Bryant P E
Br J Cancer Suppl. 1984;6:61-5.
Evidence supports the view that double-strand breaks (dsb) in the DNA of X-irradiated mammalian cells are the lesions leading to chromosome aberrations and eventual cell death. The detailed kinetics of repair of dsb in Ehrlich ascites tumour cells over long repair intervals have therefore been studied and compared under conditions simulating procedures known to cause large changes in cell survival. These conditions are: holding cells in stationary phase for 7 h after X-irradiation, transference of cells to fresh growth medium immediately after X-irradiation, and treatment with the DNA synthesis inhibitor 9-beta-D-arabinofuranosyladenine (ara A) for 30 min before, during and for 7 h after X-irradiation. These conditions have also been investigated for their effects on the frequencies of chromosome abnormalities (anaphase bridges and fragments). It is shown that conditions leading to both an inhibition of dsb repair (in the presence of ara A) as well as an acceleration of dsb repair (by fresh growth medium) lead to higher frequencies of chromosome abnormalities as compared to those for cells under stationary conditions for 7 h after irradiation. Holding dsb open for long periods with ara A may maximize the probability of formation of aberrations, however the data for fresh medium treatment show that it is not merely the rate at which dsb repair which determines the aberration frequency, and indicate the presence of other biochemical mechanisms in the cell which determine the frequency of conversion of dsb into chromosome aberrations.
有证据支持这样一种观点，即经X射线照射的哺乳动物细胞DNA中的双链断裂（dsb）是导致染色体畸变并最终导致细胞死亡的损伤。因此，在模拟已知会导致细胞存活率大幅变化的程序的条件下，研究并比较了艾氏腹水瘤细胞中dsb在长时间修复间隔内的详细修复动力学。这些条件包括：X射线照射后将细胞置于静止期7小时；X射线照射后立即将细胞转移至新鲜生长培养基；在X射线照射前、照射期间以及照射后7小时用DNA合成抑制剂9-β-D-阿拉伯呋喃糖基腺嘌呤（ara A）处理30分钟。还研究了这些条件对染色体异常（后期桥和片段）频率的影响。结果表明，与照射后在静止条件下培养7小时的细胞相比，导致dsb修复受到抑制（在ara A存在的情况下）以及dsb修复加速（通过新鲜生长培养基）的条件会导致更高频率的染色体异常。用ara A长时间使dsb保持开放状态可能会使畸变形成的概率最大化，然而新鲜培养基处理的数据表明，不仅仅是dsb修复的速率决定了畸变频率，这表明细胞中存在其他生化机制决定dsb转化为染色体畸变的频率。
