Journal ArticleDOI
Redox cycling of MPP+: Evidence for a new mechanism involving hydride transfer with xanthine oxidase, aldehyde dehydrogenase, and lipoamide dehydrogenase
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TLDR
The data suggest that MPP+ is reduced by lipoamide dehydrogenase, and the mechanism involved may be hydride transfer from the enzymes to MPP+, rather than a direct single-electron reduction.About:
This article is published in Free Radical Biology and Medicine.The article was published on 1993-08-01. It has received 66 citations till now. The article focuses on the topics: Dihydrolipoamide dehydrogenase & Redox.read more
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Parkinson's disease: Mechanisms and models
TL;DR: PD models based on the manipulation of PD genes should prove valuable in elucidating important aspects of the disease, such as selective vulnerability of substantia nigra dopaminergic neurons to the degenerative process.
Journal ArticleDOI
Classic toxin-induced animal models of Parkinson's disease: 6-OHDA and MPTP.
TL;DR: The most important properties of 6-hydroxy-dopamine and MPTP, their modes of administration, and critically examines advantages and limitations of selected animal models are discussed.
Journal ArticleDOI
Inactivation of tyrosine hydroxylase by nitration following exposure to peroxynitrite and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
Jahan Ara,Serge Przedborski,Ali Naini,Vernice Jackson-Lewis,Rosario R. Trifiletti,Joel Horwitz,Harry Ischiropoulos +6 more
TL;DR: It is reported that the rate-limiting enzyme in dopamine synthesis, tyrosine hydroxylase (TH), is a selective target for nitration following exposure of PC12 cells to either peroxynitrite or 1-methyl-4-phenylpyridiniun ion (MPP+).
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The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model: a tool to explore the pathogenesis of Parkinson's disease.
Serge Przedborski,Miquel Vila +1 more
TL;DR: Different contributing factors are reviewed, as is the sequence in which it is believed these factors are acting within the cascade of events responsible for the death of dopaminergic neurons in the MPTP model and in PD.
Journal ArticleDOI
Toxin models of mitochondrial dysfunction in Parkinson's disease
TL;DR: An overview of toxin models of mitochondrial dysfunction in experimental Parkinson's disease and mitochondrial mechanisms of neurotoxicity are provided, as well as an emerging emphasis on extranigral aspects of PD pathology.
References
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Ubisemiquinone is the electron donor for superoxide formation by complex III of heart mitochondria.
TL;DR: Experiments with succinate as electron donor in the presence of antimycin A in intact rat heart mitochondria showed that myxothiazol, which inhibits reduction of the Rieske iron-sulfur center, prevented formation of hydrogen peroxide, determined spectrophotometrically as the H2O2-peroxidase complex.
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Metabolism of the neurotoxic tertiary amine, MPTP, by brain monoamine oxidase.
TL;DR: The neurotoxic chemical MPTP is metabolized by rat brain mitochondrial fractions at a rate of 0.91 +/- 0.02 nmoles/mg protein/min, and the major metabolite has been identified as the 1-methyl-4- phenylpyridinium species.
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Dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine in mice
TL;DR: When MPTP (30 milligrams per kilogram of body weight) was administered parenterally to mice, a decrease in concentrations of neostriatal dopamine and its metabolites and a disappearance of nerve cells in the zona compacta of the substantia nigra were observed.
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Spin trapping. Kinetics of the reaction of superoxide and hydroxyl radicals with nitrones
Book
Oxidases and Related Redox Systems
TL;DR: This book contains the proceedings of a symposium on oxidases and related redoxsystems, which covered topics such as Flavoprotein oxidase and oxygenases, Peroxidases, and Cytochrome P-450 and related proteins.