Oxidative toxicity in models of neurodegeneration: Responses to melatonin

Russel J. Reiter, Joaquin J. Garcia, Juan Pie

Research output: Contribution to journalArticlepeer-review

52 Scopus citations

Abstract

In this brief review the antioxidative actions of melatonin are summarized and they are discussed relative to several models of oxidative neurotoxicity. Melatonin is a ubiquitously acting antioxidant. It has been shown to scavenge the hydroxyl radical, peroxyl radical, singlet oxygen and the peroxynitrite anion; secondarily, it also scavenges the superoxide anion radical. In addition, melatonin reportedly stimulates a number of antioxidative enzymes including glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase. On the other hand, melatonin inhibits the pro-oxidative enzyme nitric oxide synthase. Besides these actions which help to resist oxidative damage, melatonin prevents membrane rigidity, reduces polymorphonuclear cell infiltration into damaged tissue, limits the adhesion of leucocytes to endothelial cells, thereby increasing blood flow and reducing edema. Some or all of these actions may have been operative in the experimental models of oxidative neurotoxicity that were improved by melatonin treatment. In brief, melatonin has been found to protect the CNS from β-amyloid toxicity, experimental models of Parkinsonism, excitotoxicity, nitric oxide toxicity, aminolevulinic acid, lipopolysaccharide, hyperbaric hyperoxia, L-cysteine, Cyanide and ischemia/reperfusion injury.

Original languageEnglish (US)
Pages (from-to)135-142
Number of pages8
JournalRestorative Neurology and Neuroscience
Volume12
Issue number2-3
StatePublished - Jun 1 1998

Keywords

  • Alzheimer's disease
  • Antioxidant
  • Free radicals
  • Ischemia/reperfusion
  • Lipid peroxidation
  • Melatonin
  • Neurotoxicity

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience
  • Clinical Neurology

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