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ID 30980
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Abstract

Oxidative stress, including the reactive oxygen or nitrogen species generated in the enzymatical oxidationor auto-oxidation of an excess amount of dopamine, is thought to play an important role in dopaminergic neurotoxicity. Dopamine and its metabolites containing 2 hydroxyl residues exert cytotoxicityin dopaminergic neuronal cells, primarily due to the generation of highly reactive dopamine and DOPA quinones. Dopamine and DOPA quinones may irreversibly alter protein function through the formation of 5-cysteinyl-catechols on the proteins. Furthermore, the quinone formation is closely linked to other representative hypotheses such as mitochondrial dysfunction, inflammation, oxidative stress, and dysfunction of the ubiquitin-proteasome system, in the pathogenesis of neurodegenerative diseases. Therefore, pathogenic effects of the dopamine quinone have recently focused on dopaminergicneuron-specific oxidative stress. In this article, we primarily review recent studies on the pathogenicity of quinone formation, in addition to several neuroprotective approaches against dopaminequinone-induced dysfunction of dopaminergic neurons.

Keywords
dopamine quinone
quinoprotein
methamphetamine
Parkinson?s disease
L-DOPA
Amo Type
Review
Published Date
2008-06
Publication Title
Acta Medica Okayama
Volume
volume62
Issue
issue3
Publisher
Okayama University Medical School
Start Page
141
End Page
150
ISSN
0386-300X
NCID
AA00508441
Content Type
Journal Article
language
英語
File Version
publisher
Refereed
True
PubMed ID
Web of Science KeyUT