Abstract
Recent studies suggest that oxidative stress plays a significant role in the pathogenesis of atherosclerosis. This process serves as the basis for the oxidative-modification hypothesis of atherosclerosis. Several risk factors for atherothrombotic disease, such as hypercholesterolemia, hypertension, diabetes mellitus, cigarette smoking, and hyperhomocyst(e)inemia, promote oxidative reactions in the vasculature. Oxidant stress damages LDL, attracts and activates leukocytes, and stimulates platelets. In order to combat factors promoting oxidative stress, mammals have evolved several antioxidant defenses to limit oxidant injury. These defenses, which include water-soluble antioxidants (e.g., glutathione, ascorbate), lipid soluble antioxidants (e.g., α-tocopherol), and antioxidant enzymes (e.g., glutathione peroxidases) in the vasculature and extracellular space, frequently fail to afford adequate protection from the oxidative reactions that accompany atherogenesis. The antioxidant hypothesis derives from this limitation of endogenous antioxidant defenses, and posits that inadequate endogenous antioxidants promote, and antioxidant supplemementation prevents, atherothrombotis.
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Forgione, M., Loscalzo, J. (2000). The Antioxidant Hypothesis. In: Tardif, JC., Bourassa, M.G. (eds) Antioxidants and Cardiovascular Disease. Developments in Cardiovascular Medicine, vol 233. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4375-2_3
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DOI: https://doi.org/10.1007/978-94-011-4375-2_3
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