卤代化合物对肝细胞钙稳态的影响。
Impact of halogenated compounds on calcium homeostasis in hepatocytes.
作者信息
Moore L, Schoenberg D R, Long R M
机构信息
Dept. of Pharmacology, University of the Health Sciences, Bethesda, MD 20814.
出版信息
Environ Health Perspect. 1990 Mar;84:149-53. doi: 10.1289/ehp.9084149.
Halocarbons (CCl4, 1,1-dichlorethylene) cause a wide spectrum of effects and injury in hepatocytes. One early effect of these compounds is the inhibition and destruction of the endoplasmic reticulum (ER) calcium pump. Subsequent to inhibition of this pump, the ER calcium pool is depleted and cytosolic levels of calcium are increased for a prolonged period of time. This effect of halocarbons has been characterized and is similar in vivo and in vitro. The importance of this redistribution of cell calcium in expression of halocarbon injury of hepatocytes has not been fully resolved. Several degradative enzymes (phospholipases, proteases) have been implicated as calcium-dependent mediators in toxicity. Our preliminary studies of the effect of calcium redistribution suggest that activation of a calcium-sensitive endonuclease in liver does not play a central role in initiating the lethal effect of halocarbons on hepatocytes.
卤代烃（四氯化碳、1,1-二氯乙烯）会在肝细胞中引发广泛的效应和损伤。这些化合物的一个早期效应是对内质网（ER）钙泵的抑制和破坏。该泵受到抑制后，内质网钙库会耗尽，细胞溶质中的钙水平会在较长一段时间内升高。卤代烃的这种效应已得到表征，在体内和体外情况相似。细胞钙的这种重新分布在卤代烃所致肝细胞损伤表达中的重要性尚未完全阐明。几种降解酶（磷脂酶、蛋白酶）被认为是毒性作用中钙依赖性的介质。我们关于钙重新分布效应的初步研究表明，肝脏中钙敏感核酸内切酶的激活在引发卤代烃对肝细胞的致死效应中并不起核心作用。
Zotero 插件