On the oxidative damage by cadmium to kidney mitochondrial functions

Author:

Pavón Natalia1,Buelna-Chontal Mabel2,Macías-López Arturo2,Correa Francisco2,Uribe-Álvarez Cristina3,Hernández-Esquivel Luz4,Chávez Edmundo4

Affiliation:

1. Departamento de Farmacología, Instituto Nacional de Cardiología, Ignacio Chávez, Ciudad de México, México.

2. Departamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología, Ignacio Chávez, Ciudad de México, México.

3. Instituto de Fisiología Celular UNAM, Ciudad de México, México.

4. Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, Ciudad de México, México.

Abstract

In the kidney, the accumulation of heavy metals such as Cd2+ produces mitochondrial dysfunctions, i.e., uncoupling of the oxidative phosphorylation, inhibition of the electron transport through the respiratory chain, and collapse of the transmembrane electrical gradient. This derangement may be due to the fact that Cd2+ induces the transition of membrane permeability from selective to nonselective via the opening of a transmembrane pore. In fact, Cd2+ produces this injury through the stimulation of oxygen-derived radical generation, inducing oxidative stress. Several molecules have been used to avoid or even reverse Cd2+-induced mitochondrial injury, for instance, cyclosporin A, resveratrol, dithiocarbamates, and even EDTA. The aim of this study was to explore the possibility that the antioxidant tamoxifen could protect mitochondria from the deleterious effects of Cd2+. Our results indicate that the addition of 1 μmol/L Cd2+ to mitochondria collapsed the transmembrane electrical gradient, induced the release of cytochrome c, and increased both the generation of H2O2 and the oxidative damage to mitochondrial DNA (among other measured parameters). Of interest, these mitochondrial dysfunctions were ameliorated after the addition of tamoxifen.

Publisher

Canadian Science Publishing

Subject

Cell Biology,Molecular Biology,Biochemistry

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