Leeper D B, Hagemann R F
Biophys J. 1973 Feb;13(2):179-85. doi: 10.1016/S0006-3495(73)85978-8.
The recovery from radiation-induced mitotic delay in asynchronous sarcoma-180 (S-180) ascites tumor cells has been analyzed in a manner analogous to the repair of sublethal damage. 200-R increments were separated by various fraction intervals (not exceeding the time necessary for mitosis to return to control levels) for total exposures up to 1600 R. The accumulated mitotic delay after the last exposure increment, in percent of an equivalent single exposure, decreased exponentially with overall treatment time in a bimodal fashion. An initial repair process displayed a half time of 2.3 h of overall elapsed time and was followed by a slower process with a half time of 15.1 h. Such a bimodal recovery provides an explanation of why fractionation intervals long with respect to the amitotic period resulting from a single 200 R exposure enhance mitotic delay over that of equivalent single exposures, while shorter fractionation intervals diminish it. It also predicts that mitotic delay vs. dose curves should bend toward the abscissa as the exposure time is increased with large single exposures and large fractionated exposures given over short fraction intervals.
已采用类似于亚致死损伤修复的方式,分析了异步肉瘤 - 180(S - 180)腹水肿瘤细胞从辐射诱导的有丝分裂延迟中的恢复情况。对于高达1600 R的总照射量,以各种分次间隔(不超过有丝分裂恢复到对照水平所需的时间)进行200 R的增量照射。最后一次照射增量后的累积有丝分裂延迟,以等效单次照射的百分比表示,随着总体治疗时间呈双峰方式指数下降。初始修复过程的半衰期为总经过时间的2.3小时,随后是一个较慢的过程,半衰期为15.1小时。这种双峰恢复解释了为什么相对于单次200 R照射产生的无丝分裂期而言较长的分次间隔会比等效单次照射增强有丝分裂延迟,而较短的分次间隔则会使其减小。它还预测,随着暴露时间增加,在短分次间隔下给予大的单次照射和大的分次照射时,有丝分裂延迟与剂量曲线应向横坐标弯曲。