Link C J, Bohr V A
Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, MD 20892.
Biochem Biophys Res Commun. 1995 Mar 8;208(1):198-203. doi: 10.1006/bbrc.1995.1323.
3"-Azido-3'-deoxythymidine (AZT) was the first approved drug for the treatment of the AIDS; however, despite its usefulness, AZT often produces side effects that require cessation of therapy. 2',3'-Dideoxycytidine (ddC) is a related anti-retroviral agent in advanced stages of clinical testing. A previous report demonstrated that AZT decreased the repair of UV-induced DNA strand breaks in mammalian cells after ultraviolet (UV) irradiation. We studied the effect of AZT and ddC on DNA repair from the hamster DHFR gene of the major UV-induced DNA lesion, cyclobutane pyrimidine dimers (CPDs). We conclude that neither AZT nor ddC inhibited DNA replication or the gene-specific repair of CPDs in the hamster DHFR gene after 8 or 24 hrs of repair incubation at concentrations of 25 microM and 10 microM, respectively.
3'-叠氮-3'-脱氧胸苷（AZT）是首个被批准用于治疗艾滋病的药物；然而，尽管它很有用，但AZT常常会产生需要停止治疗的副作用。2'，3'-双脱氧胞苷（ddC）是处于临床试验后期的一种相关抗逆转录病毒药物。先前的一份报告表明，AZT会降低紫外线（UV）照射后哺乳动物细胞中紫外线诱导的DNA链断裂的修复。我们研究了AZT和ddC对主要紫外线诱导的DNA损伤——环丁烷嘧啶二聚体（CPD）——在仓鼠二氢叶酸还原酶（DHFR）基因中的DNA修复的影响。我们得出结论，在分别以25微摩尔和10微摩尔的浓度进行8小时或24小时的修复孵育后，AZT和ddC均未抑制仓鼠DHFR基因中CPD的DNA复制或基因特异性修复。
