The oxidative damages caused by ultraviolet radiation type C (UVC) to a tropical rodent Funambulus pennanti: role of melatonin.

Data suggests that UV radiation causes oxidative damage of the cells due to the release of inflammatory cytokines which in turn generates reactive oxygen species (ROS) that damages lipids, proteins and DNA. On the other hand, melatonin a potent antioxidant from the pineal gland under most of the conditions acts as a free radical scavenger. Our data suggests that melatonin pre-treatment (s.c. injections) significantly protected the diurnal squirrels from oxidative damages caused by UVC irradiation of 1528 mJ cm(-2) that induced suppression of delayed type hypersensitivity (DTH) responses. It also protected the rodents from UVC radiation induced increase in thiobarbituric acid reactive substances (TBARS) levels in spleen accompanied with a significant decrease in Superoxide Dismutase (SOD) activity indicating the occurrence of superoxide anion mediated damages following UVC exposure. Melatonin administration reduced the radiation induced oxidative stress in the spleen tissue as analyzed by reduced lipid damages and higher SOD activity. Under in vivo (100 μg/100g body wt.) and in vitro (250 pg/10(6) cells) conditions, melatonin pre-treatment prevented spleen tissues and splenocytes from radiation induced cell death. In conclusion we may suggest that melatonin could be one of the potent antioxidant and radio protector that may reduce UV radiation induced toxicity to the cells and hence may be clinically important.