Stages of formation in blood plasma and diagnostic value of modified low density lipoproteins

Abstract

Ligand formation in phylogenetically early low-density lipoprotein (LDL) and phylogenetically late very low-density lipoprotein (VEDE) occurs when apoB-100 acquires active conformation in association with essential polyenic fatty acids (FA) as esters with the alcohol cholesterol (СL), palmitic and oleic triglycerides (TG). AроВ-100 domen-ligand forms in LDL, and apoE/B-100 ligand, in VLDL. Cells internalize ligand lipoproteins (LP) by apoE/B-100 and apoB-100 receptor-mediated endocytosis. In E2/E3 phenotype and high blood content of - palmitic TG and palmitic VLDL, preligand TG-rich LР are accumulated in the circulation if primary structure - of postheparinic liver lipoprotein lipase and apoC-I and apoC-II is impaired. In apoB-100 receptor pathology, postligand LDL with low TG content are accumulated. All ligand-free LР are physiologically denatured by neutrophils and modified by other agents (glycotoxins) in pathology. Preligand LPform soft raised plaques in arterial intima and cause atherothrombosis, a destructive-inflammatory process. Postligand LP form flat plaques and induce atheromatosis. Atherosclerosis can be regarded as a conformation-related disease. According to NMR data, small dense atherogenic LP are palmitic VLDL with hydrated density of LDL. Excessive dietary palmitic saturated FA, Е2/E2 phenotype and apoB-100 gene deletion are the causes of arterial intima injury. Ligand-free LP and dying _ macrophages form destructive and inflammatory processes. Atheromatosis is a result of endoecology, the biological function providing ”purity” of entercellular medium.