Defective and enhanced postreplication repair in classical and variant xeroderma pigmentosum cells treated with N-acetoxy-2-acetylaminofluorene.
Xeroderma pigmentosum (XP) cells proficient in the excision repair of pyrimidine dimers (XP variants) were also found to be proficient in the excision repair of N-2-acetoxyacetylaminofluorene (AAAF)-induced lesions in their DNA, as assayed by the photolysis of 5-bromodeoxyuridine incorporated during repair. However, the time in which the small segments of newly synthesized DNA, made immediately after treatment of cells with AAAF, were joined together to form DNA of parental size by a process called postreplication repair was long in the XP variant and classical cells. Although increasing doses of AAAF increased the time for making daughter DNA of parental size for variant and classical XP cells, AAAF did not appear to affect this process in normal human cells. Treatment of variant and classical XP cells with a relatively small dose (2.5 micron) of AAAF or 2.5 J/sq m of UV radiation several hr before a 2- to 3-fold-larger dose decreased the time for the pulse-labeled DNA to appear as parental size.
D000099:Acetoxyacetylaminofluorene / Q000494:pharmacology*; D001973:Bromodeoxyuridine; D002460:Cell Line; D004260:DNA Repair / Q000187:drug effects* / Q000528:radiation effects; D004261:DNA Replication; D004273:DNA, Neoplasm / Q000096:biosynthesis; D005449:Fluorenes / Q000494:pharmacology*; D006801:Humans; D008970:Molecular Weight; D009374:Neoplasms, Experimental / Q000378:metabolism; D010782:Photolysis; D013997:Time Factors; D014466:Ultraviolet Rays; D014983:Xeroderma Pigmentosum / Q000378:metabolism*
D004273:DNA, Neoplasm; D005449:Fluorenes; D000099:Acetoxyacetylaminofluorene; D001973:Bromodeoxyuridine