Laurman W, Salmon S, Mazière C, Mazière J C, Auclair M, Theron L, Santus R
CNRS UA 524, Faculté de Médecine Saint-Antoine, Paris, France.
Atherosclerosis. 1989 Aug;78(2-3):211-8. doi: 10.1016/0021-9150(89)90225-6.
Carbon disulfide interacts in vitro with low density lipoprotein (LDL), resulting in an increased electrophoretic mobility of the particle, due to a decrease in free amino groups of apolipoprotein B-100. The processing of carbon disulfide-modified LDL through the apo B/E receptor pathway of cultured human fibroblasts is decreased as compared to that of native LDL, depending on the level of modification. Carbon disulfide-modified LDL is recognized and degraded by the scavenger pathway of macrophages, but to a lesser extent than acetylated LDL. Carbon disulfide modification decreases the ability of the LDL to down-regulate sterol synthesis and to stimulate cholesterol esterification in fibroblasts. Carbon disulfide-modified LDL markedly stimulates cholesteryl ester formation in macrophages, albeit to a lesser extent than acetylated LDL. These results indicate that after carbon disulfide modification the LDL catabolism is shifted to the scavenger pathway, and are consistent with the fact that carbon disulfide intoxication accelerates the appearance of atherosclerotic lesions.
二硫化碳在体外与低密度脂蛋白(LDL)相互作用,由于载脂蛋白B - 100的游离氨基减少,导致颗粒的电泳迁移率增加。与天然LDL相比,培养的人成纤维细胞通过载脂蛋白B/E受体途径对二硫化碳修饰的LDL的处理能力降低,这取决于修饰水平。二硫化碳修饰的LDL可被巨噬细胞的清道夫途径识别并降解,但程度低于乙酰化LDL。二硫化碳修饰降低了LDL下调成纤维细胞中甾醇合成和刺激胆固醇酯化的能力。二硫化碳修饰的LDL显著刺激巨噬细胞中胆固醇酯的形成,尽管程度低于乙酰化LDL。这些结果表明,二硫化碳修饰后LDL的分解代谢转向清道夫途径,这与二硫化碳中毒加速动脉粥样硬化病变出现的事实一致。