Brattin W J, Waller R L
Life Sci. 1984 Sep 10;35(11):1231-40. doi: 10.1016/0024-3205(84)90195-4.
Exposure of isolated rat hepatocytes to hepatotoxic halomethanes results in a 40-60% decrease in intracellular Ca2+ content. The order of halomethane potency (CBrCl3 CCl4 CHCl3) suggests that this effect requires halomethane metabolism by the hepatic mixed function oxidase system. Although the Ca2+ sequestering ability of the endoplasmic reticulum is destroyed by CBrCl3 and CCl4, it appears that much of the Ca2+ lost from the cell is mitochondrial in origin. Paradoxically, saturating concentrations of CCl4 cause a marked increase in cell Ca2+. CCl4 also causes an acute increase in cytoplasmic free Ca2+ (from about 60 nM to about 90 nM), but this effect does not appear to require CCl4 metabolism and is probably a result of direct action of CCl4 on the plasma membrane.
将分离的大鼠肝细胞暴露于具有肝毒性的卤代甲烷中，会导致细胞内钙离子含量降低40%-60%。卤代甲烷的效力顺序（三氯溴甲烷、四氯化碳、三氯甲烷）表明，这种效应需要肝脏混合功能氧化酶系统对卤代甲烷进行代谢。尽管内质网的钙离子螯合能力会被三氯溴甲烷和四氯化碳破坏，但细胞中流失的大部分钙离子似乎源自线粒体。矛盾的是，饱和浓度的四氯化碳会导致细胞钙离子显著增加。四氯化碳还会使细胞质游离钙离子急剧增加（从约60纳摩尔增加到约90纳摩尔），但这种效应似乎不需要四氯化碳代谢，可能是四氯化碳直接作用于质膜的结果。
