Dritschilo A, Piro A J, Belli J A
Int J Radiat Biol Relat Stud Phys Chem Med. 1979 Jun;35(6):549-60. doi: 10.1080/09553007914550661.
We have studied the effects of actinomycin-D (AMD) and Adriamycin (ADRM) on the repair of radiation damage in Chinese hamster cells (V79) in plateau phase growth. Suppression of potentially lethal damage repair (PLDR) was observed in the presence of non-toxic levels of AMD and minimally toxic levels of ADRM. The suppression of PLDR by AMD persisted as long as the drug was present. Removal of AMD was followed by prompt repair of potentially lethal injury suggesting that suppression of PLDR by AMD was not accompanied by fixation of injury to a non-repairable state. On the other hand, irradiated cells exposed to ADRM eventually repair potentially lethal injury in the presence of drug after an initial delay. AMD, but not ADRM, inhibited repair of sublethal radiation damage.
我们研究了放线菌素-D（AMD）和阿霉素（ADRM）对处于平台期生长的中国仓鼠细胞（V79）辐射损伤修复的影响。在无毒水平的AMD和最低毒性水平的ADRM存在下，观察到潜在致死性损伤修复（PLDR）受到抑制。只要药物存在，AMD对PLDR的抑制就持续存在。去除AMD后，潜在致死性损伤迅速修复，这表明AMD对PLDR的抑制并未伴随着损伤固定为不可修复状态。另一方面，暴露于ADRM的受辐照细胞在最初延迟后最终在药物存在的情况下修复潜在致死性损伤。AMD而非ADRM抑制亚致死性辐射损伤的修复。
