Buelna-Chontal Mabel, Hernández-Esquivel Luz, Correa Francisco, Díaz-Ruiz Jorge Luis, Chávez Edmundo
Departamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología, Ignacio Chávez, D.F. México, México.
Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, D.F. México, 14080, México.
Cell Biol Int. 2016 Dec;40(12):1349-1356. doi: 10.1002/cbin.10690. Epub 2016 Oct 26.
In this work, we studied the effect of tamoxifen and cyclosporin A on mitochondrial permeability transition caused by addition of the thiol-oxidizing pair Cu -orthophenanthroline. The findings indicate that tamoxifen and cyclosporin A circumvent the oxidative membrane damage manifested by matrix Ca release, mitochondrial swelling, and transmembrane electrical gradient collapse. Furthermore, it was found that tamoxifen and cyclosporin A prevent the generation of TBARs promoted by Cu -orthophenanthroline, as well as the inactivation of the mitochondrial enzyme aconitase and disruption of mDNA. Electrophoretic analysis was unable to demonstrate a cross-linking reaction between membrane proteins. Yet, it was found that Cu -orthophenanthroline induced the generation of reactive oxygen species. It is thus plausible that membrane leakiness is due to an oxidative stress injury.
在本研究中，我们研究了他莫昔芬和环孢素A对由添加硫醇氧化对铜 - 邻菲罗啉引起的线粒体通透性转变的影响。研究结果表明，他莫昔芬和环孢素A可规避由基质钙释放、线粒体肿胀和跨膜电位梯度崩溃所表现出的氧化膜损伤。此外，还发现他莫昔芬和环孢素A可防止铜 - 邻菲罗啉促进的硫代巴比妥酸反应物（TBARs）的生成，以及线粒体酶乌头酸酶的失活和线粒体DNA（mDNA）的破坏。电泳分析未能证明膜蛋白之间存在交联反应。然而，发现铜 - 邻菲罗啉可诱导活性氧的生成。因此，膜通透性增加可能是由于氧化应激损伤所致。
