Selenium, an antioxidant, protects against methamphetamine-induced dopaminergic neurotoxicity

Brain Res. 1999 Feb 13;818(2):575-8. doi: 10.1016/s0006-8993(98)01311-0.

Abstract

Dopaminergic changes were studied in the caudate nucleus of adult female mice after pre- and post-treatment with an antioxidant, selenium, 72 h after the multiple injections of methamphetamine (METH, 4x10 mg/kg, i.p. at 2-h interval) or an equivalent volume of saline. Selenium treatment prevented the depletion of dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in caudate nucleus resulting from the METH treatment. These data suggest that METH-induced neurotoxicity is mediated by free radical and selenium plays a protective role against METH-induced dopaminergic neurotoxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3,4-Dihydroxyphenylacetic Acid / metabolism
  • Animals
  • Antioxidants / therapeutic use*
  • Dopamine / metabolism
  • Dopamine Agents / toxicity*
  • Female
  • Homovanillic Acid / metabolism
  • Methamphetamine / antagonists & inhibitors
  • Methamphetamine / toxicity*
  • Mice
  • Mice, Inbred C57BL
  • Neuroprotective Agents / therapeutic use*
  • Selenium / therapeutic use*

Substances

  • Antioxidants
  • Dopamine Agents
  • Neuroprotective Agents
  • 3,4-Dihydroxyphenylacetic Acid
  • Methamphetamine
  • Selenium
  • Dopamine
  • Homovanillic Acid