Molecular interactions between adriamycin and x‐ray damage in mammalian tumor cells
Molecular interactions between adriamycin and x‐ray damage in mammalian tumor cells
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阿霉素与哺乳动物肿瘤细胞 X 射线损伤之间的分子相互作用
DOI：
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发表时间：
1977
影响因子：
6.4
通讯作者：
Lorna Tu
中科院分区：
文献类型：
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作者：
J. Byfield;Young C. Lee;Lorna Tu
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在体内诱导了切除修复能力（HeLa和Me - 180）细胞和切除修复缺陷（REQ）细胞的DNA降解。当X照射细胞在DNA单链断裂修复期间暴露于Ad时，少量残留断裂在修复完成后仍然存在。这些都是由Ad单独引起的。因此，Ad和X射线的作用似乎是相似的和可加性的。没有明确的证据表明Ad可以抑制X射线诱导的DNA单链断裂的修复。Ad还诱导DNA双链断裂的形成，并抑制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，并且当两种类型的病变共存时，可能有助于增强原发性X射线照射损伤的能力。
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 induces 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.