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Melatonin as a Pharmacological Agent against Neuronal Loss in Experimental Models of Huntington's Disease, Alzheimer's Disease and Parkinsonism
Author(s) -
REITER RUSSEL J.,
CABRERA JAVIER,
SAINZ ROSA M.,
MAYO JUAN CARLOS,
MANCHESTER LUCIEN C.,
TAN DUNXIAN
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb08028.x
Subject(s) - melatonin , neuroprotection , glutathione peroxidase , superoxide dismutase , chemistry , antioxidant , pharmacology , glutathione reductase , oxidative stress , nitric oxide , free radical theory of aging , glutathione , biochemistry , neuroscience , medicine , biology , enzyme , organic chemistry
This review summarizes the experimental findings related to the neuroprotective role of melatonin. In particular, it focuses on research directed at models of Huntington's disease, Alzheimer's disease and Parkinsonism. Melatonin has been shown to be highly effective in reducing oxidative damage in the central nervous system; this efficacy derives from its ability to directly scavenge a number of free radicals and to function as an indirect antioxidant. In particular, melatonin detoxifies the highly toxic hydroxyl radical as well as the peroxyl radical, peroxynitrite anion, nitric oxide, and singlet oxygen, all of which can damage macromolecules in brain cells. Additionally, melatonin stimulates a variety of antioxidative enzymes including superoxide dismutase, glutathione peroxidase and glutathione reductase. One additional advantage melatonin has in reducing oxidative damage in the central nervous system is the ease with which to crosses the blood‐brain barrier. This combination of actions makes melatonin a highly effective pharmacological agent against free radical damage. The role of physiological levels of melatonin in forestalling oxidative damage in the brain is currently being tested.