Byfield J E, Lee Y C, Tu L
Int J Cancer. 1977 Feb 15;19(2):186-93. doi: 10.1002/ijc.2910190208.
The effect of the anthracycline antibiotic, Adriamycin (Ad), on the sedimentation properties of pre-labelled mammalian DNA has been studied. Ad induces DNA degradation in vivo in both excision repair-competent (HeLa and Me-180) cells and in excision repair-deficient (REQ) cells. When X-irradiated cells are exposed to Ad during the period of repair of DNA single-strand breaks, small numbers of residual breaks persist following completion of repair. These are attributable to those induced by Ad alone. The effects of Ad and X-rays therefore appear to be similar and additive. No clear-cut evidence that Ad can inhibit the repair of X-ray-induced DNA single-strand breakage was found. Ad also induced the formation of DNA double-strand breaks and inhibits the repair of X-ray-induced base damage (repair replication). The induction of DNA strand breakage may be responsible for Ad cell toxicity and may contribute to its capacity to enhance primary X-irradiation damage when the two types of lesions co-exist.
已经研究了蒽环类抗生素阿霉素（Ad）对预先标记的哺乳动物DNA沉降特性的影响。Ad在体内可诱导具有切除修复能力的细胞（HeLa和Me-180细胞）以及切除修复缺陷（REQ）细胞中的DNA降解。当X射线照射的细胞在DNA单链断裂修复期间暴露于Ad时，修复完成后仍会残留少量的断裂。这些断裂可归因于仅由Ad诱导产生的断裂。因此，Ad和X射线的作用似乎相似且具有累加性。未发现明确证据表明Ad能够抑制X射线诱导的DNA单链断裂的修复。Ad还诱导了DNA双链断裂的形成，并抑制了X射线诱导的碱基损伤的修复（修复复制）。DNA链断裂的诱导可能是Ad细胞毒性的原因，并且当两种类型的损伤共存时，可能有助于其增强初次X射线照射损伤的能力。
