Oxidant stress: a key determinant of atherothrombosis

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Abstract
ROS (reactive oxygen species) are normal products of oxidative cellular metabolism. These biochemically active free-radical derivatives of molecular oxygen serve as normal signalling molecules in the vasculature; however, an excess of vascular ROS flux occurs in the setting of risk factors for atherothrombosis or established atherothrombosis. The oxidant stress that ROS generate promotes endothelial dysfunction, causes oxidative injury to vascular cells, oxidizes lipoproteins and accelerates atherothrombogenesis. Antioxidant enzymes that are important in limiting vascular oxidant stress include the superoxide dismutases, catalase, glutathione peroxidases and glucose-6-phosphate dehydrogenase. The consequences of acquired and inherited deficiencies of these antioxidant enzymes for vascular oxidant stress, endothelial dysfunction and atherothrombosis will be reviewed.

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