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. Immunocytochemical 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.
CITATION STYLE
Haberland, M. E., Fong, D., & Cheng, L. (1988). Malondialdehyde-altered protein occurs in atheroma of watanabe heritable hyperlipidemic rabbits. Science, 241(4862), 215–218. https://doi.org/10.1126/science.2455346
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