Poli G, Cottalasso D, Pronzato M A, Chiarpotto E, Biasi F, Corongiu F P, Marinari U M, Nanni G, Dianzani M U
Department of Experimental Medicine and Oncology, University of Turin, Italy.
Cell Biochem Funct. 1990 Jan;8(1):1-10. doi: 10.1002/cbf.290080102.
The onset of the lipoprotein secretory block provoked by CCl4 in the whole animal was monitored after purification of liver Golgi membranes. Both lipid transit through the apparatus and hexosylation of the lipoprotein are markedly inhibited 5-15 min after poisoning. Pre-treating the animal with alpha-tocopherol, shown to prevent lipid peroxidation without modifying the covalent binding due to CCl4 metabolites, affords little protection against lipid accumulation in the Golgi, but total preservation of galactosyl transferase activity. While haloalkylation therefore appears to be the major mechanism of damage in the early phases of CCl4-induced derangement of lipid secretion, lipid peroxidation is probably more involved later; this is indicated by the marked, though never complete, protection against fatty liver afforded at 24 h after CCl4 poisoning by supplementation of the membrane with alpha-tocopherol.
在纯化肝脏高尔基体膜后，监测了四氯化碳在整个动物体内引发的脂蛋白分泌阻滞的起始情况。中毒后5 - 15分钟，脂质通过该细胞器的转运以及脂蛋白的己糖基化均受到显著抑制。用α - 生育酚预处理动物，已证明其可防止脂质过氧化而不改变四氯化碳代谢产物引起的共价结合，这对高尔基体中脂质积累几乎没有保护作用，但能完全保留半乳糖基转移酶活性。因此，虽然卤代烷基化似乎是四氯化碳诱导脂质分泌紊乱早期阶段损伤的主要机制，但脂质过氧化可能在后期起更大作用；这一点由在四氯化碳中毒24小时后通过向膜中补充α - 生育酚对脂肪肝提供的显著（尽管从未完全）保护所表明。
