Genotoxicity of 2,4,6-trichlorophenol in V79 Chinese hamster cells.
The genotoxicity of the rodent carcinogen 2,4,6-trichlorophenol (TCP) was studied without exogenous metabolic activation in V79 Chinese hamster cells. TCP did not induce mutation at the hprt locus to 6-thioguanine resistance or structural chromosome aberrations. However, it produced statistically significant, dose-related increases in hyperdiploidy and micronuclei. From these results it appears that TCP causes chromosome malsegregation as its major mode of genotoxic action.
Jansson
K
K
Department of Cell Biology, University of Jyväskylä, Finland.
Jansson
V
V
D000818:Animals; D002273:Carcinogens / Q000494:pharmacology*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D002733:Chlorophenols / Q000494:pharmacology*; D002869:Chromosome Aberrations; D006224:Cricetinae; D003412:Cricetulus; D004171:Diploidy; D004305:Dose-Response Relationship, Drug; D004351:Drug Resistance; D005020:Ethyl Methanesulfonate / Q000494:pharmacology; D007041:Hypoxanthine Phosphoribosyltransferase / Q000235:genetics; D015162:Micronucleus Tests; D009152:Mutagenicity Tests; D009153:Mutagens / Q000494:pharmacology*; D013866:Thioguanine / Q000494:pharmacology
D002273:Carcinogens; D002733:Chlorophenols; D009153:Mutagens; D005020:Ethyl Methanesulfonate; D007041:Hypoxanthine Phosphoribosyltransferase; D013866:Thioguanine; C024564:2,4,6-trichlorophenol