Melatonin-induced reduction in age-related accumulation of oxidative damage in mice

The ever-increasing understanding of oxygen radical-linked diseases, including the biological process of aging, has stimulated general interest in modulating these biological events. Melatonin has been reported to have antioxidant properties in addition to its known hormonal activities. However, reports on low-level chronic administration with its anti-aging influence are scanty. Hence, the present study was aimed to investigate the influence of low-dose chronic administration (0.10 mg/kg bodyweight/day for 3 months) of melatonin again stage-induced oxidative stress in mice tissues, namely brain, liver, spleen and kidney. Sixteen-month-old mice were supplemented with melatonin (0.10 mg/kg body weight/day) for three months and then autopsied (at the age of19 months) for the biochemical estimation of lipid peroxidation, reduced glutathione (GSH), glutathione disulphide (GSSG), glutathione peroxidase (GSH-Px) and serum phosphatase activity. Results indicate that age-induced augmentation (compared to 6–8-week-old mice)in the level of lipid peroxidation, GSSG and acid phosphatase is significantly (P < 0.001)ameliorated in melatonin-treated mice. Age-induced decline in the level of GSH, GSH-Px and alkaline phosphatase activity is inhibited significantly by the long-term administration of melatonin. The findings indicate that low-dose chronic administration of melatonin acts as a free radical scavenger and anti-aging agent. This revised version was published online in July 2006 with corrections to the Cover Date.