Melatonin protects against membrane alterations affected by 'Artificial Light at Night' in a circadian-disrupted model of rat

Artificial Light at Night (ALAN) causes alteration in the redox status and membrane-bound transporters. Melatonin has pleiotropic effects on normal physiology and acts as a potential antioxidant. This study was undertaken to evaluate the effects of ALAN-induced alterations in the membrane transporters, oxidative stress biomarkers and to evaluate the protective effects of melatonin supplementation prior to exposure of light in a circadian-disrupted model of rat. Young male Wistar rats 250 +/- 20 g were randomly segregated into following groups; Group (I) control, Group (II) melatonin-treated group (10 mg/kg, orally), Group (III) ALAN (500 lux), Group (IV) ALAN with melatonin, for 10 days. Results show that melatonin is an effective mediator of membrane-bound transporters revealed by activation of Na+/K+-ATPase (NKA), plasma membrane Ca2+-ATPase (PMCA) and suppression of Na+/H+ exchanger (NHE) activity. Oxidative stress biomarkers such as total thiol (T-SH), sialic acid (SA), lipid hydroperoxides (LHs) and protein carbonylation (PC) are also restored to the normal level after supplementation of melatonin. These findings demonstrate the protective effect of melatonin on membrane-bound enzymes along with other oxidative stress biomarkers against light-mediated oxidative damage in erythrocyte membrane.