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ID 30980
JaLCDOI
フルテキストURL
著者
Miyazaki, Ikuko Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kaken ID researchmap
Asanuma, Masato Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
抄録

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.

キーワード
dopamine quinone
quinoprotein
methamphetamine
Parkinson?s disease
L-DOPA
Amo Type
Review
発行日
2008-06
出版物タイトル
Acta Medica Okayama
62巻
3号
出版者
Okayama University Medical School
開始ページ
141
終了ページ
150
ISSN
0386-300X
NCID
AA00508441
資料タイプ
学術雑誌論文
言語
English
論文のバージョン
publisher
査読
有り
PubMed ID
Web of Science KeyUT