Hypercholesterolemia is a major risk for atherogenesis. Recent evidence suggests that oxidative modification of the major cholesterol-carrying lipo protein, low-density lipoprotein (LDL), renders it more atherogenic. Not only does oxidized LDL (Ox-LDL) have enhanced uptake by macro phages, which contributes directly to foam cell formation, it may also adversely affect many other aspects of arterial wall metabolism and thus contribute further to the atherogenic process. Inhibition of the oxidation of LDL may be another approach to inhibiting atherogenesis, additive to or even synergistic with lowering of plasma LDL levels.