UVB irradiation severely induces systemic tissue injury by augmenting oxidative load in a tropical rodent: Efficacy of melatonin as an antioxidant

•The UVB radiation induced oxidative stress in the spleen tissue.•Increase in LPO and decreased antioxidative enzymes aggravated conditions.•Melatonin partially recovered the oxidative damages when administered prior to the radiation.•Apoptosis was suppressed by melatonin.•Melatonin pre-treatment was beneficial in partly restoring tissue homeostasis.

Tropical animals are regularly exposed to solar UV radiation. The generation and accumulation of free radicals as a result of UVB incidence causes tissue damage. In the present study we report that the irradiation of Funambulus pennanti by 1.5 J/cm2 of UVB caused significant oxidative damage to the spleen. The systemic immunity suffered collateral damage as depicted by results of total leukocyte count (TLC) while an increase in the thiobarbituric acid reactive substances (TBARS) and decline in the activities of enzymes superoxide dismutase (SOD), Glutathione peroxidase (GSH-Px) and Catalase (CAT) denoted oxidative tissue damage. Melatonin the indole-amine with known antioxidative properties when administered subcutaneously (s.c 100 μg/100 gm body weight), before the UVB irradiation recovered the damages caused by UVB radiation in the spleen. The action of melatonin was direct and might have involved its membrane receptor (MT1) as well as nuclear receptor (RORα) indicating the fact that the mode of action of melatonin in ameliorating UVB radiation induced free radical load may be receptor mediated. Our study hence reports for the first time that UVB radiation incurred oxidative damage to the spleen and suppressed the normal tissue functions. This UVB mitigated oxidative stress was recovered by the free radical scavenging and anti-apoptotic functions of melatonin when administered prior to UVB irradiation.