Approaches to prevent dopamine quinone-induced neurotoxicity

Neurochem Res. 2009 Apr;34(4):698-706. doi: 10.1007/s11064-008-9843-1. Epub 2008 Sep 4.

Abstract

Dopamine (DA) and its metabolites containing two hydroxyl residues exert cytotoxicity in dopaminergic neuronal cells, primarily due to the generation of highly reactive DA and DOPA quinones. 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 such as Parkinson's disease and methamphetamine-induced neurotoxicity. Therefore, pathogenic effects of the DA quinone have focused on dopaminergic neuron-specific oxidative stress. Recently, various studies have demonstrated that some intrinsic molecules and several drugs exert protective effects against DA quinone-induced damage of dopaminergic neurons. In this article, we review recent studies on some neuroprotective approaches against DA quinone-induced dysfunction and/or degeneration of dopaminergic neurons.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Dopamine / analogs & derivatives*
  • Dopamine / physiology
  • Humans
  • Methamphetamine / toxicity
  • Neurodegenerative Diseases / chemically induced
  • Neurodegenerative Diseases / drug therapy
  • Neurodegenerative Diseases / metabolism*
  • Neurons / metabolism*
  • Neuroprotective Agents / pharmacology
  • Neuroprotective Agents / therapeutic use
  • Oxidative Stress*
  • Parkinsonian Disorders / drug therapy
  • Parkinsonian Disorders / metabolism*

Substances

  • Neuroprotective Agents
  • Methamphetamine
  • dopamine quinone
  • Dopamine