Abstract

Gamma radiation induces the generation of free radicals, leading to serious cellular damages in biological systems. Radioprotectors act as prophylactic agents that are administered to shield normal cells and tissues from the deleterious effects of radiation. Melatonin synergistically acts as an immune-stimulator and antioxidant. We investigated the possible radioprotective role of melatonin (100 mg/kg i.p.) against lethal-whole-body radiation- (10 Gy) induced sickness, body weight loss, and mortality in rats. Results of the present study suggest that exposure to lethal-whole-body radiation incurred mortality, body weight loss, and apoptosis and it also depleted the immunity and the antioxidant status of the rats. Our results show that melatonin pretreatment provides protection against radiation induced mortality, oxidative stress, and immune-suppression. The melatonin pretreated irradiated rats showed less change in body weight as compared to radiation only group. On the other hand, melatonin appeared to have another radioprotective role, suggesting that melatonin may reduce apoptosis through a caspase-3-mediated pathway by blocking caspase-3 activity.

Highlights

  • Ionizing radiation is commonly used in diagnostic, therapeutic, and industrial settings

  • Mortality occurring after whole-body radiation, in addition to damages to hematopoietic and other tissues that have not been checked, may be attributed to inhibition of the immune system; that is, irradiation causes immunosuppression leading to death of the rats [23]

  • Results obtained from our study indicated that treatment with melatonin (100 mg/kg) ameliorates the deleterious effects of 10 Gy irradiation by increasing the Total Antioxidant Capacity (TAC) level and antioxidant enzymes activity and decreasing nitric oxide (NO) and MDA levels

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Summary

Introduction

Ionizing radiation is commonly used in diagnostic, therapeutic, and industrial settings. Researches for new strategies to prevent radiation damage are in progress. Some of these efforts are based on prevention from oxidative stress, as it is the main factor responsible for radiation-induced damage [2]. Ionizing radiation interacts with biological systems to produce free radicals or reactive oxygen species (ROS), which attack various cellular components including DNA, proteins, and membrane lipids, leading to serious cellular damage [3]. To control the onset of ROS, cells have developed their own antioxidant defense system, which includes enzymatic and nonenzymatic components. The antioxidant enzymes, superoxide dismutase (SOD), the first line of defense against oxygen-derived free radicals, catalyse the dismutation of the superoxide anion (O2∙−) into hydrogen peroxide (H2O2). NO reacts rapidly with the superoxide anion (O2∙−) to form peroxynitrite (ONOO−), which in itself is cytotoxic and readily decomposes into the highly reactive and toxic hydroxyl radical (∙OH) and nitrogen

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