Ikushima T, Aritomi H, Morisita J
Biology Division, Kyoto University of Education, Japan.
Mutat Res. 1996 Nov 4;358(2):193-8. doi: 10.1016/s0027-5107(96)00120-0.
To verify the hypothesis that the induction of a novel, efficient repair mechanism for chromosomal DNA breaks may be involved in the radioadaptive response, the repair kinetics of DNA damage has been studied in cultured Chinese hamster V79 cells with single-cell gel electrophoresis. The cells were adapted by priming exposure with 5 cGy of gamma-rays and 4-h incubation at 37 degrees C. There were no indication of any difference in the initial yields of DNA double-strand breaks induced by challenging doses from non-adapted cells and from adapted cells. The rejoining of DNA double-strand breaks was monitored over 120 min after the adapted cells were challenged with 5 or 1.5 Gy, doses at the same level to those used in the cytogenetical adaptive response. The rate of DNA damage repair in adapted cells was higher than that in non-adapted cells, and the residual damage was less in adapted cells than in non-adapted cells. These results indicate that the radioadaptive response may result from the induction of a novel, efficient DNA repair mechanism which leads to less residual damage, but not from the induction of protective functions that reduce the initial DNA damage.
为验证诱导一种新的、高效的染色体DNA断裂修复机制可能与辐射适应性反应有关这一假说,采用单细胞凝胶电泳技术研究了培养的中国仓鼠V79细胞中DNA损伤的修复动力学。细胞经5 cGy γ射线预照射并在37℃孵育4小时进行适应性处理。未发现来自未适应性处理细胞和适应性处理细胞的激发剂量所诱导的DNA双链断裂初始产率有任何差异。在用5或1.5 Gy照射适应性处理细胞后120分钟内监测DNA双链断裂的重新连接情况,这两个剂量与细胞遗传学适应性反应中使用的剂量水平相同。适应性处理细胞中DNA损伤的修复速率高于未适应性处理细胞,且适应性处理细胞中的残留损伤少于未适应性处理细胞。这些结果表明,辐射适应性反应可能是由于诱导了一种新的、高效的DNA修复机制,从而导致残留损伤减少,而不是由于诱导了减少初始DNA损伤的保护功能。