Abstract

Photoperiod refers to the relative duration of light and dark that an animal experiences over the course of a 24 h period. Light is the principal stimulus that causes profound physiological and behavioural changes in all living organism. By manipulating photoperiod, melatonin production changes and its secretion drives enduring changes in many physiological systems of our body. Taking into consideration that light can affect pineal function and melatonin can be used as reactive oxygen species scavenger, act as a potent antioxidant and immunomodulator in mammals, the present experiment was designed and conducted to explore the consequences of constant light exposure on oxidative stress and antioxidant status on kidney and spleen of rat. 16 young adult female rats were randomly divided into 3 groups. The 4 rats of first group were employed as Control. These animals were kept under a 12 h light (600 lux, 60 days)/12 h dark cycle. The 8 rats of second group were maintained under constant light condition (600 lux, 60 days). After 60 days of constant light exposure second group of rats were randomly divided into two. One of these group of rats were designated as constant light exposed rats (LL) and another group of rats exposed to constant light is treated with melatonin (LL+MEL) for 21 days. The 4 rats of third group were only supplemented melatonin (MEL). The results showed that constant light exposure (60 days, 600 lux) resulted in an increased lipid peroxidation rate in kidney and spleen tissue and could effectively disturb the immune cells function through excessive generation of free radicals and decreased antioxidant enzymes activity (superoxide dismutase, catalase, glutathione peroxidase) through physiological or functional pinealectomy. Exogenous melatonin administration (200 µg/100 g body weight/day) suppressed the constant light induced oxidative stress and increase the activity of antioxidant enzymes in kidney and spleen of rat. Hence, melatonin has a nephroprotective and immunoprotective effects following photoperiodic stress induced cellular damages in female rat model.

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