Chávez E, Holguín J A
Departamento de Bioquímica, Instituto Nacional de Cardiología, México, D.F.
J Biol Chem. 1988 Mar 15;263(8):3582-7.
Addition of Hg2+ to mitochondria of rat kidney induces efflux of intramitochondrial Ca2+. This reaction is accompanied by a diminution of the NAD(P)H/NAD(P) ratio and a decrease of the internal negative membrane potential. These effects were enhanced by dithiothreitol. The binding of mercuric ions to mitochondria saturates with a maximal binding of 9 nmol min-1 mg-1. The stoichiometry between Ca2+ released and Hg2+ bound showed that in the presence of dithiothreitol, the binding of approximately 1 nmol of Hg2+/mg of protein suffices to induce the release of the accumulated Ca2+. In the electrophoretic analysis of Hg-labeled mitochondrial proteins it was found that 203Hg2+ bound mainly to proteins that have molecular masses of 20 and 30 kDa. It is proposed that Hg2+-induced Ca2+ release is due to modification of--SH groups of these latter proteins.
向大鼠肾脏线粒体中添加Hg2+会诱导线粒体内Ca2+外流。此反应伴随着NAD(P)H/NAD(P)比值的降低和内膜负电位的下降。二硫苏糖醇会增强这些效应。汞离子与线粒体的结合会饱和，最大结合量为9 nmol min-1 mg-1。释放的Ca2+与结合的Hg2+之间的化学计量关系表明，在二硫苏糖醇存在的情况下，每毫克蛋白质结合约1 nmol的Hg2+就足以诱导积累的Ca2+释放。在对汞标记的线粒体蛋白质进行电泳分析时发现，203Hg2+主要与分子量为20 kDa和30 kDa的蛋白质结合。有人提出，Hg2+诱导的Ca2+释放是由于后一种蛋白质的-SH基团发生了修饰。
