title: Malondialdehyde-altered protein occurs in atheroma of Watanabe heritable hyperlipidemic rabbits.
abstract: It has been proposed that chemically reactive lipids released during lipid peroxidation convert low density lipoprotein (LDL), the major carrier of plasma cholesterol, to an abnormal form and that receptor-mediated clearance of this altered LDL produces cholesteryl ester deposition in macrophage-derived foam cells of atheroma. Immuno-cytochemical analyses now reveal the presence of protein modified by malondialdehyde, a peroxidative end product, which colocalizes with the extracellular deposition of apolipoprotein B-100 protein of LDL in atheroma from Watanabe heritable hyperlipidemic rabbits. These findings provide direct evidence for the existence in vivo of protein modified by a physiological product of lipid peroxidation within arterial lesions.
authors: Department of Medicine, UCLA School of Medicine 90024.
authors: M E
authors: ME
authors: Haberland
authors: D
authors: D
authors: Fong
authors: L
authors: L
authors: Cheng
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B / Q000378:metabolism*; D001161:Arteriosclerosis / Q000378:metabolism / Q000473:pathology*; D004195:Disease Models, Animal; D000939:Epitopes; D006949:Hyperlipidemias / Q000235:genetics / Q000473:pathology*; D008054:Lipid Peroxides; D008314:Malonates; D008315:Malondialdehyde; D011817:Rabbits
chemical_list: D000911:Antibodies, Monoclonal; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B; D000939:Epitopes; D008054:Lipid Peroxides; D008314:Malonates; D008315:Malondialdehyde