Schneiderman M H, Schneiderman G S, Mühlmann-Díaz M C, Bedford J S
J. Bruce Henriksen, M.D. Cancer Research Laboratories, University of Nebraska Medical Center, Omaha 68198-1045, USA.
Radiat Res. 1996 Jan;145(1):17-23.
Cell progression into mitosis and chromatid aberration frequencies were compared in two Chinese hamster ovary (CHO) cell lines after incorporation of 125IdUrd. Asynchronous, exponentially growing populations of CHO K1 and the DNA repair-deficient, radiation-sensitive CHO irs-20 cells were compared after a 10-min exposure to 14.8 kBq/ml 125IdUrd. Essentially no differences were seen for either end point between the cells of the two cell lines. As the cells in S phase at the time of labeling entered the mitotic cell selection window, the number of mitotic cells of each cell line declined to approximately 60% of the respective unlabeled control. Chromosome analysis of the mitotically selected cells indicated an 125I decay-dependent increase in the number of chromatid aberrations in cells of both cell lines. The appearance of aberrations together with the known rates of production and rejoining of DNA double-strand breaks show that cells are able to progress through G2 phase and into mitosis in the presence of such breaks. The data suggest that DNA damage may be necessary, but is not sufficient to cause a radiation-induced blockade of cell progression through G2 phase.
在掺入125I脱氧尿苷后,比较了两种中国仓鼠卵巢(CHO)细胞系中细胞进入有丝分裂的进程和染色单体畸变频率。将处于指数生长期的CHO K1细胞和DNA修复缺陷、对辐射敏感的CHO irs - 20细胞的非同步群体在14.8 kBq/ml 125I脱氧尿苷中暴露10分钟后进行比较。在这两个细胞系的细胞之间,在任何一个终点上基本上都没有观察到差异。当标记时处于S期的细胞进入有丝分裂细胞选择窗口时,每个细胞系的有丝分裂细胞数量下降到各自未标记对照的约60%。对有丝分裂选择的细胞进行染色体分析表明,两个细胞系的细胞中染色单体畸变的数量都有依赖于125I衰变的增加。畸变的出现以及已知的DNA双链断裂产生和重新连接的速率表明,细胞能够在存在此类断裂的情况下通过G2期并进入有丝分裂。数据表明,DNA损伤可能是必要的,但不足以导致辐射诱导的细胞通过G2期的进程受阻。