Rashed Engy R, El-Daly Menna A, Abd-Elhalim Sawsan A, El-Ghazaly Mona A
Department of Drug Radiation Research, National Center for Radiation Research and Technology, Atomic Energy Authority, PO Box 29, Nasr City, Cairo, Egypt.
Department of Biochemistry, Faculty of Science, Helwan University, Cairo, Egypt.
Radiat Environ Biophys. 2016 Nov;55(4):451-460. doi: 10.1007/s00411-016-0665-2. Epub 2016 Aug 26.
The current study aimed to investigate the effect of different low doses of gamma irradiation on hyperglycemia-induced brain injury. The aim was further extended to investigate the sub-chronic effect of low dose radiation on the neuronal damage induced by diabetes. To induce diabetes, male albino rats were injected with dexamethasone (10 mg/kg/day, for 9 successive days, subcutaneously). Different diabetic groups were irradiated with 0.1, 0.25 and 0.5 Gy. The effect of low dose gamma irradiation on the hyperglycemia-induced brain damage based was analyzed at two levels: oxidative stress and apoptosis. The brain contents of glutathione, malondialdhyde and total nitrate/nitrite were measured to assess the oxidative stress. In order to evaluate the extent of the apoptotic changes in brain, tissue caspase-3 expression was detected using immunohistochemistry and the degree of DNA fragmentation was estimated. Moreover, brain tissues were examined using light microscopy to evaluate the histological changes in different groups and serum lactate dehydrogenase activity was determined as an indicator for the brain tissue damage. Results indicated that exposure to 0.5 Gy ameliorated the hyperglycemia and subsequently inhibited oxidative stress and apoptosis. Radiation exposure at this dose level also increased the survival rate of diabetic animals.
本研究旨在探讨不同低剂量γ射线辐射对高血糖诱导的脑损伤的影响。该目标进一步扩展至研究低剂量辐射对糖尿病诱导的神经元损伤的亚慢性影响。为诱导糖尿病,给雄性白化大鼠皮下注射地塞米松(10毫克/千克/天,连续9天)。不同糖尿病组分别接受0.1、0.25和0.5戈瑞的辐射。基于氧化应激和细胞凋亡两个层面分析低剂量γ射线辐射对高血糖诱导的脑损伤的影响。检测谷胱甘肽、丙二醛和总硝酸盐/亚硝酸盐的脑含量以评估氧化应激。为评估脑内凋亡变化程度,采用免疫组织化学检测组织半胱天冬酶-3表达并估算DNA片段化程度。此外,使用光学显微镜检查脑组织以评估不同组的组织学变化,并测定血清乳酸脱氢酶活性作为脑组织损伤的指标。结果表明,暴露于0.5戈瑞可改善高血糖,随后抑制氧化应激和细胞凋亡。此剂量水平的辐射暴露还提高了糖尿病动物的存活率。