ABSTRACT
INTRODUCTION: Oxidative stress is a common factor in cataract. Considering the antioxidant properties of hesperidin as a flavanone glycoside from the flavonoid family with radioprotective effect, this study aimed to determine the protective effect of this flavanone glycoside on reducing oxidative stress in the eye lens tissue of mature rats caused by gamma irradiation. MATERIALS AND METHODS: A total of 48 adult rats were randomly divided into six groups, namely, control, Dimethyl sulfoxide (DMSO), hesperidin, radiation, radiation + DMSO, and radiation + hesperidin. 15 Gy irradiation was carried out using Cobalt-60 teletherapy instrument with a source-to-surface distance of 80 cm at a dose rate of 98.5 cGy/min. 2 days following irradiation, we removed the rats' lenses and analyzed them to determine the effects of hesperidin. RESULTS: The comparison of control and intervention groups after irradiation showed that malondialdehyde (MDA) level in the lens tissue was significantly higher in the irradiation groups than the control group. Furthermore, a significant difference between radiation and radiation + hesperidin groups were observed. The level of glutathione (GSH) in the lens tissue was significantly lower in the irradiation groups compared to the control group. Nonetheless, significant elevation of GSH in the radiation + hesperidin group compared to radiation group was seen. CONCLUSIONS: Radiation exposure reduced GSH and enhanced MDA levels in the lens tissue. However, GSH and MDA levels were modulated after hesperidin consumption. These results show the antioxidative properties of hesperidin in the lens and demonstrated that radiation complications such as cataract can be reduced by hesperidin through reducing oxidative stress.
ABSTRACT
Reactive oxygen species (ROS) are generated by ionizing radiation, and one of the organs commonly affected by ROS is the lung. Radiation-induced lung injury including pneumonia and lung fibrosis is a dose-limiting factor in radiotherapy (RT) of patients with thorax irradiation. Administration of antioxidants has been proved to protect against ROS. The present study was aimed to assess the protective effect of hesperidin (HES) against radiation-induced lung injury of male rats. Fifty rats were divided into three groups. G1: Received no HES and radiation (sham). G2: Underwent γ-irradiation to the thorax. G3: Received HES and underwent γ-irradiation. The rats were exposed to a single dose of 18 Gy using cobalt-60 unit and were administered HES (100 mg/kg) for 7 days before irradiation. Histopathological analysis was performed 24 h and 8 weeks after RT. Histopathological results in 24 h showed radiation-induced inflammation and presence of more inflammatory cells as compared to G1 (P < 0.05). Administration of HES significantly decreased such an effect when compared to G2 (P < 0.05). Histopathological evaluation in 8 weeks showed a significant increase in mast cells, inflammation, inflammatory cells, alveolar thickness, vascular thickness, pulmonary edema, and fibrosis in G2 when compared to G1 (P < 0.05). HES significantly decreased inflammatory response, fibrosis, and mast cells when compared to G2 (P < 0.05). Administration of HES resulted in decreased radiation pneumonitis and radiation fibrosis in the lung tissue. Thus, the present study showed HES to be an efficient radioprotector against radiation-induced damage in the lung of tissue rats.
ABSTRACT
This study was carried out to evaluate radioprotective effects of hesperidin (HES) administration before the irradiation on the cardiac oxidative stress and histopathological changes in an experimental rat model. The cardiovascular complications of radiation exposure cause morbidity and mortality in patients who received radiotherapy. HES, an antioxidant flavonoid found in citrus fruits, suggests the protection against the tissue damage. Fifty-eight rats were divided into four groups: Group 1 received phosphate buffered saline (PBS) and sham radiation; Group 2, HES and sham radiation; Group 3, PBS and radiation; and Group 4, HES and radiation. The rats were exposed to single dose of 18 Gy of 6 MV X-ray. One hundred milligrams per kilogram doses of HES was administered for 7 days before irradiation. The estimation of superoxide dismutase (SOD), malondialdehyde (MDA), and histopathological analyses was performed at 24 h and 8 weeks after radiation exposure. The irradiation of chest area resulted in an elevated MDA level and decreased SOD activity. Moreover, long-term pathological lesions of radiation were inflammation, fibrosis, the increased number of mast cells and macrophages, and development of plaque, vascular leakage, myocardial degeneration, and myocyte necrosis. Although the administration of HES decreases inflammation, fibrosis, mast cell and macrophage numbers, and myocyte necrosis, it did not result in reduced thrombus, myocardium degeneration, and vascular leakage. In conclusion, these results suggest that HES can perform a radioprotection action. The protective effect of HES may be attributable to its immunomodulatory effects and free radical-scavenging properties.
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BACKGROUND: Radiotherapy of the thorax often causes lung inflammation leading to fibrosis. OBJECTIVES: The aim of this study was to investigate whether the use of glycyrrhizic acid (GLA) could improve the development of lung fibrosis in irradiated animals. MATERIALS AND METHODS: Wistar rats were divided into four groups. Group A rats received thoracic irradiation. Rats in group B received GLA and irradiation. Group C received GLA and no irradiation. Group D received no GLA and irradiation. GLA was administered at a dose of 4 mg/kg body weight using an intraperitoneal injection one hour before thoracic irradiation. Radiation therapy was delivered on a Cobalt-60 unit using a single fraction of 16 Gy. The animals were sacrificed at 32 weeks following thoracic irradiation. The lungs were dissected and blind histopathological evaluation was performed. RESULTS: Histopathologically, a decrease (statistically not significant) in the thickening of alveolar or bronchial wall, formation of fibrous bands, and superimposed collagen were noted in the animals in group B as compared to the animals in group A. CONCLUSION: In this experimental study, administration of GLA one hour before thoracic irradiation may be a protective agent against radiation-induced fibrosis in animals and this model could be used in future studies.
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OBJECTIVE: Free radicals generated by ionizing radiation attack various cellular components such as lipids. The lung is a very radiosensitive organ and its damage is a doselimiting factor in radiotherapy treatments. Melatonin (MLT), the major product of the pineal gland acts as a radioprotective agent. This study aims to investigate the radioprotective effects of MLT on malondialdehyde (MDA) levels and histopathological changes in irradiated lungs. MATERIALS AND METHODS: In this experimental study, a total of 62 rats were divided into five groups. Group 1 received no MLT and radiation (unT), group 2 received oral MLT (oM), group 3 received oral MLT and their thoracic areas were irradiated with 18 Gy (oMR), group 4 received MLT by intraperitoneal (i.p.) injection and their thoracic areas were irradiated with 18 Gy (ipM-R), group 5 received only 18 Gy radiation in the thoracic area (R). Following radiotherapy, half of the animals in each group were sacrificed at 48 hours for evaluation of lipid peroxidation and early phase lung injuries. Other animals were sacrificed in the eighth week of the experiment for evaluation of the presence of late phase radiation induced lung injuries. RESULTS: Pre-treatment of rats with either i.p injection (p<0.05) and oral administration of MLT (p<0.001) significantly reduced MDA levels in red blood cell (RBC) samples compared to the R group. Furthermore, i.p. injection of MLT decreased MDA levels in plasma and tissue (p<0.05). In the early phase of lung injury, both administration of MLT significantly increased lymphocyte (p<0.05) and macrophage frequency (p<0.001). MLT reduced the lung injury index in the lungs compared to the R group (p<0.05). CONCLUSION: The result of this study confirms the radioprotective effect of MLT on lipid peroxidation, and in both early and late phases of radiation induced lung injuries in an animal model.
ABSTRACT
AIM: We aimed to determine the changes in TNF-α expression and Malondialdehyde (MDA) level in a short time after irradiation. Furthermore, we evaluated the effect of melatonin on the modulation of TNF-α gene expression. BACKGROUND: The radio-sensitivity of the cervical spinal cord limits the dose of radiation which can be delivered to tumors in the neck region. There is increasing evidence that TNF-α has a role in the development of the acute phase of spinal cord injury. MATERIALS/METHODS: Four groups of rats were investigated. Group 1 (vehicle treatment) served as the control. Group 2 (radiation) was treated with the vehicle, and 30 min later, the rats were exposed to radiation. Group 3 (radiation + melatonin) was given an oral administration of melatonin (100 mg/kg body weight) and 30 min later exposed to radiation in the same manner as in group 2. Group 4 (melatonin-only) was also given an oral administration of melatonin (100 mg/kg body weight). 5 mg/kg of melatonin was administered daily to rats in groups 3 and 4, and the vehicle was administered daily to rats in groups 1 and 2. RESULTS: Three weeks after irradiation, TNF-α gene up-regulated almost 5 fold in the irradiated group compared to the normal group. TNF-α gene expression in the melatonin pretreatment group, compared to the radiation group, was significantly down-regulated 3 weeks after irradiation (p < 0.05). MDA levels increased after irradiation and then significantly decreased under melatonin treatment. CONCLUSION: We suggest that inhibition of TNF-α expression by oral administration of melatonin may be a therapeutic option for preventing radiation-induced spinal cord injury.
