Mourelle M, Villalon C, Amezcua J L
Department of Pharmacology and Toxicology, Centro de Investigación, Mexico City, Mexico.
J Hepatol. 1988 Jun;6(3):337-42. doi: 10.1016/s0168-8278(88)80051-5.
Pretreatment of rats with colchicine (10 micrograms/day) for 7 days protected against CCl4-induced acute liver damage. CCl4 intoxication was demonstrated histologically and by increased serum activities of glutamic-pyruvic transaminase, alkaline phosphatase and gamma-glutamyl transpeptidase. Furthermore, an increase in liver lipid peroxidation and a decrease in plasma membrane gamma-glutamyl transpeptidase activity were found. Colchicine increased the LD50 of CCl4 2.5-fold and prevented the release of intracellular enzymes, as well as the decrease in gamma-glutamyl transpeptidase activity in the plasma membrane. It also completely prevented the lipid peroxidation produced by CCl4 and limited the extent of the histological changes. Our results suggest that the protective effect of colchicine may be mediated through its action on an early toxic event, because treatment of the animals with colchicine produced a significant decrease in CCl4-induced lipid peroxidation.
用秋水仙碱（10微克/天）对大鼠进行预处理7天，可预防四氯化碳诱导的急性肝损伤。通过组织学检查以及血清谷丙转氨酶、碱性磷酸酶和γ-谷氨酰转肽酶活性升高来证实四氯化碳中毒。此外，还发现肝脂质过氧化增加以及质膜γ-谷氨酰转肽酶活性降低。秋水仙碱使四氯化碳的半数致死剂量增加了2.5倍，并防止了细胞内酶的释放以及质膜中γ-谷氨酰转肽酶活性的降低。它还完全阻止了四氯化碳产生的脂质过氧化，并限制了组织学变化的程度。我们的结果表明，秋水仙碱的保护作用可能是通过其对早期毒性事件的作用介导的，因为用秋水仙碱治疗动物可使四氯化碳诱导的脂质过氧化显著降低。
