Oxidation of lipoproteins and atherosclerosis.

The fatty streak is the earliest lesion of atherosclerosis. This lesion contains foam cells which are primarily derived from blood monocytes. The accumulation of cholesterol in macrophages is explained by the uptake of modified low-density lipoprotein (LDL). An in vivo modification of lipoproteins might be oxidation. The oxidized LDL showed several chemicophysical modifications. The first demonstrated effect of LDL oxidation was its increased susceptibility to uptake by cultured macrophages. Furthermore, oxidized LDL exhibits a chemotactic activity, and a cytotoxicity. An hypothesis that explains the appearance and development of atherosclerotic lesions and is based on obtained in vitro is exposed. LDL-like lipoproteins extracted from human aorta had some of properties of oxidized LDL, such as the recognition of materials present in atheroma by antibodies against oxidized LDL and the presence of autoantibodies against oxidized LDL in human sera are in favor of the pathogenetically important role of the oxidation of LDL.