Methamphetamine-induced neuronal damage: A possible role for free radicals

M. J. De Vito, G. C. Wagner

Research output: Contribution to journalArticlepeer-review

234 Scopus citations

Abstract

The hypothesis that methamphetamine-induced neuronal damage is mediated by the production of free radicals was evaluated by pretreating rats with either antioxidants or a Superoxide dismutase (SOD) inhibitor. It was found that methamphetamine (dose range 6.25-25.0 mg/kg) caused long-lasting depletions of dopamine and serotonin in the striatum and that pretreatment with the antioxidants, ascorbic acid (10-100 mg/kg), ethanol(1 g/kg), mannitol (2 g/kg), or vitamin E (2 g/kg), attenuated these depletions, whereas pretreatment with the Superoxide dismutase inhibitor diethyldithiocarbamate (200-400 mg/kg) exacerbated the depletions. The alteration of this effect by four different antioxidants, as well as an inhibitor of superoxidase dismutase, indicated that oxygen-free radicals may have a role in the methamphetamineinduced neurotoxicity.

Original languageEnglish (US)
Pages (from-to)1145-1150
Number of pages6
JournalNeuropharmacology
Volume28
Issue number10
DOIs
StatePublished - Oct 1989

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Cellular and Molecular Neuroscience

Keywords

  • Parkinson's disease
  • dopamine
  • methamphetamine

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