Elevated reactive oxygen species and antioxidant enzyme activities in animal and cellular models of Parkinson's disease.
Biochim Biophys Acta
; 1362(1): 77-86, 1997 Nov 28.
Article
em En
| MEDLINE
| ID: mdl-9434102
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Doença de Parkinson Secundária
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Encéfalo
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Espécies Reativas de Oxigênio
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Neurônios
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Antioxidantes
Tipo de estudo:
Prognostic_studies
Limite:
Animals
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Humans
Idioma:
En
Ano de publicação:
1997
Tipo de documento:
Article