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      Effects of coenzyme Q10 supplementation on activities of selected antioxidative enzymes and lipid peroxidation in hypertensive patients treated with indapamide. A pilot study

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          Abstract

          Introduction

          An increase in oxidative stress is strongly documented in hypertensive patients. In blood vessels, oxidative stress increases the production of superoxide anion (O 2 •−) that reacts with nitric oxide (NO) and impairs the ability of endothelium to relax. Many reports indicate a beneficial effect of coenzyme Q10 (CoQ) in hypertension. Coenzyme Q10 therapy may lower O 2 •− and thus decrease the complications associated with hypertension. The aim of our study was to evaluate the effects of CoQ supplementation on antioxidative enzyme activities and lipid peroxidation in elderly hypertensive patients.

          Material and methods

          We determined the activities of superoxide dismutase (SOD-1) and glutathione peroxidase (GSH-Px) and the concentration of malondialdehyde (MDA) in erythrocytes of 27 elderly (mean age 72.5 ±6.1 year) hypertensive patients treated with indapamide at baseline and after 12 weeks of CoQ supplementation (60 mg twice a day) in comparison with 30 healthy elderly volunteers (mean age 76.8 ±8.5 year).

          Results

          Decrease of SOD-1 ( p < 0.001) and insignificant reduction of GSH-Px activities and increase of MDA ( p < 0.001) level were observed in hypertensive patients in comparison to healthy volunteers before supplementation. Coenzyme Q10 administration resulted in a significant increase only in SOD-1 activity ( p < 0.001).

          Conclusions

          The present study indicates that CoQ improves the most important component of the antioxidant defence system – SOD-1, which is responsible for O 2 •− scavenging. Coenzyme Q10 may be used as an additional therapeutic agent for prophylaxis and treatment of hypertension in elderly patients.

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          Most cited references40

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          Estimation of product of lipid peroxidation (malonyl dialdehyde) in biochemical systems.

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            Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase.

            The Sod2 gene for Mn-superoxide dismutase (MnSOD), an intramitochondrial free radical scavenging enzyme that is the first line of defense against superoxide produced as a byproduct of oxidative phosphorylation, was inactivated by homologous recombination. Homozygous mutant mice die within the first 10 days of life with a dilated cardiomyopathy, accumulation of lipid in liver and skeletal muscle, and metabolic acidosis. Cytochemical analysis revealed a severe reduction in succinate dehydrogenase (complex II) and aconitase (a TCA cycle enzyme) activities in the heart and, to a lesser extent, in other organs. These findings indicate that MnSOD is required for normal biological function of tissues by maintaining the integrity of mitochondrial enzymes susceptible to direct inactivation by superoxide.
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              Oxidative stress, caloric restriction, and aging.

              Under normal physiological conditions, the use of oxygen by cells of aerobic organisms generates potentially deleterious reactive oxygen metabolites. A chronic state of oxidative stress exists in cells because of an imbalance between prooxidants and antioxidants. The amount of oxidative damage increases as an organism ages and is postulated to be a major causal factor of senescence. Support for this hypothesis includes the following observations: (i) Overexpression of antioxidative enzymes retards the age-related accrual of oxidative damage and extends the maximum life-span of transgenic Drosophila melanogaster. (ii) Variations in longevity among different species inversely correlate with the rates of mitochondrial generation of the superoxide anion radical (O2) and hydrogen peroxide. (iii) Restriction of caloric intake lowers steady-state levels of oxidative stress and damage, retards age-associated changes, and extends the maximum life-span in mammals.
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                Author and article information

                Journal
                Arch Med Sci
                AMS
                Archives of Medical Science : AMS
                Termedia Publishing House
                1734-1922
                1896-9151
                07 September 2010
                30 August 2010
                : 6
                : 4
                : 513-518
                Affiliations
                [1 ]Department and Clinic of Geriatrics, Nicolaus Copernicus University Collegium Medicum, Bydgoszcz, Poland
                [2 ]Department of Biochemistry, Nicolaus Copernicus University Collegium Medicum, Bydgoszcz, Poland
                [3 ]Department of Nephrology, Hypertension and Family Medicine, Medical University of Lodz, Poland
                [4 ]Department of Hypertension, Medical University of Lodz, Poland
                Author notes
                Corresponding author: Dr Jolanta Czuczejko, Department of Biochemistry Nicolaus Copernicus University, Collegium Medicum, 24 Karlowicza Str., 85-092 Bydgoszcz, Poland, Phone: +48 52585 3755, Fax: +48 52585 3771. E-mail: joczu@ 123456wp.pl
                Article
                15172
                10.5114/aoms.2010.14461
                3284064
                22371793
                9c5d670f-15ed-44fd-bbd1-b72abafccb41
                Copyright © 2010 Termedia & Banach

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 13 April 2010
                : 28 June 2010
                : 19 July 2010
                Categories
                Clinical Research

                Medicine
                hypertension,glutathione peroxidase,superoxide dismutase,oxidative stress,aging
                Medicine
                hypertension, glutathione peroxidase, superoxide dismutase, oxidative stress, aging

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