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Elevated reactive oxygen species and antioxidant enzyme activities in animal and cellular models of Parkinson's disease

1997; Elsevier BV; Volume: 1362; Issue: 1 Linguagem: Inglês

10.1016/s0925-4439(97)00070-7

1879-260X

David S. Cassarino, Christopher P. Fall, Russell H. Swerdlow, Trisha S. Smith, Erik M Halvorsen, Scott W. Miller, Janice P Parks, W. Davis Parker, James P. Bennett,

Neurological diseases and metabolism

The dopaminergic neurotoxin N-methyl,4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) causes a syndrome in primates and humans which mimics Parkinson's disease (PD) in clinical, pathological, and biochemical findings, including diminished activity of complex I in the mitochondrial electron transport chain. Reduced complex I activity is found in sporadic PD and can be transferred through mitochondrial DNA, suggesting a mitochondrial genetic etiology. We now show that MPTP treatment of mice and N-methylpyridinium (MPP+) exposure of human SH-SY5Y neuroblastoma cells increases oxygen free radical production and antioxidant enzyme activities. Cybrid cells created by transfer of PD mitochondria exhibit similar characteristics; however, PD cybrids' antioxidant enzyme activities are not further increased by MPP+ exposure, as are the activities in control cybrids. PD mitochondrial cybrids are subject to metabolic and oxidative stresses similar to MPTP parkinsonism and provide a model to determine mechanisms of oxidative damage and cell death in PD.