Lipoprotein oxidation in dyslipidemia: insights into general mechanisms affecting lipoprotein oxidative behavior.
Atherosclerosis susceptibility associated with elevations in specific populations of apolipoprotein-B-containing particles may involve increased oxidation of lipoproteins and associated changes in their biological properties. Lipoprotein oxidation may be potentiated by the greater mass of oxidizable lipoprotein substrates, as well as by a greater intrinsic susceptibility of the specific forms of lipoproteins that arise in these disorders. The atherogenic consequences of increased lipoprotein oxidation may be further enhanced by a greater relative potency or toxicity of the oxidized products of these lipoprotein subpopulations. This review addresses these facets of lipoprotein oxidation in several forms of dyslipidemia, and in view of both differences between and commonalities among these disorders, proposes that lipoprotein oxidative behavior is determined by a complex array of physical, chemical, and metabolic factors.
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Department of Molecular and Nuclear Medicine, Lawrence Berkeley Laboratory, University of California, Berkeley, USA.
D001055:Apolipoproteins B / Q000097:blood / Q000737:chemistry; D005231:Fatty Acids, Unsaturated / Q000097:blood; D006801:Humans; D006861:Hydrogen Peroxide; D006949:Hyperlipidemias / Q000097:blood*; D015227:Lipid Peroxidation; D008074:Lipoproteins / Q000097:blood*; D010084:Oxidation-Reduction
D001055:Apolipoproteins B; D005231:Fatty Acids, Unsaturated; D008074:Lipoproteins; D006861:Hydrogen Peroxide