Dalvi R R, Howell C D
Drug Chem Toxicol. 1978;1(2):191-202. doi: 10.3109/01480547809034435.
Alterations in the activity of drug-metabolizing enzymes and the concentration of cytochrome p-450 from liver microsomes of rats pretreated with phenobarbital for enzyme induction and later given a single oral dose (0.4 ml/kg) of carbon disulfide (CS2) have been examined. In vitro incubations of these microsomes with parathion and malathion showed no significant change in the amount of cytochrome p-450 from that present in the corresponding controls. This inhibition of oxidative desulfuration of these insecticides by microsomes from CS2-treated animals could be attributed to the prior binding with cytochrome p-450 of sulfur released from CS2 as confirmed from the results of spectral binding of SKF 525-A, parathion and malathion. These results lead to the conclusion that CS2, parathion and malathion undergo oxidative desulfuration in an analogous manner and that the metabolism of the insecticides is impaired in liver previously exposed to CS2.
已对用苯巴比妥预处理以诱导酶,随后单次口服剂量(0.4毫升/千克)二硫化碳(CS2)的大鼠肝脏微粒体中药物代谢酶活性和细胞色素P-450浓度的变化进行了研究。这些微粒体与对硫磷和马拉硫磷的体外孵育显示,细胞色素P-450的量与相应对照相比无显著变化。CS2处理动物的微粒体对这些杀虫剂氧化脱硫的抑制作用可归因于CS2释放的硫与细胞色素P-450的预先结合,这从SKF 525-A、对硫磷和马拉硫磷的光谱结合结果得到证实。这些结果得出结论,CS2、对硫磷和马拉硫磷以类似方式进行氧化脱硫,并且在先前暴露于CS2的肝脏中杀虫剂的代谢受到损害。