Antioxidants, Journal Year: 2025, Volume and Issue: 14(4), P. 430 - 430

Published: April 2, 2025

Low-density lipoprotein (LDL) chemically modified by reactive oxygen species (ROS), for example, leaking from red blood cells in the vascular compartment, more readily crosses endothelium than does nonoxidatively LDL to enter tissue fluid. Oxidatively (oxLDL) may also be created fluid ROS design, inflammatory white cells, or simply other as a consequence of metabolism. As well oxLDL, glycatively (glycLDL) is formed circulation. High-density (HDL) appears capable decreasing burden lipid peroxides on exposed glucose and its metabolites. The mechanism this that has received most attention antioxidant activity HDL, which due large part presence paraoxonase 1 (PON1). PON1 intimately associated with apolipoprotein A1 component HDL’s domains into cell membranes can transferred. It frequently overlooked hydrolyze substrates, it essential remain virtue hydrophobic amino acid sequences within micellar environment, during isolation serum genetically culture. Otherwise, retain capacity water-soluble such phenyl acetate, whilst failing lipid-soluble molecules. OxLDL probably glycLDL, once they have crossed arterial receptor-mediated transcytosis, are rapidly taken up monocytes process involves scavenger receptors, leading subendothelial foam formation. These precursors atheroma, inducing cross lesion proliferation migration myocytes present wall developing lesion, where transform fibroblasts. atheroma progresses central extracellular lake cholesteryl ester following necrosis apoptosis an overlying fibrous cap continuing grow concentrically around involving oxLDL glycLDL. Within wall, additional generated secreted leakage generally when couplet reduced. important HDL opposes atherogenesis, provide better avenue inquiry identification vulnerable individuals provision new therapies emerged emphasis placed role RCT.

Language: Английский