Abstract
Oxidation of human plasma lipoprotein (LP) was studied in the presence of exogenous hypochlorite anion (OCl −) or OCl − generated in the “myeloperoxidase + H 2O 2 + Cl −” system. OCl − effectively initiates peroxidation of lipids extracted from LP and those within LP particles, as can be judged from accumulation of secondary (thiobarbituric acid [TBA] reactive) and final (Schiff bases) products of lipid peroxidation (LPO) in LP after incubation with myeloperoxidase or exogenous OCl −. Very low density and low density lipoproteins classified as atherogenic LP are more sensitive to OCl −-induced LPO than high density lipoproteins. These data allow us to propose that OCl − secreted by activated neutrophils and monocyte-macrophages can produce oxidative modification of LP in vivo. The latter is known as a risk factor in the development of atherosclerosis.
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