周平坤,隋建丽,杨素红.低剂量辐射对细胞 DNA 修复兴奋效应[J].中华放射医学与防护杂志,1997,17(3):155-158.Zhou Pingkun,Sui Jianli and Yang Suhong.Hormetic effect of low dose radiation on cellular DNA repair[J].Chin J Radiol Med Prot,1997,17(3):155-158
低剂量辐射对细胞 DNA 修复兴奋效应
Hormetic effect of low dose radiation on cellular DNA repair
投稿时间:1996-12-24  修订日期:1997-01-19
DOI:
中文关键词:  低剂量辐射  兴奋效应  DNA修复  基因突变  DNA结合蛋白
英文关键词:Low dose radiation  Hormesis  DNA repair  Gene mutation  DNA bound protein
基金项目:国际原子能机构协作项目
作者单位
周平坤 100850 北京放射医学研究所 
隋建丽 100850 北京放射医学研究所 
杨素红 100850 北京放射医学研究所 
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中文摘要:
      目的 研究低剂量电离辐射对细胞DNA双链断裂修复及基因突变适应性的兴奋效应, 并探测辐射诱导DNA结合蛋白。方法 实验用小鼠SR-1细胞, 60Coγ射线照射;用6-巯基鸟嘌呤筛选hprt基因突变克隆;脉冲电场凝胶电泳检测DNA双链断裂;Southwestern印迹杂交探测DNA结合蛋白。结果 细胞受1cGy预照射后18小时、24小时显着降低3Gy照射诱发的hprt基因突变频率。预先受单次1cGy照射刺激, 或每天照射一次, 连续10天, 显着增加3Gy照射细胞的DNA双链断裂修复效率。1cGy照射细胞后16小时提取的核蛋白中, 探测到损伤DNA结合蛋白的诱导合成。结论 低剂量辐射通过调节某些细胞辐射反应调控基因表达, 诱导合成DNA修复反应蛋白, 增强细胞DNA修复能力, 减少基因突变的发生, 提高细胞维持遗传稳定性机能。
英文摘要:
      Objective To study radio adaptive response of mutagenesis and repair of DNA double-strand breaks (DSB) in mammalian cells induced by low dose γ-rays, and to detect low dose radiation-induced proteins. Methods Mouse SR-1 Cells were irradiated with 60Coγ-rays.Mutations at hprt locus were assayed by 6-thioguanine selective culture method.DNA DSBs were measured by pulsed field gel electrophoresis.Southwestern blot hybridization was employed to detect radiation induced proteins.Results Preexposure of SR-1 cells to 1 cGy at 18h and 24h before challenging dose significantly decreased the frequency of hprt gene mutations induced by following 3 Gy challenge.Preexposure of SR-1 cells to single 1 cGy as well as to 1 cGy per day for 10 successive days significantly increased the cellular capacity of rejoining 3 Gy induced DNA DSBs.A newly synthesized protein bound to damaged DNA was detected at 16h after 1 cGy exposure. Conclusion Proteins possibly involved in the process of DNA repair were induced by low dose radiation upregulating the expression of some specific genes.Such induced proteins lead to increase of cellular DNA repair capacity as well as radio adaptive response of cells to gene mutations.
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