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Oxidative toxicity in models of neurodegeneration: responses to melatonin.
Restor Neurol Neurosci. 1998 Jun; 12(2-3):135-42.RN

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 beta-amyloid toxicity, experimental models of Parkinsonism, excitotoxicity, nitric oxide toxicity, aminolevulinic acid, lipopolysaccharide, hyperbaric hyperoxia, L-cysteine, cyanide and ischemia/reperfusion injury.

Authors+Show Affiliations

Department of Cellular and Structural Biology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284-7762, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12671308

Citation

Reiter, R J., et al. "Oxidative Toxicity in Models of Neurodegeneration: Responses to Melatonin." Restorative Neurology and Neuroscience, vol. 12, no. 2-3, 1998, pp. 135-42.
Reiter RJ, Garcia JJ, Pie J. Oxidative toxicity in models of neurodegeneration: responses to melatonin. Restor Neurol Neurosci. 1998;12(2-3):135-42.
Reiter, R. J., Garcia, J. J., & Pie, J. (1998). Oxidative toxicity in models of neurodegeneration: responses to melatonin. Restorative Neurology and Neuroscience, 12(2-3), 135-42.
Reiter RJ, Garcia JJ, Pie J. Oxidative Toxicity in Models of Neurodegeneration: Responses to Melatonin. Restor Neurol Neurosci. 1998;12(2-3):135-42. PubMed PMID: 12671308.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative toxicity in models of neurodegeneration: responses to melatonin. AU - Reiter,R J, AU - Garcia,J J, AU - Pie,J, PY - 2003/4/3/pubmed PY - 2003/4/3/medline PY - 2003/4/3/entrez SP - 135 EP - 42 JF - Restorative neurology and neuroscience JO - Restor Neurol Neurosci VL - 12 IS - 2-3 N2 - 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 beta-amyloid toxicity, experimental models of Parkinsonism, excitotoxicity, nitric oxide toxicity, aminolevulinic acid, lipopolysaccharide, hyperbaric hyperoxia, L-cysteine, cyanide and ischemia/reperfusion injury. SN - 0922-6028 UR - https://www.unboundmedicine.com/medline/citation/12671308/Oxidative_toxicity_in_models_of_neurodegeneration:_responses_to_melatonin_ DB - PRIME DP - Unbound Medicine ER -
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