Selective killing of carcinogen-treated SV40-transformed Chinese hamster cells by a defective parvovirus.
SV40-transformed Chinese hamster cells (CO631) were treated with 7, 12-dimethylbenz[alpha]anthracene, 4-nitroquinoline-N-oxide, or benzo[alpha]pyrene, respectively, at sublethal concentrations. Infection of these cells with the helper-dependent parvovirus, AAV-5 immediately prior to, or at the time of exposure to the chemical carcinogens resulted in effective killing of cells exposed to the combination virus plus carcinogen, AAV infection without additional treatment did not have a significant effect on cell survival. AAV infections have recently been shown to efficiently inhibit gene amplification induced by various initiators and herpes simplex virus infections. Data may suggest that gene amplification is an adaptive cellular response to initiating events resulting in enhanced cell survival.
D015112:4-Nitroquinoline-1-oxide / Q000633:toxicity; D015127:9,10-Dimethyl-1,2-benzanthracene / Q000633:toxicity; D000818:Animals; D001564:Benzo(a)pyrene; D001580:Benzopyrenes / Q000633:toxicity; D002273:Carcinogens / Q000633:toxicity*; D002470:Cell Survival; D002472:Cell Transformation, Viral; D006224:Cricetinae; D003412:Cricetulus; D003673:Defective Viruses / Q000502:physiology*; D007700:Kinetics; D010321:Parvoviridae / Q000502:physiology*; D013539:Simian virus 40 / Q000235:genetics*
D001580:Benzopyrenes; D002273:Carcinogens; D001564:Benzo(a)pyrene; D015112:4-Nitroquinoline-1-oxide; D015127:9,10-Dimethyl-1,2-benzanthracene