Massey T E, Walker R M, McElligott T F, Racz W J
Toxicology. 1982;25(2-3):187-200. doi: 10.1016/0300-483x(82)90029-4.
Pretreatment of mice with phenobarbital, an inducer of oxidative drug metabolism, had no effect on the early hypothermic effect of a toxic dose of acetaminophen, while pretreatment with metyrapone, SKF-525A, or piperonyl butoxide (inhibitors of mixed-function oxidase) enhanced the hypothermia. In mice treated with acetaminophen alone, brain parent drug levels correlated with the degree of hypothermia, while liver drug levels did not. Also, intracerebroventricular injection of acetaminophen resulted in significant hypothermia within 20 min. These results indicate that the early hypothermia caused by acetaminophen in mice is due to the parent drug, not to its toxic reactive metabolite, and that the effect is mediated centrally. The observation that piperonyl butoxide and SKF-525A themselves caused significant hypothermia indicates that the use of these compounds should be avoided when body temperature is being followed in drug metabolism experiments.
用苯巴比妥(一种氧化药物代谢诱导剂)对小鼠进行预处理,对毒性剂量对乙酰氨基酚的早期体温过低效应没有影响,而用甲吡酮、SKF - 525A或胡椒基丁醚(混合功能氧化酶抑制剂)进行预处理则增强了体温过低。在用对乙酰氨基酚单独处理的小鼠中,脑内母药水平与体温过低程度相关,而肝脏药物水平则不然。此外,脑室内注射对乙酰氨基酚在20分钟内导致显著的体温过低。这些结果表明,对乙酰氨基酚在小鼠中引起的早期体温过低是由于母药,而非其有毒的活性代谢物,且该效应是由中枢介导的。胡椒基丁醚和SKF - 525A本身会引起显著体温过低这一观察结果表明,在药物代谢实验中监测体温时应避免使用这些化合物。