Melatonin improves ultraviolet B-induced oxidative damage and inflammatory conditions in cutaneous tissue of a diurnal Indian palm squirrel Funambulus pennanti.

BACKGROUND

Skin is exposed to various abiotic and biotic factors. Solar radiation, of which ultraviolet (UV) rays are a principle component, increases the free radical load, and the accumulation of reactive oxygen species (ROS) causes lipid peroxidation, DNA damage and apoptosis, and is also associated with inflammatory responses recruiting molecules [nuclear factor (NF)-κB, interleukin (IL)-6] that can potentially further aggravate the damaged milieu of the cells. One of the potent causes of skin cancers is exposure to UV rays. UV radiation generates a wide range of biological responses such as adaptive, inflammatory and immunological reactions in the skin.

OBJECTIVE

To examine the effects of pretreatment with melatonin on UVB (290-320 nm) radiation-mediated damage to the skin of a diurnal rodent Funambulus pennanti.

RESULTS

The UVB radiation (1·5 J cm(-2) for 30 min daily on the shaved abdominal area) for 4 days caused a significant increase in the lipid peroxidation products (thiobarbituric acid reactive substances, TBARS) and decreased the activity of the antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) of the skin. Pretreatment with melatonin (100 μg 100 g(-1) bodyweight subcutaneously) improved the damage induced by UVB radiation on the skin and might act via a receptor-independent mechanism. No significant effect of melatonin pretreatment was found on the expression pattern of MT1 (melatonin membrane receptor) and RORα (nuclear retinoic orphan receptor alpha), which suggests a receptor-independent action. However, NF-κB and inflammatory cytokine IL-6 levels were downregulated in the squirrels pretreated with melatonin before the UVB radiation.

CONCLUSION

UVB radiation induced oxidative stress in the skin culminating in an inflammatory response. The action of melatonin in protecting the skin from oxidative damage occurs in a receptor-independent manner by lowering the oxidative damage and inflammatory response. On the other hand, melatonin decreased the expression of NF-κB and the circulating proinflammatory cytokine IL-6, suggesting an anti-inflammatory action in protecting the skin from UVB radiation.