Moore L, Ray P
Toxicol Appl Pharmacol. 1983 Oct;71(1):54-8. doi: 10.1016/0041-008x(83)90044-3.
Pretreatment of rats with isopropanol enhanced both hepatotoxicity and calcium pump inhibition after CCl4 exposure in vivo or in vitro. Animals were given isopropanol (1.25 ml/kg) 18 hr before CCl4 (0.01 to 1.0 ml/kg). CCl4 hepatotoxicity, judged as increased appearance of glutamic-pyruvate transaminase in serum, was enhanced by isopropanol pretreatment. Pretreatment of rats with isopropanol made CCl4 as much as 20- to 30-fold more potent as an inhibitor of the calcium pump. Inhibition of another endoplasmic reticulum enzyme, glucose 6-phosphatase, was also enhanced by isopropanol pretreatment. In contrast to the effect of CCl4 in control animals, in isopropanol-pretreated rats given CCl4, depletion of liver glutathione was observed. Altered CCl4 metabolism in isopropanol-pretreated animals may result in production of increased amounts of phosgene (or other metabolites) responsible for inhibition of the liver microsome calcium pump and glutathione depletion.
用异丙醇对大鼠进行预处理，可增强其在体内或体外接触四氯化碳后的肝毒性及对钙泵的抑制作用。在给予四氯化碳（0.01至1.0毫升/千克）前18小时，给动物注射异丙醇（1.25毫升/千克）。通过血清中谷丙转氨酶出现增多来判断，异丙醇预处理增强了四氯化碳的肝毒性。用异丙醇对大鼠进行预处理后，四氯化碳作为钙泵抑制剂的效力提高了20至30倍。异丙醇预处理还增强了对另一种内质网酶葡萄糖6 -磷酸酶的抑制作用。与对照动物中四氯化碳的作用不同，在给予四氯化碳的异丙醇预处理大鼠中，观察到肝脏谷胱甘肽耗竭。异丙醇预处理动物中四氯化碳代谢的改变可能导致产生更多量的光气（或其他代谢产物），从而导致肝脏微粒体钙泵受到抑制和谷胱甘肽耗竭。
