Trela B A, Carlson G P, Chadwick R W, Copeland M F
Toxicol Lett. 1986 Jul-Aug;32(1-2):133-40. doi: 10.1016/0378-4274(86)90059-7.
Mercuric chloride was administered once i.p. to female Fischer-344 rats at doses of 0, 0.2, 0.6 and 1.8 mg/kg. Although there were no alterations in the urinary excretion of lactate dehydrogenase, significant elevations in the activities of urinary (U) alkaline phosphatase, glutamic-pyruvic transaminase (GPT) and glutamic-oxalacetic transaminase (GOT) indicated that mercuric chloride was nephrotoxic. There was no evidence of hepatotoxicity as hepatic glucose-6-phosphatase and serum sorbitol dehydrogenase were essentially unaffected by mercuric chloride administration. The activities of ethylmorphine demethylase, hexobarbital oxidase and aldrin epoxidase determined in vitro were not inhibited by mercuric chloride although aniline hydroxylase activity was decreased. Of the four phase-II reactions measured, only the glucuronidation of chloramphenicol was diminished by treatment with mercuric chloride. Results from the in vivo studies on the metabolism of lindane, which indicated no change in the excretion of free or conjugated metabolites, were in close agreement with the in vitro data suggesting that the nephrotoxic effects of mercuric chloride do not alter the urinary excretion of the model substrate lindane.
将氯化汞以0、0.2、0.6和1.8 mg/kg的剂量经腹腔注射一次给予雌性Fischer-344大鼠。虽然乳酸脱氢酶的尿排泄没有变化,但尿碱性磷酸酶、谷丙转氨酶(GPT)和谷草转氨酶(GOT)活性的显著升高表明氯化汞具有肾毒性。没有肝毒性的证据,因为肝葡萄糖-6-磷酸酶和血清山梨醇脱氢酶基本上不受氯化汞给药的影响。体外测定的乙基吗啡脱甲基酶、己巴比妥氧化酶和艾氏剂环氧化酶的活性不受氯化汞抑制,尽管苯胺羟化酶活性降低。在测定的四个II期反应中,只有氯霉素的葡萄糖醛酸化因氯化汞处理而减少。关于林丹代谢的体内研究结果表明,游离或结合代谢物的排泄没有变化,这与体外数据密切一致,表明氯化汞的肾毒性作用不会改变模型底物林丹的尿排泄。