中文摘要：

目的 通过观察γ射线照射后IRM-2辐射抗性小鼠DNA链的断裂及修复,探讨IRM-2小鼠辐射抗性产生的可能机理.方法 采用脉冲场凝胶电泳法,测定不同剂量γ射线诱发IRM-2小鼠及其亲本ICR/JCL和615小鼠脾细胞DNA单、双链断裂及照射后不同时间DNA链断裂的修复动力学.结果 对照组IRM-2小鼠本底DNA损伤较低,即ssb和dsb的数目低于未照射的亲本ICR 和615小鼠（P＜0.01）.不同剂量（1、2、4 和 8 Gy）照射后,IRM-2小鼠ssb 和dsb的数量均明显低于经相同剂量照射的亲本ICR 和 615小鼠（P＜0.05和P＜0.01）.在较低剂量2 Gy 时,IRM-2 小鼠与亲本小鼠相比,dsb和ssb修复无统计学差异;当分别接受4、8 Gy大剂量照射后,IRM-2 小鼠表现出较高的修复效率,即IRM-2 小鼠0.5h 和1h dsb、ssb修复速率比亲本小鼠快（P＜0.05和P＜0.01）,而且修复后剩余的损伤远低于亲本小鼠.结论 电离辐射后IRM-2小鼠DNA链断裂量较低,DNA链断裂的修复速率比亲本小鼠快,因此能及时快速地抵抗辐射造成的损伤,具有较强的辐射抗性.

英文摘要：

Objective To investigate the radioresistance mechanism of IRM - 2 mice through measuring DNA single - strand break （SSB） and double - strands break （DSB） as well as their repair. Methods Pulsed - field gel electrophoresis was used to measure DSB and SSB in IRM - 2 mice and their parental mice ICR/JCL and 615 mice after exposure to different doses of γ - ray at different postirradiation time. Results The initial DNA damages , ie the quantities of DSB and SSB in unirradiation IRM - 2 mice were less serious than that of their parental mice ICR/JCL and 615 mice（ P 〈0.01 ）. The percentage of DSB and SSB in IRM -2 mice was significantly lower than that of ICR./JCL and 615 mice after exposure to various doses of γ- ray（P 〈0.01 and P 〈0.05）. There were not statistic differences in DSB and SSB repair between IRM -2 mice and their parental mice after exposure to 2Gy radiation. The DNA damage repair rate induced by 4Gy and 8Gy radiation in IRM - 2 mice was rapid, ie the repair rate of SSB and DSB after 0.5b and lh postirradiation in IRM -2 mice was higher than that of their parental mice （P 〈0.01 and P 〈0.05 ）. And remaining damages after repair in IRM -2 mice were lower than that of ICR/JCL and 615 mice. Conclusion The DNA damages in IRM - 2 mice were lower than that of their parental mice after exposure to ionizing radiation. Moreover, the repair rate of SSB and DSB was higher than that of their parental mice, which perhaps were the radioresistance causes of IRM - 2 mice. Therefore IRM - 2 mice are naturally resistant to DNA damages induced by ionizing radiation.