Article ID Journal Published Year Pages File Type
9880350 Journal of the Neurological Sciences 2005 9 Pages PDF
Abstract
The mutant protein rendered G93ASOD1 cells more sensitive to mitochondrial dysfunction induced by stimuli that alter cellular free radical homeostasis, like serum withdrawal, depletion of glutathione by ethacrynic acid or rotenone-mediated inhibition of complex I of the mitochondrial electron transport chain. In conclusion, even a small amount of mutant SOD1 put motor neurons in a condition of oxidative stress and mitochondrial damage that causes cell vulnerability and death.
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Life Sciences Biochemistry, Genetics and Molecular Biology Ageing
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