Holmberg M
National Institute of Radiation Protection, Stockholm, Sweden.
Mutat Res. 1990 Oct;232(2):267-72. doi: 10.1016/0027-5107(90)90133-o.
Quiescent human lymphocytes were X-irradiated and allowed to repair for various times at 37 degrees C before the cells were challenged with the DNA-repair inhibitor ara-C. The observed yield of chromosome exchange aberrations (dicentrics) was about twice the yield induced by X-rays alone, if ara-C was added immediately after irradiation. The yield as a function of the repair time between X-irradiation and ara-C treatment decreased with a half-life of 15-30 min and was almost down to the baseline yield for X-rays alone after 1 h. This shows that an exchange aberration can be formed from a short-lived DNA break. In contrast, previously published results from dose-split experiments demonstrate that the half-life of the interacting DNA breaks is of the order of several hours. A model is proposed which can account for the different estimates of the time course of the interactions involved in the process which leads to an exchange aberration.
将静止的人类淋巴细胞进行X射线照射，并在37摄氏度下让其修复不同时间，然后用DNA修复抑制剂阿糖胞苷（ara-C）处理这些细胞。如果在照射后立即添加ara-C，观察到的染色体交换畸变（双着丝粒）的产额约为仅由X射线诱导产额的两倍。作为X射线照射与ara-C处理之间修复时间的函数，产额以15 - 30分钟的半衰期下降，并且在1小时后几乎降至仅由X射线诱导的基线产额。这表明交换畸变可由短暂存在的DNA断裂形成。相比之下，先前发表的剂量分割实验结果表明，相互作用的DNA断裂的半衰期约为几个小时。提出了一个模型，该模型可以解释导致交换畸变的过程中所涉及相互作用时间进程的不同估计。
