Abstract
Oxidative reactions caused by cigarette smoke (CS) chemicals have been shown to initiate crucial events in atherogenesis. However, physicians and scientists are confronted with the paradoxical situation that an antioxidative treatment of smokers improves acute smoking effects but hardly has any impact on long term outcome of cardiovascular diseases (CVD). In this review we make an attempt to explain this paradox. First, smoke-derived free radicals and oxidants are part of CS causing a pro-oxidative state in the circulatory system. Further, smoke chemicals down-regulate antioxidant defence enzymes that would counteract the oxidative burden by cigarette smoke. With the prolonged exposure to smoke, oxidation catalysing metals accumulate in the vessel wall and mediate local oxidation reactions. Therefore, pharmacological intervention relying on nonselective antioxidants often appears to be ineffective. Consequently a novel strategy for the prevention and treatment of CVD caused by smoking is suggest, relying on a combined application of antioxidants, substitution of factors important for physiological oxidant defence, and metal-detoxifying agents.
Keywords: cigarette smoke extract, atherosclerosis, endothelial, dysfunction, injury, in vitro, vitamine C, vitamine E, antioxidants, oxidation
Current Medicinal Chemistry
Title: Smoking, Oxidative Stress and Cardiovascular Diseases-Do Anti-Oxidative Therapies Fail?
Volume: 14 Issue: 16
Author(s): D. Bernhard and X.L. Wang
Affiliation:
Keywords: cigarette smoke extract, atherosclerosis, endothelial, dysfunction, injury, in vitro, vitamine C, vitamine E, antioxidants, oxidation
Abstract: Oxidative reactions caused by cigarette smoke (CS) chemicals have been shown to initiate crucial events in atherogenesis. However, physicians and scientists are confronted with the paradoxical situation that an antioxidative treatment of smokers improves acute smoking effects but hardly has any impact on long term outcome of cardiovascular diseases (CVD). In this review we make an attempt to explain this paradox. First, smoke-derived free radicals and oxidants are part of CS causing a pro-oxidative state in the circulatory system. Further, smoke chemicals down-regulate antioxidant defence enzymes that would counteract the oxidative burden by cigarette smoke. With the prolonged exposure to smoke, oxidation catalysing metals accumulate in the vessel wall and mediate local oxidation reactions. Therefore, pharmacological intervention relying on nonselective antioxidants often appears to be ineffective. Consequently a novel strategy for the prevention and treatment of CVD caused by smoking is suggest, relying on a combined application of antioxidants, substitution of factors important for physiological oxidant defence, and metal-detoxifying agents.
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Cite this article as:
D. Bernhard and X.L. Wang , Smoking, Oxidative Stress and Cardiovascular Diseases-Do Anti-Oxidative Therapies Fail?, Current Medicinal Chemistry 2007; 14 (16) . https://dx.doi.org/10.2174/092986707781058959
DOI https://dx.doi.org/10.2174/092986707781058959 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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