Tamoxifen inhibits mitochondrial membrane damage caused by disulfiram

被引：7

作者：

Pavon, Natalia ^{[1
]}

Buelna-Chontal, Mabel ^{[2
]}

Correa, Francisco ^{[2
]}

Yoval-Sanchez, Belem ^{[3
]}

Belmont, Javier ^{[3
]}

Hernandez-Esquivel, Luz ^{[3
]}

Rodriguez-Zavala, Jose S. ^{[3
]}

Chavez, Edmundo ^{[3
]}

机构：

[1] Inst Nacl Cardiol Ignacio Chavez, Dept Farmacol, Mexico City, DF, Mexico

[2] Inst Nacl Cardiol Ignacio Chavez, Dept Biomed Cardiovasc, Mexico City, DF, Mexico

[3] Inst Nacl Cardiol Ignacio Chavez, Dept Bioquim, Mexico City, DF, Mexico

来源：

BIOCHEMISTRY AND CELL BIOLOGY | 2017年 / 95卷 / 05期

关键词：

disulfiram; mitochondria; tamoxifen; oxidative stress; OXIDATIVE STRESS; PERMEABILITY TRANSITION; CA-2+ RELEASE; CELLS; MECHANISMS; APOPTOSIS; REAGENTS; HYPERTHYROIDISM; SUPEROXIDE; CYSTEINE;

D O I：

10.1139/bcb-2017-0027

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In this work, we studied the protective effects of tamoxifen (TAM) on disulfiram (Dis)-induced mitochondrial membrane insult. The results indicate that TAM circumvents the inner membrane leakiness manifested as Ca2+ release, mitochondrial swelling, and collapse of the transmembrane electric gradient. Furthermore, it was found that TAM prevents inactivation of the mitochondrial enzyme aconitase and detachment of cytochrome c from the inner membrane. Interestingly, TAM also inhibited Dis-promoted generation of hydrogen peroxide. Given that TAM is an antioxidant molecule, it is plausible that its protection may be due to the inhibition of Dis-induced oxidative stress.

引用

页码：556 / 562

页数：7

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