Differences in structural changes and pathophysiologic effects of low-density lipoproteins upon accumulation of acylhydroperoxy derivatives in their outer phospholipid monolayer or upon chemical modification of apoprotein b-100 by natural dicarbonyl

Abstract

Nanoparticles of the lipid-transporting system of the organism - low-density lipoproteins (LDL) of blood plasma are easily subjected to free radical peroxidation with formation of their main modified forms - oxidized LDL itself (containing hydroperoxy-acyls in phospholipids of the outer layer of particles) and dicarbonyl-modified LDL (apoprotein B-100 of which was chemically modified by the Maillard reaction). Based on the study of free radical oxidation kinetics of LDL, it was found that the existing in the literature designation “oxidized lipoproteins” is incorrect because it does not reveal the nature of oxidative modification of LDL. It is shown that “atherogenic” LDL (particles of which are actively captured by cultured macrophages) are not the oxidized LDL (in which LOOH-derivatives of phospholipids are formed by enzymatic oxidation of of C-15 lipoxygenase of rabbit reticulocytes), but dicarbonyl-modified LDL. The important role of dicarbonyl-modified LDL in the molecular mechanisms of atherogenesis and endothelial dysfunction is discussed.