2008年6月
Dopaminergic neuron-specific oxidative stress caused by dopamine itself
Acta Medica Okayama
- ,
- 巻
- 62
- 号
- 3
- 開始ページ
- 141
- 終了ページ
- 150
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.18926/AMO/30980
- 出版者・発行元
- OKAYAMA UNIV MED SCHOOL
Oxidative stress, including the reactive oxygen or nitrogen species generated in the enzymatical oxidation or 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 cytotoxicity in 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 dopaminergic neuron-specific oxidative stress. In this article, we primarily review recent studies on the pathogenicity of quinone formation, in addition to several neuroprotective approaches against dopamine quinone-induced dysfunction of dopaminergic neurons.
- リンク情報
- ID情報
-
- DOI : 10.18926/AMO/30980
- ISSN : 0386-300X
- Web of Science ID : WOS:000257130300001