Andrabi K, Kaul N, Ganguly N K, Dilawari J B
Department of Experimental Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh.
Biochem Int. 1989 Jun;18(6):1287-95.
In situ perfusion of rat liver with carbon tetrachloride (10-15 mM at a final concentration of lul/ml of mineral oil) resulted in a significant (p less than 0.01) loss of microsomal Ca2+ over 5-15 min of exposure. Mitochondrial Ca2+ content increased sharply (2 fold) with concomitant increase in the cytosolic free Ca2+. The changes were associated with a significant (p less than 0.01) decrease in plasma membrane Ca2+ - ATPase activity, reflected by impaired Ca2+ efflux and Ca2+ exchange properties. Our data indicates that impairment of plasma membrane Ca2+ flux contributes substantially to the overall disruption of calcium homeostasis induced by carbon tetrachloride.
用四氯化碳(最终浓度为10 - 15 mM,每毫升矿物油含1微升)对大鼠肝脏进行原位灌注,在暴露5 - 15分钟后,微粒体Ca2+显著(p小于0.01)流失。线粒体Ca2+含量急剧增加(2倍),同时胞质游离Ca2+也增加。这些变化与质膜Ca2+ - ATP酶活性显著(p小于0.01)降低有关,表现为Ca2+外流和Ca2+交换特性受损。我们的数据表明,质膜Ca2+通量受损在很大程度上导致了四氯化碳诱导的钙稳态整体破坏。