MALONDIALDEHYDE-ALTERED PROTEIN OCCURS IN ATHEROMA OF WATANABE HERITABLE HYPERLIPIDEMIC RABBITS
MALONDIALDEHYDE-ALTERED PROTEIN OCCURS IN ATHEROMA OF WATANABE HERITABLE HYPERLIPIDEMIC RABBITS
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DOI：
10.1126/science.2455346
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发表时间：
1988-07-08
期刊：
影响因子：
56.9
通讯作者：
CHENG, L
中科院分区：
文献类型：
--
作者：
HABERLAND, ME;FONG, D;CHENG, L
有人认为，在脂质过氧化过程中释放的化学反应脂质将血浆胆固醇的主要载体低密度脂蛋白(低密度脂蛋白)转变为异常形式，而受体介导的这种改变的低密度脂蛋白的清除会在动脉粥样硬化的巨噬细胞来源的泡沫细胞中产生胆固醇酯沉积。免疫细胞化学分析显示，在渡边遗传性高脂血症兔的动脉粥样硬化中，存在被丙二醛修饰的蛋白质，丙二醛是一种过氧化终产物，与低密度脂蛋白的载脂蛋白B-100蛋白细胞外沉积共存。这些发现为动脉病变中存在被脂质过氧化生理产物修饰的蛋白质提供了直接证据。
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.