Role of Sodium Selenite in Ameliorating the Oxidative Stress of Gamma Radiation Exposure. | ||||
| The Egyptian Journal of Hospital Medicine | ||||
| Article 6, Volume 27, Issue 1, April 2007, Page 188-199 PDF (495.36 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/ejhm.2007.17721 | ||||
 View on SCiNiTO | ||||
| Author | ||||
| Hanafi N. | ||||
| Radiation Biology Department, National Centre for Radiation Research and Technology, Atomic Energy Authority, Cairo, Egypt | ||||
| Abstract | ||||
| Back ground: This work aims to investigate the role of Sodium Selenite (NaSeO3) in ameliorating the oxidative stress of gamma radiation exposure. The relation between the antioxidant status, the histopahological changes and the immunohistological expression of p53 was evaluated. Materials and methods: Adult male Swiss albino mice weighing 25-30g were used in this work. Lipid peroxidation and GSH activity levels were estimated in liver and intestinal tissues. Histopathological observations in addition to the immunohistological expression of p53 were also assayed. Experimental animals treated daily with 0.7μg /ml /kg body weight of NaSeO3 for two weeks. Some animals were exposed to 5Gy γ-irradiation and others exposed to 5Gy γ-irradiation and treated with NaSeO3. Results: Due to ROS production, 5Gy γ-radiation induced a highly significant increase in lipid peroxidation and a significant decrease in GSH activity level in liver and intestine tissues. NaSeO3 supplementation revealed NS change in lipid peroxidation of liver and intestine tissues, while GSH levels recorded a significant increase as compared to the control group. Combined treatments with NaSeO3 supplementation and 5Gy γ-radiation revealed a significant amelioration in lipid peroxidation and GSH levels as compared to the irradiated groups. The histopathological observations went parallel to the biochemical records, while p53 expression was treatments and organs dependent. Conclusion: NaSeO3 supplementation recorded ameliorated effects against cellular damage caused by radiation oxidative stress. | ||||
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