Dopaminergic neuron-specific oxidative stress caused by dopamine itself

Research output: Contribution to journalReview articlepeer-review

134 Citations (Scopus)


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. Copyright

Original languageEnglish
Article number1
JournalActa medica Okayama
Issue number3
Publication statusPublished - Jun 2008


  • Dopamine quinone
  • L-DOPA
  • Methamphetamine
  • Parkinson's disease
  • Quinoprotein

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


Dive into the research topics of 'Dopaminergic neuron-specific oxidative stress caused by dopamine itself'. Together they form a unique fingerprint.

Cite this