Effects of amphetamines on mitochondrial function: Role of free radicals and oxidative stress

Jeffrey M. Brown, Bryan K. Yamamoto

Research output: Contribution to journalArticle

136 Scopus citations

Abstract

Amphetamine-like psychostimulants are associated with long-term decreases in markers for monoaminergic neurons, suggesting neuronal loss and/or damage within the brain. This long-term "toxicity" results from formation of free radicals, particularly reactive oxygen species (ROS) and reactive nitrogen species (RNS), although the mechanism(s) of ROS and RNS formation are unclear. Mitochondria are a major source of ROS and mitochondrial dysfunction has been linked to some neurodegenerative disorders. Amphetamines also inhibit mitochondrial function, although the mechanism involved in the inhibition is uncertain. This review coordinates findings on the multiple pathways for ROS and RNS and describes a hypothesis involving mitochondrial inhibition in the initiation of amphetamine-induced cellular necrosis.

Original languageEnglish (US)
Pages (from-to)45-53
Number of pages9
JournalPharmacology and Therapeutics
Volume99
Issue number1
DOIs
StatePublished - Jul 1 2003
Externally publishedYes

Keywords

  • Amphetamine
  • Free radicals
  • Mitochondria
  • Oxidative stress
  • Reactive nitrogen species
  • Reactive oxygen species

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

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