DNA damage, cell survival and DNA repair in Chinese hamster ovary cells after in vitro metabolic activation of dimethylnitrosamine and benzo[a]pyrene.
Both benzo[a]pyrene (BP) and dimethylnitrosamine (DMN) cause a dose-related increase in single-strand DNA lesions in CHO cells after in vitro metabolic activation, as detected by alkaline sucrose gradients (ASG) sedimentation analysis. This type of DNA damage and cell survival are inversely related with DMN, whereas there is negligible cell killing with BP even at concentrations producing maximal DNA damage. However, high concentrations of BP do result in a reduction in colony size, suggesting a diminished growth rate rather than increased lethality. Up to 80% of the DNA lesions induced by BP and detectable by alkaline sucrose gradient sedimentation may be repaired within 6 h, whereas less than 30% of the DNA damage caused by DMN is apparently removed 24 h after treatment, implying that DNA repair may be involved in the differential lethality of CHO cells exposed to DMN and BP.
D000818:Animals; D001580:Benzopyrenes / Q000378:metabolism* / Q000494:pharmacology; D001711:Biotransformation; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects*; D006224:Cricetinae; D004247:DNA / Q000235:genetics; D004260:DNA Repair / Q000187:drug effects*; D004128:Dimethylnitrosamine / Q000378:metabolism* / Q000494:pharmacology; D008970:Molecular Weight; D009153:Mutagens
D001580:Benzopyrenes; D009153:Mutagens; D004247:DNA; D004128:Dimethylnitrosamine