Abstract
Increasing evidence exists that oxidative modification of low density lipoprotein (LDL) plays an important role in the pathogenesis of atherosclerosis. Lipid peroxidation processes degrade polyunsaturated fatty acids of the LDLโlipids to hydroperoxyacids and further breakdown products, which themselves modify the apolipoprotein B. These oxidized LDLโparticles are taken up via the scavenger receptor of tissueโmacrophages in an uncontrolled manner and lead to the formation of lipid laden foam cells, which are present in fatty streaks. Oxidized LDL (oxLDL) is detectable in atherosclerotic plagues immunochemically. Autoantibodies against oxLDL are detectable in serum and their titers correlate with the progression of atherosclerosis. The oxidation resistance of LDL is in part dependent of its antioxidant content (vitamin E, carotenoids, ubiquinolโ10). Oral supplementation of vitamin E increases significantly the oxidation resistance of LDL while ฮฒโcarotene supplementation seems to increase the oxidation resistance only of certain individuals. A clinical trial has demonstrated an inverse correlation of severity of myocardial infarction and oxidation resistance of LDL.