Stacey N H, Klaassen C D
J Toxicol Environ Health. 1982 Feb;9(2):267-76. doi: 10.1080/15287398209530160.
Recent evidence has renewed interest in the hypothesis that Ca plays a central role in cell death. It was previously found that Cd and CuCl2 cause loss of viability of isolated hepatocytes. It was therefore of interest to determine whether Ca was intimately involved with the toxic effect of these metals. Some of the chemicals that were previously shown to be toxic through a mechanism involving Ca (amphotericin B, lysolecithin, and Ca ionophore A23187) were also included in the study. Hepatocytes were incubated with one of these chemicals and samples taken at various time points up to 120 min for estimation of cell viability (intracellular K+ and leakage of aspartate aminotransferase) and lipid peroxidation. The toxic effects due to Cd or Cu were not ameliorated on omission of Ca from the incubation medium. Furthermore, of the other three chemicals investigated, only the toxic properties of the Ca ionophore were effectively blocked by incubation in a Ca-free medium. The results of this study do not support the hypothesis that Ca plays a ubiquitous role in the death of liver cells.
最近的证据重新引发了人们对钙在细胞死亡中起核心作用这一假说的兴趣。此前发现镉和氯化铜会导致分离的肝细胞活力丧失。因此，确定钙是否与这些金属的毒性作用密切相关很有意义。该研究还纳入了一些先前被证明通过涉及钙的机制产生毒性的化学物质（两性霉素B、溶血卵磷脂和钙离子载体A23187）。将肝细胞与这些化学物质之一一起孵育，并在长达120分钟的不同时间点取样，以评估细胞活力（细胞内钾离子和天冬氨酸转氨酶泄漏）和脂质过氧化。从孵育培养基中去除钙后，镉或铜引起的毒性作用并未改善。此外，在所研究的其他三种化学物质中，只有钙离子载体的毒性特性在无钙培养基中孵育时被有效阻断。这项研究的结果不支持钙在肝细胞死亡中普遍起作用这一假说。
