ancona, Italy.
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Sohmiya M, Tanaka M, Tak NW, Yanagisawa M, Tanino Y, Suzuki Y, Okamoto K, Yamamoto Y. Redox status of plasma coenzyme Q10 indicates elevated systemic oxidative stress in Parkinson's disease. J Neurol Sci 2004; 223:161-6. [PMID: 15337618 DOI: 10.1016/j.jns.2004.05.007] [Citation(s) in RCA: 110] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/21/2003] [Revised: 02/20/2004] [Accepted: 05/11/2004] [Indexed: 11/15/2022]
Abstract
Oxidative stress is suggested to play an important role in the pathogenesis of Parkinson's disease (PD). However, no elevation of plasma oxidative stress marker has been reported. We measured percent content of the oxidized form of coenzyme Q10 in total coenzyme Q10 (%CoQ-10) because %CoQ-10 has been shown to be a sensitive marker of oxidative stress. A slight but significant elevation in %CoQ-10 was observed in PD patients when compared with age/gender-matched normal subjects, suggesting elevated systemic oxidative stress in PD patients.
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Affiliation(s)
- Makoto Sohmiya
- Department of Neurology, Gunma University Graduate School of Medicine, 3-39-22 Showamachi, Maebashi, Gunma 371-8511, Japan.
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Turunen M, Olsson J, Dallner G. Metabolism and function of coenzyme Q. BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES 2004; 1660:171-99. [PMID: 14757233 DOI: 10.1016/j.bbamem.2003.11.012] [Citation(s) in RCA: 730] [Impact Index Per Article: 34.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
Coenzyme Q (CoQ) is present in all cells and membranes and in addition to be a member of the mitochondrial respiratory chain it has also several other functions of great importance for the cellular metabolism. This review summarizes the findings available to day concerning CoQ distribution, biosynthesis, regulatory modifications and its participation in cellular metabolism. There are a number of indications that this lipid is not always functioning by its direct presence at the site of action but also using e.g. receptor expression modifications, signal transduction mechanisms and action through its metabolites. The biosynthesis of CoQ is studied in great detail in bacteria and yeast but only to a limited extent in animal tissues and therefore the informations available is restricted. However, it is known that the CoQ is compartmentalized in the cell with multiple sites of biosynthesis, breakdown and regulation which is the basis of functional specialization. Some regulatory mechanisms concerning amount and biosynthesis are established and nuclear transcription factors are partly identified in this process. Using appropriate ligands of nuclear receptors the biosynthetic rate can be increased in experimental system which raises the possibility of drug-induced upregulation of the lipid in deficiency. During aging and pathophysiological conditions the tissue concentration of CoQ is modified which influences cellular functions. In this case the extent of disturbances is dependent on the localization and the modified distribution of the lipid at cellular and membrane levels.
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Affiliation(s)
- Mikael Turunen
- Department of Biochemistry and Biophysics, Stockholm University, Arrhenius Laboratories for Natural Sciences, SE-106 91 Stockholm, Sweden.
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Tang PH, Miles MV, Steele P, DeGrauw A, Chuck G, Schroer L, Pesce A. Anticoagulant effects on plasma coenzyme Q(10) estimated by HPLC with coulometric detection. Clin Chim Acta 2002; 318:127-31. [PMID: 11880122 DOI: 10.1016/s0009-8981(02)00003-7] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/27/2022]
Abstract
BACKGROUND The proportion of reduced coenzyme Q(10) (Q(10)H(2)) in total coenzyme Q(10) (TQ(10)), referred to as the Q(10)H(2):TQ(10) ratio, may be used as a possible marker of in vivo oxidative stress. However, the ranges for Q(10)H(2):TQ(10) ratio from previous reports are quite variable. Sample handling and preparation appear to have a profound effect on the stability of Q(10)H(2). METHODS Paired tests were used to estimate TQ(10), Q(10)H(2), oxidized coenzyme Q(10) (Q(10)), and Q(10)H(2):TQ(10) ratio in patient samples collected in vacutainers containing heparin or EDTA. Sample tubes were immediately placed on ice and promptly centrifuged. After harvesting plasma, 100 microl of plasma was extracted with 1-propanol and centrifuged. The supernatant was injected directly into a high-performance liquid chromatography (HPLC) system. RESULTS Significantly higher values (p=0.0015) of TQ(10), Q(10)H(2), and Q(10)H(2):TQ(10) ratio were noted in heparinized plasma as compared to EDTA plasma; Q(10) concentrations were lower in heparinized plasma. When vacutainers containing specimen were opened and kept refrigerated, the Q(10)H(2):TQ(10) ratios in heparinized samples were stable over 7 h with variation <3%. Blood Q(10)H(2) in closed heparin vacutainers kept refrigerated was stable up to 24 h. CONCLUSIONS Our results indicate that the heparinized plasma is superior to the EDTA plasma in all measurements for coenzyme Q(10).
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Affiliation(s)
- Peter H Tang
- Division of Pediatric Neurology, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA.
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Schwartzbaum JA, Cornwell DG. Oxidant stress and glioblastoma multiforme risk: serum antioxidants, gamma-glutamyl transpeptidase, and ferritin. Nutr Cancer 2002; 38:40-9. [PMID: 11341043 DOI: 10.1207/s15327914nc381_7] [Citation(s) in RCA: 17] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/31/2022]
Abstract
Case-control studies of serum antioxidants are difficult to interpret, because antioxidants may be altered by the disease under study. However, because glioblastoma multiforme (GBM) is a relatively rare disease, a cohort study would require a large sample observed for many years. In the present case-control pilot study (34 cases and 35 controls), we evaluated the association between serum levels of ascorbic acid (AA) and alpha- and gamma-tocopherol (alpha-T and gamma-T) measured before diagnostic surgery. To control for influence of GBM on serum AA, alpha-T, and gamma-T, we adjusted for oxidant stress indexes (gamma-glutamyl transpeptidase and uric acid) and an acute-phase response index (serum ferritin). When adjusted, AA is inversely related to GBM (p for trend = 0.007). In addition, AA interacts with alpha-T to further reduce GBM risk (test for interaction, p = 0.04). gamma-T is not associated with GBM (p = 0.71). However, gamma-glutamyl transpeptidase (p = 0.004), coenzyme Q (p = 0.01), and ferritin (p = 0.009) are positively and uric acid (p = 0.000) is negatively related to GBM. We conclude that 1) AA and alpha-T are jointly related to GBM after adjustment for GBM-produced oxidant stress and 2) there is a strong association between the presence of GBM and oxidant stress.
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Affiliation(s)
- J A Schwartzbaum
- Division of Epidemiology and Biometrics, College of Medicine and Public Health, Ohio State University, and Comprehensive Cancer Center, Columbus, OH 43210, USA
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Tang PH, Miles MV, DeGrauw A, Hershey A, Pesce A. HPLC Analysis of Reduced and Oxidized Coenzyme Q10 in Human Plasma. Clin Chem 2001. [DOI: 10.1093/clinchem/47.2.256] [Citation(s) in RCA: 121] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/12/2022]
Abstract
AbstractBackground: The percentage of reduced coenzyme Q10 (CoQ10H2) in total coenzyme Q10 (TQ10) is decreased in plasma of patients with prematurity, hyperlipidemia, and liver disease. CoQ10H2 is, however, easily oxidized and difficult to measure, and therefore reliable quantification of plasma CoQ10H2 is of clinical importance.Methods: Venous blood was collected into evacuated tubes containing heparin, which were immediately placed on ice and promptly centrifuged at 4 °C. The plasma was harvested and stored in screw-top polypropylene tubes at −80 °C until analysis. After extraction with 1-propanol and centrifugation, the supernatant was injected directly into an HPLC system with coulometric detection.Results: The in-line reduction procedure permitted transformation of CoQ10 into CoQ10H2 and avoided artifactual oxidation of CoQ10H2. The electrochemical reduction yielded 99% CoQ10H2. Only 100 μL of plasma was required to simultaneously measure CoQ10H2 and CoQ10 over an analytical range of 10 μg/L to 4 mg/L. Intra- and interassay CVs for CoQ10 in human plasma were 1.2–4.9% across this range. Analytical recoveries were 95.8–101.0%. The percentage of CoQ10H2 in TQ10 was ∼96% in apparently healthy individuals. The method allowed analysis of up to 40 samples within an 8-h period.Conclusions: This optimized method for CoQ10H2 analysis provides rapid and precise results with the potential for high throughput. This method is specific and sufficiently sensitive for use in both clinical and research laboratories.
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Affiliation(s)
- Peter H Tang
- Division of Pediatric Neurology, The Children’s Hospital Medical Center, 3333 Burnet Ave., Cincinnati, OH 45229-3039
| | - Michael V Miles
- Division of Pediatric Neurology, The Children’s Hospital Medical Center, 3333 Burnet Ave., Cincinnati, OH 45229-3039
| | - Antonius DeGrauw
- Division of Pediatric Neurology, The Children’s Hospital Medical Center, 3333 Burnet Ave., Cincinnati, OH 45229-3039
| | - Andrew Hershey
- Division of Pediatric Neurology, The Children’s Hospital Medical Center, 3333 Burnet Ave., Cincinnati, OH 45229-3039
| | - Amadeo Pesce
- Department of Pathology and Laboratory Medicine, College of Medicine, University of Cincinnati, 231 Bethesda Ave., Cincinnati, OH 45267-0559
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Reichenbach J, Schubert R, Schwan C, Müller K, Böhles HJ, Zielen S. Antioxidative capacity in patients with common variable immunodeficiency. J Clin Immunol 2000; 20:221-6. [PMID: 10941831 DOI: 10.1023/a:1006645731813] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/12/2022]
Abstract
Highly reactive oxygen species (ROS) are involved in T-cell activation and in the defense against environmental pathogens. An imbalance of ROS generation, detoxifying scavenger enzymes, and molecules with antioxidant capacity could contribute to the increased susceptibility to cancer and infections in severe humoral immunodeficiency. We studied antioxidant status, i.e., plasma antioxidant capacity (TEAC), retinol, alpha-to-copherol, ubiquinol, and the number of activated T cells in 16 patients with common variable immunodeficiency (CVID) compared to age-matched healthy controls. As expected, patients showed significantly increased levels of activated HLA-DR and CD45RO-expressing T cells. Plasma levels of the endogenous ROS scavenger ubiquinol (Q 10) were significantly lower in patients as compared to controls. However, patients showed only slightly reduced levels of TEAC as well as the exogenous antioxidants retinol and alpha-tocopherol. Although no correlation of the number of activated T cells and antioxidant capacity could be demonstrated, an increase in ROS and a diminished reactive oxygen scavenger capacity may be involved in the disease process in patients with common variable immunodeficiency.
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Affiliation(s)
- J Reichenbach
- Department of Pediatrics, Rheinische Friedrich-Wilhelms Universität, Bonn Germany
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