On the oxidative damage by cadmium to kidney mitochondrial functions.
Biochem Cell Biol
; 97(2): 187-192, 2019 04.
Article
en En
| MEDLINE
| ID: mdl-30332552
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.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Cadmio
/
Estrés Oxidativo
/
Potencial de la Membrana Mitocondrial
/
Peróxido de Hidrógeno
/
Riñón
/
Mitocondrias
Límite:
Animals
Idioma:
En
Revista:
Biochem Cell Biol
Asunto de la revista:
BIOQUIMICA
Año:
2019
Tipo del documento:
Article
Pais de publicación:
Canadá