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Mutagenicity testing on o-phenylphenol
227 decreased as compared with Difco agar. DNA~iamaging activity of some chemicals and their metabolites were identified by using a criterion that many more cells of 45T should be killed than 17A. It was clear from the data that pretreatment with phenobarbital resulted in inactivation for DNA-damaging activity of AF2, and pretreatment with carbon tetrachloride killed conversely many cells of 45T due to inhibition of metabolizing enzyme for AF2. Although a probably activated effect of DMNA was revealed in the present study, it seems that host-mediated rec-assay is insensitive for screening the labile substances such as active metabolites of DMNA when compared with the Salmonella G46 data.
a Present address:
Tobishi Pharmaceutical Co. Ltd., Tokyo.
A b b r e v i a t i o n s : AF2, 2-(2-furyl)-3-(5-nitro-2-fttryl)acrylamide; DMNA, dimethylnitrosamine.
31 Shirasu, Y., M. Moriya, K. Kato, H. Tezuka, R. Henmi, A. Shingu, M. Kaneda and S. Teramoto, Institute of Environmental Toxicology, Kodaira-shi, T o k y o (Japan) Mutagenicity testing o n o-phenylphenol A series of mutagenicity studies was conducted on the fungicide o-phenylphenol (OPP). Microbial studies: The rec-assay usingB, subtilis H17 and M45, the reversion assays with and without metabolic activation employing E. coli WP2 hcr- and 5 S. typhimurium TA strains (1535, 1537, 1538, 98 and 100), and the hostmediated assay with S. typhimurium G46 were performed on OPP. In the hostmediated assay, 7-week-old JCL-ICR male mice were orally treated with 200 or 600 mg/kg of OPP for 5 consecutive days. Negative results were obtained in all the tests. Cytogenetic studies: Four-week-old Wistar male rats were treated orally with OPP in daily doses of 50, 100, 200, 400 and 800 mg/kg for 5 days or in single doses of 250, 500, 1000, 2000 and 4000 mg/kg. They were killed 24 h after the final treatment. The bone-marrow cells were examined for chromosomal abnormalities. OPP produced no structural and numerical aberrations at any dose tested. Dominant-lethal studies: Dally oral doses of OPP were administered to C3H male mice at 100 or 500 mg/kg for 5 days. Each treated male mouse was mated with 2 untreated virgin females from the same stock weekly for 6 weeks. OPP induced no dominant-lethal mutations at any stage of the spermatogenesis.
32 Shirasu, Y., H. Tezuka, R. Henmi, S. Teramoto, A. Shingu and M. Kaneda, The Institute of Environmental Toxicology, Kodaira-shi, T o k y o (Japan)
a Present address:
Tobishi Pharmaceutical Co. Ltd., Tokyo.
A b b r e v i a t i o n s : AF2, 2-(2-furyl)-3-(5-nitro-2-fttryl)acrylamide; DMNA, dimethylnitrosamine.
31 Shirasu, Y., M. Moriya, K. Kato, H. Tezuka, R. Henmi, A. Shingu, M. Kaneda and S. Teramoto, Institute of Environmental Toxicology, Kodaira-shi, T o k y o (Japan) Mutagenicity testing o n o-phenylphenol A series of mutagenicity studies was conducted on the fungicide o-phenylphenol (OPP). Microbial studies: The rec-assay usingB, subtilis H17 and M45, the reversion assays with and without metabolic activation employing E. coli WP2 hcr- and 5 S. typhimurium TA strains (1535, 1537, 1538, 98 and 100), and the hostmediated assay with S. typhimurium G46 were performed on OPP. In the hostmediated assay, 7-week-old JCL-ICR male mice were orally treated with 200 or 600 mg/kg of OPP for 5 consecutive days. Negative results were obtained in all the tests. Cytogenetic studies: Four-week-old Wistar male rats were treated orally with OPP in daily doses of 50, 100, 200, 400 and 800 mg/kg for 5 days or in single doses of 250, 500, 1000, 2000 and 4000 mg/kg. They were killed 24 h after the final treatment. The bone-marrow cells were examined for chromosomal abnormalities. OPP produced no structural and numerical aberrations at any dose tested. Dominant-lethal studies: Dally oral doses of OPP were administered to C3H male mice at 100 or 500 mg/kg for 5 days. Each treated male mouse was mated with 2 untreated virgin females from the same stock weekly for 6 weeks. OPP induced no dominant-lethal mutations at any stage of the spermatogenesis.
32 Shirasu, Y., H. Tezuka, R. Henmi, S. Teramoto, A. Shingu and M. Kaneda, The Institute of Environmental Toxicology, Kodaira-shi, T o k y o (Japan)