Moore L
Biochim Biophys Acta. 1984 Nov 7;777(2):216-20. doi: 10.1016/0005-2736(84)90423-1.
In vitro exposure of hepatocytes or liver microsomes to t-butyl hydroperoxide resulted in a marked decrease of liver microsomal calcium pump activity. Decreased calcium pump activity was dependent upon both concentration and time. Liver microsomes could be protected from this effect by glutathione or dithiothreitol. In addition to decreased calcium pump activity, exposure of liver microsomes to t-butyl hydroperoxide produced a concentration-dependent aggregation of microsomal membrane protein as determined by polyacrylamide gel electrophoresis. Inhibition of microsomal calcium pump activity was observed when intact hepatocytes were incubated, in vitro, with t-butyl hydroperoxide. However, aggregation of microsomal membrane protein was not observed when hepatocytes were incubated with t-butyl hydroperoxide. The effects produced by exposure of liver microsomes to this compound do not appear to be a complete model of actions of the compound on intact cells.
肝细胞或肝微粒体在体外暴露于叔丁基过氧化氢会导致肝微粒体钙泵活性显著降低。钙泵活性的降低取决于浓度和时间。谷胱甘肽或二硫苏糖醇可保护肝微粒体免受这种影响。除了钙泵活性降低外,通过聚丙烯酰胺凝胶电泳测定,肝微粒体暴露于叔丁基过氧化氢还会产生浓度依赖性的微粒体膜蛋白聚集。当完整的肝细胞在体外与叔丁基过氧化氢孵育时,观察到微粒体钙泵活性受到抑制。然而,当肝细胞与叔丁基过氧化氢孵育时,未观察到微粒体膜蛋白聚集。肝微粒体暴露于该化合物所产生的影响似乎并非该化合物对完整细胞作用的完整模型。