[Back to Issue 11 ToC] [Back to Journal Contents] [Back to Biochemistry (Moscow) Home page]

Differences in Structural Changes and Pathophysiological Effects of Low-Density Lipoprotein Particles upon Accumulation of Acylhydroperoxy Derivatives in Their Outer Phospholipid Monolayer or upon Modification of Apoprotein B-100 by Natural Dicarbonyls


Vadim Z. Lankin1,a*, Alla K. Tikhaze1, and Galina G. Konovalova1

1Chazov National Medical Research Center of Cardiology, Ministry of Health of the Russian Federation, 121552 Moscow, Russia

* To whom correspondence should be addressed.

Received August 4, 2023; Revised September 20, 2023; Accepted September 20, 2023
Nanoparticles of the lipid-transporting system of the organism, low-density lipoproteins (LDL) of blood plasma, are prone 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 in which chemically modified via the Maillard reaction). Based on the study of free radical oxidation kinetics of LDLs, it was found that the existing in the literature designation of “oxidized lipoproteins” is incorrect because it does not reveal the nature of oxidative modification of LDLs. It was shown in this study that the “atherogenic” LDLs (particles of which are actively captured by the cultured macrophages) are not the oxidized LDL (in which LOOH-derivatives of phospholipids are formed by enzymatic oxidation by C-15 lipoxygenase of rabbit reticulocytes), but dicarbonyl-modified LDLs. Important role of the dicarbonyl-modified LDLs in the molecular mechanisms of atherogenesis and endothelial dysfunction is discussed.
KEY WORDS: oxidized low-density lipoproteins (LDL), dicarbonyl-modified LDL, free radical oxidation, “atherogenic” LDL, oxidative stress, carbonyl stress

DOI: 10.1134/S0006297923110196