Blöcher D, Pohlit W
Int J Radiat Biol Relat Stud Phys Chem Med. 1982 Sep;42(3):329-38. doi: 10.1080/09553008214551241.
The induction and repair of DNA double strand breaks (dsb) in early stationary Ehrlich ascites tumour cells by X-rays was determined using an improved sedimentation technique in neutral sucrose gradients. The disappearance of dsb was followed during post-irradiation incubation of the cells and was interpreted as dsb repair. Kinetics were approximated by exponential functions with time constants of t37 = 3.0 +/- 0.7 hours ('conditioned' medium) and t37 = 2.0 +/- 0.5 hours (growth medium). Maximal repair was reached after 24 hours and the relationship of the remaining breaks with dose was interpreted on the basis of a recombination repair model. Using these dsb data and on the assumption of one dsb being a lethal event, cell survival curves were calculated for different repair times and compared with experimental curves. It was shown that cell survival curves can be interpreted on the basis of one unrepaired dsb being a lethal event, when dsb repair continues for about 11 hours after plating the cells on nutrient agar.
采用改进的中性蔗糖梯度沉降技术，测定了X射线对早期静止期艾氏腹水瘤细胞中DNA双链断裂（dsb）的诱导和修复情况。在细胞照射后孵育期间跟踪dsb的消失情况，并将其解释为dsb修复。动力学可用指数函数近似，在“条件”培养基中时间常数t37 = 3.0 +/- 0.7小时，在生长培养基中t37 = 2.0 +/- 0.5小时。24小时后达到最大修复，基于重组修复模型解释了剩余断裂与剂量的关系。利用这些dsb数据，并假设一个dsb是致死事件，计算了不同修复时间的细胞存活曲线，并与实验曲线进行比较。结果表明，当细胞接种到营养琼脂上后dsb修复持续约11小时时，细胞存活曲线可以基于一个未修复的dsb是致死事件来解释。
