PL EN


Preferences help
enabled [disable] Abstract
Number of results
2007 | 67 | 1 | 63-70
Article title

Melatonin attenuates radiation-induced learning deficit and brain oxidative stress in mice

Selected contents from this journal
Title variants
Languages of publication
EN
Abstracts
EN
Oxidative stress has been implicated in cognitive impairment in both experimental animals and humans. This implication has led to the notion that antioxidant defence mechanisms in the brain are not sufficient to prevent oxidative damage, and that dietary intake of a variety of antioxidants might be beneficial for preserving brain function. The present study, therefore, aimed to investigate the protective effect of melatonin against radiation-induced impairment in the learning ability of mice. Twenty days oral administration of melatonin (0.1 mg/kg b.w.), followed by an acute exposure to gamma-radiation (6 Gy), inhibited the radiation-induced decline in learning ability. Biochemical estimation of brain protein carbonyls, malondialdehide (MDA) and reduced glutathione (GSH) in these mice indicated that radiation-induced augmentation of protein oxidation and lipid peroxidation had been significantly ameliorated in melatonin treated, irradiated mice. Radiation-induced deficit of glutathione was also normalized by melatonin administration, as there was no statistical difference from normal at P<0.001. Results indicate the antioxidative as well as neuroprotective properties of melatonin against the radiation. These findings support results showing melatonin as a free radical scavenger.
Publisher

Year
Volume
67
Issue
1
Pages
63-70
Physical description
Contributors
author
author
author
author
References
Document Type
ARTICLE
Publication order reference
Kailash Manda, National Institute of Radiological Sciences, Chiba-263-8555, Japan
Identifiers
YADDA identifier
bwmeta1.element.element-from-psjc-f615fc57-bbb4-35ea-90c0-d1474d24408c
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.