Service de biochimie A, hôpital Saint-Antoine, 184, rue du faubourg Saint-Antoine, 75571 Paris Cedex 12
In the physiological state, anti-oxidant systems can equilibrate the production of free radicals derived from oxygen (or reactive oxygen species, ROS). In cardiovascular pathology, an imbalance can emerge related to the overproduction of ROS with a potential defect in anti-oxidant defences. Such a phenomenon particularly arises during the development of atherosclerosis where oxidized LDL are captured by scavenger cells leading to the accumulation of lipids in sub-endothelium and creating a lipid core in the atherosclerotic plaque. Oxidative stress occurs in all the stages of atherosclerosis development and in many ways; for example through the mitogenic effects of oxidized LDL, by the chemotactic and genotoxic properties of the products of lipoperoxidation, by the formation of advanced glycation end-products and by the production of nitrogen monoxide. Moreover, oxidative stress is a major consequence of myocardial ischemia, in particular by the activation of endothelial xanthine-oxidase; ROS arising from this activation are directly incriminated in post-infarction arrythmia. In recent decades, many assays for oxidative stress markers have been developed, such as products of oxidization of lipids (malonedialdehyde, 4-hydroxy-nonenal...), proteins (oxidized albumin) or nucleotides (8-hydroxy-deoxyguanosine), also pro-oxidative enzymes (e.g. myeloperoxidase), or enzymes (superoxide dismutase, glutathione peroxidase, catalase...), vitamins (A, E, C) and glutathione for anti-oxidant protection. Retrospective studies have shown the interest of some of these markers, in particular glutathione peroxidase, myeloperoxidase and oxidized albumin, for the diagnosis and the prognosis of acute coronary syndromes, independently of other cardiovascular risk factors.