Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9880350 | Journal of the Neurological Sciences | 2005 | 9 Pages |
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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Authors
Milena Rizzardini, Alessandra Mangolini, Monica Lupi, Paolo Ubezio, Caterina Bendotti, Lavinia Cantoni,