Tamoxifen inhibits mitochondrial oxidative stress damage induced by copper orthophenanthroline. (26th October 2016)

• Record Type: Journal Article
• Authors: Buelna‐Chontal, Mabel; Hernández‐Esquivel, Luz; Correa, Francisco; Díaz‐Ruiz, Jorge Luis; Chávez, Edmundo
• Is Part Of: Cell biology international. Volume 40:Number 12(2016)
• Page Start: 1349
• Page End: 1356
• Publication Date: 2016-10-26
• Subjects: copper -- mitochondria -- oxidative stress -- permeability transition -- tamoxifen; Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10690
• Languages: English
• ISSNs: 1065-6995

Abstract

Abstract: 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 2+ ‐orthophenanthroline. The findings indicate that tamoxifen and cyclosporin A circumvent the oxidative membrane damage manifested by matrix Ca 2+ 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 2+ ‐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 2+ ‐orthophenanthroline induced the generation of reactive oxygen species. It is thus plausible that membrane leakiness is due to an oxidative stress injury.