Smoking is a significant independent risk factor for cardiovascular disease and is a leading cause of structural and functional alterations of the cardiovascular system. Increasing evidence supports the hypothesis that oxidative stress and endothelial dysfunction are the fundamental pathophysiological mechanisms linking cigarette smoking to cardiovascular disease. The cardiovascular system is a rich source of NADPH oxidase - derived reactive oxygen species, which under pathological conditions play a fundamental role in vascular damage. Endothelium-derived nitric oxide (NO) plays a major role in the regulation of vascular tone, structure, and function, and endothelial dysfunction could be considered the first step in the pathogenesis of atherosclerosis and cardiovascular disease. Indeed, the bioavailability of NO is modulated by reactive oxygen species that degrade NO, uncouple NO synthase, and inhibit synthesis. Reduced bioavailability of NO and consequent endothelial dysfunction are involved in the initiation, progression and complications of atherosclerosis and also are predictive of future cardiovascular events. Thus, although data from clinical trials exploring the role of antioxidants on cardiovascular risk and disease are equivocal as yet, the role of oxidative stress in cardiovascular disease is an important area of research, which is likely to continue to be fruitful. This review focuses on possible interactions between oxidative stress, endothelial dysfunction and cigarette smoking - favouring the atherosclerotic process and cardiovascular disease - also focusing on the potential role for antioxidants in the prevention of adverse cardiovascular outcomes.
Keywords: Oxidative stress, cigarette smoking, endothelial dysfunction, nitric oxide, reactive oxygene species, atherosclerosis, cardiovascular disease
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