LDL particles constitute the predominant form of transport of cholesterol towards tissues, and a major risk factor for atheroma. The pathogenesis of atherosclerosis is, as yet, far from completely elucidated and, indeed, within the LDL particles themselves, there is a structural heterogeneity. Approximately fifteen subfractions have been isolated so far, presenting differing profiles in normal and hyperlipidemic subjects. Some of these subgroups seem to be linked with an atherogenic potential, this is the case for the smaller and the more dense of the particles. LDL particles are normally cleared from the blood stream via the BE receptor, whose synthesis is regulated by the intracellular content of cholesterol. The particules must however undergo several, in vivo and in vitro, transformations which modify their metabolism and are all the more important when their half life is prolonged. These transformations, and in particular oxydation, lead, via the macrophage pathway, to the accumulation of cholesterol, the creation of foam cells, and ultimately to the formation of the lipid streak. Antioxydants therefore open the way to new therapeutic pathways by acting in synergy with cholesterol lowering agents.