Excision repair in ataxia telangiectasia, Fanconi's anemia, Cockayne syndrome, and Bloom's syndrome after treatment with ultraviolet radiation and N-acetoxy-2-acetylaminofluorene.
Excision repair of damage due to ultraviolet radiation, N-acetoxy-2-acetyl-aminofluorene and a combination of both agents was studied in normal human fibroblasts and various cells from cancer prone patients (ataxia telangiectasia, Fanconi's anemia, Cockayne syndrome and Bloom's syndrome). Three methods giving similar results were used: unscheduled DNA synthesis by radioautography, photolysis of bromodeoxyuridine incorporated into parental DNA during repari, and loss of sites sensitive to an ultraviolet endonuclease. All cell lines were proficient in repair of ultraviolet and acetoxy acetylaminofluorene damage and at saturation doses of both agents repair was additive. We interpret these data as indicating that the rate limiting step in excision repair of ultraviolet and acetoxy acetylaminofluorene is different and that there are different enzyme(s) working on incision of both types of damages.
D001260:Ataxia Telangiectasia / Q000378:metabolism*; D001973:Bromodeoxyuridine / Q000494:pharmacology; D002460:Cell Line; D004247:DNA / Q000096:biosynthesis / Q000528:radiation effects*; D004260:DNA Repair; D003851:Deoxyribonucleases; D004392:Dwarfism / Q000378:metabolism*; D004720:Endonucleases; D005198:Fanconi Syndrome / Q000378:metabolism*; D005347:Fibroblasts; D006801:Humans; D010782:Photolysis; D014466:Ultraviolet Rays
D004247:DNA; D003851:Deoxyribonucleases; D004720:Endonucleases; D001973:Bromodeoxyuridine