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FEBS Lett. 2003 May 22;543(1-3):179-83.

Ca2+-induced oxidative stress in brain mitochondria treated with the respiratory chain inhibitor rotenone.

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1
Departamento de Patologia Cli;nica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, SP 13083-970, Campinas, Brazil.

Abstract

In this study we show that micromolar Ca(2+) concentrations (>10 microM) strongly stimulate the release of reactive oxygen species (ROS) in rotenone-treated isolated rat forebrain mitochondria. Ca(2+)-stimulated mitochondrial ROS release was associated with membrane lipid peroxidation and was directly correlated with the degree of complex I inhibition by rotenone. On the other hand, Ca(2+) did not increase mitochondrial ROS release in the presence of the complex I inhibitor 1-methyl-4-phenylpyridinium. Cyclosporin A had no effect on Ca(2+)-stimulated mitochondrial ROS release in the presence of rotenone, indicating that mitochondrial permeability transition is not involved in this process. We hypothesized that Ca(2+)-induced mitochondrial oxidative stress associated with partial inhibition of complex I may be an important factor in neuronal cell death observed in the neurodegenerative disorder Parkinson's disease.

PMID:
12753929
[Indexed for MEDLINE]
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