Chávez E, Zazueta C, Bravo C
Departamento de Bioquímica Instituto Nacional de Cardiología, Ignacio Chávez, México.
J Bioenerg Biomembr. 1989 Jun;21(3):335-45. doi: 10.1007/BF00762725.
The effect of the alcohol-deterrent drug, disulfiram, on mitochondrial Ca2+ content was studied. Addition of this drug (20 microM) to mitochondria induces a complete loss of accumulated Ca2+. The calcium release is accompanied by a collapse of the transmembrane potential, mitochondrial swelling, and a diminution of the NAD(P)H/NAD(P) radio. These effects of disulfiram depend on Ca2+ accumulation; thus, ruthenium red reestablished the membrane delta psi and prevents the oxidation of pyridine nucleotides. The binding of disulfiram to the membrane sulfhydryls appeared to depend on the metabolic state of mitochondria, as well as on the mitochondrial configuration. In addition, it is shown that modification of 9 nmol -SH groups per mg protein suffices to induce the release of accumulated Ca2+.
研究了戒酒药物双硫仑对线粒体钙含量的影响。向线粒体中添加该药物（20微摩尔）会导致积累的钙完全丧失。钙释放伴随着跨膜电位的崩溃、线粒体肿胀以及NAD(P)H/NAD(P)比值的降低。双硫仑的这些作用取决于钙的积累；因此，钌红可恢复膜电位差并防止吡啶核苷酸的氧化。双硫仑与膜巯基的结合似乎取决于线粒体的代谢状态以及线粒体的形态。此外，研究表明每毫克蛋白质修饰9纳摩尔的巯基就足以诱导积累的钙释放。
