Zhou P K, Liu X Y, Sun W Z, Zhang Y P, Wei K
Department of Biochemistry, Institute of Radiation Medicine, Beijing, PRC.
Mutagenesis. 1993 Mar;8(2):109-11. doi: 10.1093/mutage/8.2.109.
The effect of pre-exposure of cultured mouse SR-1 cells to a low dose of gamma-rays on the induction of mutations at the hprt locus by subsequent high dose radiation or bleomycin was studied. When cells were pre-exposed to 0.01 Gy gamma-rays, the induction of mutations by a 3 Gy gamma-ray dose given 18 or 24 h later was significantly reduced as compared with those which did not receive the low dose pre-exposure. When cells were challenged with 5 or 10 micrograms/ml bleomycin for 12 h, which can produce double-strand breaks in DNA, instead of 3 Gy gamma-rays, a similar mutagenetic adaptive response was observed. We conclude that this resistance to radiation- or bleomycin-induced mutation is attributed to the induction of a DNA double-strand break repair mechanism.
研究了将培养的小鼠SR-1细胞预先暴露于低剂量γ射线对随后高剂量辐射或博来霉素诱导hprt基因座突变的影响。当细胞预先暴露于0.01 Gy γ射线时,与未接受低剂量预暴露的细胞相比,在18或24小时后给予3 Gy γ射线剂量所诱导的突变显著减少。当用5或10微克/毫升博来霉素处理细胞12小时(其可在DNA中产生双链断裂)来替代3 Gy γ射线时,观察到了类似的诱变适应性反应。我们得出结论,这种对辐射或博来霉素诱导突变的抗性归因于DNA双链断裂修复机制的诱导。