Modification of human low density lipoprotein by lipid peroxidation.

Abstract

Elevated levels of low density lipoprotein (LDL) have been linked to an increased risk of atherosclerotic vascular diseases, however, the molecular mechanisms by which LDL is involved in atherogenesis are largely unknown. Recently, several reports appeared suggesting that LDL may be oxidatively modified by free radical reactions and that this oxidized LDL exhibits some of the properties which could explain the formation of early atherosclerotic lesions.1,2 The fatty streaks in plaques originate mainly from lipid laden foam cells, which are derived from smooth muscle cells or macrophages. Cultured macrophages accumulate large amounts of cholesterol-lipids and obtain a foam-cell like appearance if incubated with acetylated LDL,3 malonaldehyde-treated LDL4 or oxidized LDL.5 The uptake of these modified forms of LDL occurs through the so called scavenger receptor, which is not down regulated by the internalized LDL and which obviously recognizes LDL particles which are more negativly charged than native LDL. For acetylated LDL3 or malonaldehyde-treated LDL,4 it has been shown with some certainty that the increased negative surface charge is due to the neutralization (acetylation, Schiffs base formation) of positive charges of lysine amino groups in apo B.6,7 The commonly used index for the change of the negative charge is the increased relative electrophoretic mobility.KeywordsLipid Oxidation ProductRelative Electrophoretic MobilityFluorescent ChromophoreLipid Lade Foam CellLipophilic AldehydeThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.