Oxidative modification of low-density lipoprotein (LDL) has been implicated in the pathogenesis of coronary artery disease (CAD). Macrophages take up oxidized LDL via scavenger receptors, which is not regulated by cellular cholesterol contents, and oxidized LDL stimulates cholesterol esterification and this results in cellular cholesterol accumulation and foam cell formation. Several papers have reported a positive correlation between the severity of coronary atherosclerosis and the oxidative susceptibility of LDL. Small, dense LDL, LDL rich in polyunsaturated fatty acids (PUFA) or LDL poor in antioxidants (vitamin E, beta-carotene, CoQ10) should be more susceptible to lipid peroxidation and possibly more atherogenic. Therefore, to prevent CAD, it is important not only to reduce LDL cholesterol levels but also to suppress the oxidative modification of LDL.