Affiliations: Department of Cellular and Structural Biology, The
University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio,
TX 78284-7762, USA
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 B-amyloid toxicity,
experimental models of Parkinsonism, excitotoxicity, nitric oxide toxicity,
aminolevulinic acid, lipopolysaccharide, hyperbaric hyperoxia, L-cysteine,
cyanide and ischemia/reperfusion injury.
