Repair of deoxyribonucleic acid lesions caused by adriamycin and ellipticine.
Repair of deoxyribonucleic acid lesions caused by adriamycin and ellipticine.
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DOI：
10.1016/0006-2952(82)90500-7
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发表时间：
1982-05
影响因子：
5.8
通讯作者：
W. Ross;M. Smith
中科院分区：
文献类型：
--
作者：
W. Ross;M. Smith
插入剂阿霉素和椭圆形碱引起哺乳动物细胞中DNA单链和双链断裂以及DNA-蛋白质交联。在等毒性剂量下，椭圆形霉素引起这些病变的频率比阿霉素高得多。然而，阿霉素诱导的DNA效应缓慢和不完全修复超过24小时后，药物去除，而椭圆形的影响几乎完全修复30分钟内。椭圆形诱导的病变修复观察到只有当细胞稀释（~100倍）后，药物治疗，这表明显着量的药物可能已被隔离在细胞膜。细胞稀释不改变阿霉素的作用。DNA损伤的去除是温度依赖性的。最后，DNA单链和双链断裂以及DNA-蛋白质交联的修复率的相似性支持了它们在功能上相关的假设。
The intercalating agents adriamycin and ellipticine caused DNA single and double strand breaks and DNA-protein crosslinks in mammalian cells. Ellipticine caused a much higher frequency of each of these lesions than adriamycin, at equitoxic doses. However, adriamycin-induced DNA effects were slowly and incompletely repaired over 24 hr after drug removal while the effects of ellipticine were virtually completely repaired within 30 min. Repair of ellipticine-induced lesions was observed only if cells were diluted (~100-fold) after drug treatment, suggesting that significant amounts of drug may have been sequestered in the cellular membranes. Cell dilution did not alter the effects of adriamycin. Removal of the DNA lesions was temperature dependent. Finally, the similarity in the rates of repair for DNA single and double strand breaks and DNA-protein crosslinks supports the hypothesis that they are functionally related.