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• W2104841128 abstract "Abstract: The effect of the neurotoxic nitric oxide derivative, the peroxynitrite anion (ONOO−), on the activity of the mitochondrial respiratory chain complexes in cultured neurones and astrocytes was studied. A single exposure of the neurones to ONOO− (initial concentrations of 0.01–2.0 mM) caused, after a subsequent 24-h incubation, a dose-dependent decrease in succinate-cytochrome c reductase (60% at 0.5 mM) and in cytochrome c oxidase (52% at 0.5 mM) activities. NADH-ubiquinone-1 reductase was unaffected. In astrocytes, the activity of the mitochondrial complexes was not affected up to 2 mM ONOO−. Citrate synthase was unaffected in both cell types under all conditions studied. However, lactate dehydrogenase activity released to the culture medium was increased by ONOO− in a dose-dependent manner (40% at 0.5 mM ONOO−) from the neurones but not from the astrocytes. Neuronal glutathione concentration decreased by 39% at 0.1 mM ONOO−, but astrocytic glutathione was not affected up to 2 mM ONOO−. In isolated brain mitochondria, only succinate-cytochrome c reductase activity was affected (22% decrease at 1 mM ONOO−). We conclude that the acute exposure of ONOO− selectively damages neurones, whereas astrocytes remain unaffected. Intracellular glutathione appears to be an important factor for ameliorating ONOO−-mediated mitochondrial damage. This study supports the hypothesis that the neurotoxicity of nitric oxide is mediated through mitochondrial dysfunction." @default.
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• W2104841128 date "2002-11-23" @default.
• W2104841128 modified "2023-09-30" @default.
• W2104841128 title "Effect of Peroxynitrite on the Mitochondrial Respiratory Chain: Differential Susceptibility of Neurones and Astrocytes in Primary Culture" @default.
• W2104841128 doi "https://doi.org/10.1046/j.1471-4159.1995.64051965.x" @default.
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