Disrupted mitochondrial electron transport function increases expression of anti-apoptotic Bcl-2 and Bcl-XL proteins in SH-SY5Y neuroblastoma and in Parkinson disease cybrid cells through oxidative stress

Abstract excerpt

Death of dopamine neurons in Parkinson disease (PD) may arise from consequences of the complex I (C-I) defect in the mitochondrial electron transport chain (ETC). Whether cells activate programmed death (apoptosis) pathways derives, in part, from relative activities of proteins such as bcl-2 and bcl-X(L), that have anti-apoptotic actions. We studied the responses of bcl-2 and bcl-X(L) genes in pharmacologic...

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