The Role of Oxidative Modification and Antioxidants in LDL Metabolism and Atherosclerosis

Abstract

Recent studies have shown that low-density lipoprotein (LDL), when incubated with certain cell types in culture (including endothelial cells, smooth muscle cells and macrophages) is subject to a number of alterations in its physical and chemical properties¹. Most interestingly, this ‘modified’ LDL is endocytosed by macrophages up to 20 times more rapidly than native LDL^1,2. It is possible that the formation of foam cells from macrophages in the developing atherosclerotic plaque could be the result of the generation of similar ‘modified’ LDL particles by cells of the artery wall. Because the route for endocytosis of ‘modified’ LDL largely bypasses the normal ApoB/E receptor, target cells such as the macrophage are unable to regulate their intake of this ligand and so accumulate large amounts of cholesteryl esters intracellularly.