DNA repair in cultured mouse cells of increasing population doubling level.
Cultures of mouse cells of various population doubling levels (PDL) were examined for DNA-repair capabilities as estimated by (i) the excision of pyrimidine dimers; (ii) unscheduled DNA synthesis (UDS) in response to UV-irradiation or N-methyl-N'-nitrosoguanidine (MNNG) treatment; (iii) the levels of two DNA-repair enzyme activities, uracil DNA glycosylase and AP endonuclease. The responses to ultraviolet light and MNNG decreased rapidly within the first two PDL and more slowly thereafter until essentially no repair was detected by PDL 12. A continuous cell line which emerged from the cultured cells after a crises period had some restoration of repair capability. The amount of uracil DNA glycosylase activity decreased by approximately 40% before the crises period then decreased by 90% in the continuous cell line. In contrast, the amount of AP endonuclease activity present in the precrises cells showed no significant change until PDL 12, then increased 6-7-fold in the continuous cell line.
D000818:Animals; D002455:Cell Division / Q000187:drug effects / Q000528:radiation effects; D002478:Cells, Cultured; D045647:DNA Glycosylases; D004260:DNA Repair; D004261:DNA Replication / Q000187:drug effects / Q000528:radiation effects*; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase; D043223:Deoxyribonuclease IV (Phage T4-Induced); D004622:Embryo, Mammalian; D004706:Endodeoxyribonucleases / Q000378:metabolism; D008769:Methylnitronitrosoguanidine / Q000633:toxicity*; D051379:Mice; D008807:Mice, Inbred BALB C; D009699:N-Glycosyl Hydrolases / Q000378:metabolism; D011740:Pyrimidine Dimers / Q000528:radiation effects; D014466:Ultraviolet Rays; D051981:Uracil-DNA Glycosidase
D011740:Pyrimidine Dimers; D008769:Methylnitronitrosoguanidine; D004706:Endodeoxyribonucleases; D043223:Deoxyribonuclease IV (Phage T4-Induced); D045647:DNA Glycosylases; D009699:N-Glycosyl Hydrolases; D051981:Uracil-DNA Glycosidase; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase