3"-Azido-3'-deoxythymidine and 2',3'-dideoxycytidine do not inhibit gene-specific DNA repair in hamster cells.
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.
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Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, MD 20892.
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D000818:Animals; D016466:CHO Cells; D002999:Clone Cells; D006224:Cricetinae; D004247:DNA / Q000187:drug effects / Q000528:radiation effects; D004249:DNA Damage; D004260:DNA Repair / Q000187:drug effects*; D004261:DNA Replication / Q000187:drug effects*; D005796:Genes / Q000187:drug effects*; D007700:Kinetics; D013997:Time Factors; D014466:Ultraviolet Rays; D016047:Zalcitabine / Q000494:pharmacology*; D015215:Zidovudine / Q000494:pharmacology*
D015215:Zidovudine; D016047:Zalcitabine; D004247:DNA