Statins as Antioxidants

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A critical balance exists between NO and superoxide (O2-). Under physiologic conditions, NO levels are 1,000 times those of O2-, and the normal antioxidant mechanisms are able to detoxify small amounts of reactive oxygen species (ROS). During ischemia-reperfusion and inflammatory disorders, these defenses are overwhelmed and oxidant-mediated injury ensues, including peroxidation of cell membranes, impaired NO bioactivity, induction of leuko-cyte-endothelial adhesion, and thrombosis. Oxidative stress also contributes to the pathogenesis of chronic vascular diseases such as atherosclerosis, diabetes, and hypertension.

The NADPH oxidase is a major source of O2- within the vascular wall, and Rac-GTPase is an important regulator of this enzyme in EC, VSMC, and phagocytes. Statins block the translocation of GTP-bound Rac to the membrane, consequently reducing transcription of critical NADPH sub-units and vascular wall production of ROS in response to various stimuli, such as angiotensin II and PKC agonists. An increase in catalase expression has also been observed in aortic walls of spontaneously hypertensive rats treated with statins [4]. A direct scavenging effect of fluvastatin on hydroxyl and superoxide radicals has been described, providing another antioxidant mechanism of statins.

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