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Tamoxifen inhibits mitochondrial oxidative stress damage induced by copper orthophenanthroline
Author(s) -
BuelnaChontal Mabel,
HernándezEsquivel Luz,
Correa Francisco,
DíazRuiz Jorge Luis,
Chávez Edmundo
Publication year - 2016
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10690
Subject(s) - mitochondrial permeability transition pore , oxidative stress , reactive oxygen species , chemistry , tbars , tamoxifen , inner mitochondrial membrane , mitochondrion , transmembrane protein , oxidative phosphorylation , oxidizing agent , biophysics , biochemistry , microbiology and biotechnology , biology , apoptosis , programmed cell death , lipid peroxidation , organic chemistry , genetics , receptor , cancer , breast cancer
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.