Masuda Y, Nakayama N
Biochem Pharmacol. 1983 Nov 1;32(21):3127-35. doi: 10.1016/0006-2952(83)90194-6.
Oral administration of diethyldithiocarbamate (DTC) and carbon disulfide (CS2) protected mice against CHCl3-induced kidney injury, as evidenced by normalization of delayed plasma phenolsulfonphthalein clearance, suppression of increased kidney calcium content and prevention of renal tubular necrosis. In CCl4-treated mice, in which liver microsomal monooxygenase activities were decreased markedly, and kidney microsomal aniline hydroxylase and p-nitroanisole demethylase activities were increased to about twice those of the untreated mice, renal toxicity of CHCl3 was greatly potentiated, and the latter effect was also blocked by both agents. DTC and CS2 per se markedly decreased kidney microsomal aniline hydroxylase and p-nitroanisole demethylase activities at 1 hr after oral administration, accompanying a moderate loss of cytochrome P-450 content, in both normal and CCl4-treated mice. The protection was not due to hypothermia, because pretreatment with DTC or CS2 (p.o.) also prevented the hypothermia induced by CHCl3. The mechanism of the protection may have involved inhibition of metabolic activation of CHCl3 in the kidney rather than in the liver.
口服二乙氨基二硫代甲酸盐（DTC）和二硫化碳（CS2）可保护小鼠免受氯仿诱导的肾损伤，这表现为延迟的血浆酚红清除率恢复正常、肾脏钙含量增加受到抑制以及肾小管坏死得到预防。在四氯化碳处理的小鼠中，肝脏微粒体单加氧酶活性显著降低，而肾脏微粒体苯胺羟化酶和对硝基苯甲醚脱甲基酶活性增加至未处理小鼠的约两倍，氯仿的肾毒性大大增强，并且这两种药物也能阻止后一种效应。在正常小鼠和四氯化碳处理的小鼠中，口服给药1小时后，DTC和CS2本身均显著降低肾脏微粒体苯胺羟化酶和对硝基苯甲醚脱甲基酶活性，同时细胞色素P - 450含量适度减少。这种保护作用并非由于体温过低，因为用DTC或CS2（口服）预处理也能预防氯仿诱导的体温过低。保护机制可能涉及抑制氯仿在肾脏而非肝脏中的代谢活化。
