ABSTRACT
Ocular morbidity is widely observed when radiotherapy includes the orbit. Oxidative stress generated by irradiation is responsible for this complication. In different studies, it has been shown that melatonin has antioxidative properties and a radioprotective role. The aim of this study was to evaluate the antioxidant role of melatonin against radiation-induced oxidative injury in rats' lenses after total cranial irradiation. Thirty-six adult female Sprague-Dawley rats were divided into six groups. Group I was the control group, group II only received total cranial gamma irradiation of 5 Gy, group III was exposed as the second group but at the dose of 8 Gy, group IV received 30 mg/kg melatonin 30 minutes prior to radiation plus total cranial irradiation of 5 Gy plus 5 mg/kg melatonin daily through intraperitoneal injection for ten days after irradiation, group V was treated similar to the fourth group, i. e. received irradiation plus melatonin, but at the dose of 8 Gy, and group VI only received melatonin [30 mg/kg on the first day and 5 mg/kg on the following days]. Ten days after irradiation, all rats were sacrificed and their eyes were enucleated to measure the biochemical parameters i. e. malondialdehyde [MDA] and glutathione [GSH]. The levels of MDA in rat lenses increased and the levels of glutathione in lenses decreased after gamma ray irradiation but these parameters were still within normal limits in rats that received melatonin. It could be concluded that melatonin is useful in preventing radiation-induced oxidative injury due to its antioxidative and free radical scavenging properties
ABSTRACT
Radiation myelopathy [RM] is known as a serious complication of head and neck radiation therapy. Furthermore, the radioprotective roles of melatonin have been investigated on different tissues. The aim of this study was to assess the radio protective effects of melatonin on biochemical, histopathological and clinical manifestations of RM in the rat cervical spinal cord. Four groups of rats were investigated as follows: The control group was treated with vehicle. The second group [melatonin only] was intraperitoneally injected with 100 mg/kg melatonin. The third group's [radiation] cervical spinal cord area was irradiated with 22 Gy cobalt-60 gamma-rays. The fourth group [melatonin plus irradiation] received 100 mg/kg melatonin intraperitoneally, and after 30 minutes their spinal cord area was irradiated with 22 Gy gamma radiation. Five animals from each group were randomly selected. 72 hours, 8 and 22 weeks after irradiation for analysis of malondialdehyde [MDA] and glutathione [GSH] levels, and underwent histopathological studies. The MDA levels in the irradiation group were significantly higher than in the control group [p < 0.001]. Furthermore, the GSH levels in this group were significantly lower than that of those in the control group [p < 0.001]. Administration of melatonin markedly reduced MDA [p < 0.001] and increased GSH [p < 0.05] levels in this group. Demyelination and clinical signs of myelopathy were decreased in the melatonin plus irradiation group in comparison to the irradiated group. Our study confirms the radioprotective effects of melatonin at early stages of biochemical, as well as late histological and clinical changes in the spinal cord