Bernstein J, Santacana G
Res Commun Chem Pathol Pharmacol. 1987 Apr;56(1):49-74.
The effect of ethanol on calcium transport by the liver cell was studied by using a rat liver slice preparation. Ethanol was shown to decrease by about 30% the rate constant for 45Ca efflux from the intracellular compartment. This inhibitory effect of ethanol was not observed in the absence of Ca2+ or Na+ from the incubation medium. Ethanol was also shown to greatly increase non-insulin calcium uptake by liver slices. This effect of ethanol appeared to be dose dependent and was not observed in the absence of Na+ from the incubation medium. The ability of ethanol to increase calcium uptake by the hepatocyte was completely blocked by 1 mM Amiloride. Amiloride, however, did not affect the increased entry of either Na+ or Ca2+ produced by 10 mM Ouabain, a specific inhibitor of the sodium pump. Carbon tetrachloride (CCl4), a well known hepatotoxin, also increased calcium uptake by the hepatocyte. Amiloride, however, was not able to block the CCl4-induced calcium uptake. These results suggest that ethanol activates a Na+ entry pathway, probably represented by a Na+/H+ exchanger, which in turn stimulates an entry of Ca2+ through a Na+/Ca2+ exchange mechanism located in the plasma membrane of the hepatocyte.
采用大鼠肝切片制备物研究了乙醇对肝细胞钙转运的影响。结果表明,乙醇可使45Ca从细胞内区室流出的速率常数降低约30%。在孵育介质中不存在Ca2+或Na+时,未观察到乙醇的这种抑制作用。乙醇还可使肝切片对非胰岛素钙的摄取大幅增加。乙醇的这种作用似乎呈剂量依赖性,且在孵育介质中不存在Na+时未观察到。1 mM氨氯吡咪可完全阻断乙醇增加肝细胞钙摄取的能力。然而,氨氯吡咪并不影响由10 mM哇巴因(一种钠泵特异性抑制剂)所导致的Na+或Ca2+进入增加。四氯化碳(CCl4)是一种众所周知的肝毒素,它也可增加肝细胞对钙的摄取。然而,氨氯吡咪无法阻断CCl4诱导的钙摄取。这些结果表明,乙醇激活了一条Na+进入途径,可能由Na+/H+交换体所代表,进而通过位于肝细胞质膜上的Na+/Ca2+交换机制刺激Ca2+进入。