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      Evidence for Alterations in Circulating Low-Molecular-Weight Antioxidants and Increased Lipid Peroxidation in Smokers on Hemodialysis

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          Abstract

          Background/Aim: Cardiovascular disease is the major cause of mortality in dialysis patients, accounting for about 40% of deaths in most large registries. Oxidative stress has been strongly implicated in the pathogenesis of these events. As end-stage renal disease is a state of elevated free radical activity, the aim of the present study was to investigate the negative impact of smoking in 57 male hemodialysis patients. Methods: The patients, who were 20–85 years of age (mean age 51.0 ± 14 years), had been on hemodialysis for at least 6 months before participating in this study. Fasting blood sampling for serum lipid, albumin, urate and lipophilic antioxidants such as tocopherols, carotenes, ascorbate and lipid peroxides was performed. Results: The plasma malondialdehyde (MDA) concentration was significantly higher in hemodialysis patients who smoked compared to hemodialysis patients who were nonsmokers (1.92 ± 0.52 vs. 1.59 ± 0.42 nmol/ml, p = 0.006). No association was found between levels of MDA in smokers and parameters such as body mass index, serum cholesterol, serum triglycerides and smoking index. There were no significant differences in the plasma levels of uric acid, α-tocopherol, γ-tocopherol, δ-tocopherol, α-carotene, β-carotene and retinol between the two groups. A significantly lower level of plasma ascorbate was observed in hemodialysis patients who smoked compared to the nonsmoking hemodialysis patients or healthy controls (4.59 ± 4.0 vs. 9.57 ± 4.0 and 10.16 ± 4.6 µg/ml, p < 0.05). Moreover, in smokers, the plasma levels of ascorbate were negatively correlated with the levels of plasma MDA (r = –0.43, p < 0.001) of each patient. Partial correlation analysis of the plasma levels of the measured antioxidants and the smoking index revealed a negative correlation between the plasma levels of lipid-normalized lycopene and the smoking index (r = –0.53, p < 0.05). Conclusion: Our data suggest that cigarette smoking further increases plasma-circulating products of lipid peroxidation, which are already increased in nonsmoking hemodialysis patients as compared to matched healthy controls. The lower plasma levels of ascorbate in hemodialysis patients who smoke suggest that these patients may be more susceptible to oxidative tissue damage caused by smoking.

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          Most cited references 7

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          Increase in circulating products of lipid peroxidation (F2-isoprostanes) in smokers. Smoking as a cause of oxidative damage.

          It has been hypothesized that the pathogenesis of diseases induced by cigarette smoking involves oxidative damage by free radicals. However, definitive evidence that smoking causes the oxidative modification of target molecules in vivo is lacking. We conducted a study to determine whether the production of F2-isoprostanes, which are novel products of lipid peroxidation, is enhanced in persons who smoke. We measured the levels of free F2-isoprostanes in plasma, the levels of F2-isoprostanes esterified to plasma lipids, and the urinary excretion of metabolites of F2-isoprostanes in 10 smokers and 10 nonsmokers matched for age and sex. The short-term effects of smoking (three cigarettes smoked over 30 minutes) and the effects of two weeks of abstinence from smoking on levels of F2-isoprostanes in the circulation were also determined in the smokers. Plasma levels of free and esterified F2-isoprostanes were significantly higher in the smokers (242 +/- 147 and 574 +/- 217 pmol per liter, respectively) than in the nonsmokers (103 +/- 19 and 345 +/- 65 pmol per liter; P = 0.02 for free F2-isoprostanes and P = 0.03 for esterified F2-isoprostanes). Smoking had no short-term effects on the circulating levels of F2-isoprostanes. However, the levels of free and esterified F2-isoprostanes fell significantly after two weeks of abstinence from smoking (250 +/- 156 and 624 +/- 214 pmol per liter, respectively, before the cessation of smoking, as compared with 156 +/- 67 and 469 +/- 108 pmol per liter after two weeks' cessation; P = 0.03 for free F2-isoprostanes and P = 0.02 for esterified F2-isoprostanes). The increased levels of F2-isoprostanes in the circulation of persons who smoke support the hypothesis that smoking can cause the oxidative modification of important biologic molecules in vivo.
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            Malondialdehyde and thiobarbituric acid-reactivity as diagnostic indices of lipid peroxidation and peroxidative tissue injury

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              Free radicals and the heart.

              Because of the molecular configuration, most free radicals are highly reactive and can cause cell injury. Protective mechanisms have evolved to provide defense against free-radical injury. Any time these defense systems are overwhelmed, such as during disease states, cell dysfunction may occur. In this review we discuss cellular sources as well as the significance of free radicals, oxidative stress, and antioxidants. A probable role of oxidative stress in various cardiac pathologies has been also analyzed. Although some methods for the detection of free radicals as well as oxidative stress have been cited, better methods to study the quantity as well as subcellular distribution of free radicals are needed in order to understand fully the role of free radicals in both health and disease.
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2001
                2001
                25 May 2001
                : 88
                : 2
                : 127-133
                Affiliations
                aDepartment of Internal Medicine, Kuang Tien General Hospital, Taichung, bGraduate Institute of Clinical Medical Science, Chang Gung University, Taoyuan, cDepartment of Biochemistry and Center for Cellular and Molecular Biology, National Yang-Ming University, Taipei, Taiwan
                Article
                45972 Nephron 2001;88:127–133
                10.1159/000045972
                11399914
                © 2001 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 1, Tables: 3, References: 47, Pages: 7
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/45972
                Categories
                Original Paper

                Cardiovascular Medicine, Nephrology

                Smoking, Lipid peroxidation, Hemodialysis, Antioxidants

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