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Biochemistry Division, National Cancer Center Research Institute, Tsukiji, Chuo-ku, Tokyo, Japan 104
The chemical carcinogens, 4-nitroquinoline 1-oxide and 4-nitropyridine 1-oxide, and their carcinogenic or noncarcinogenic derivatives were tested by a slight modification of the rapid screening method for mutagens and carcinogens described by Slater, Anderson, and Rosenkranz. N-Methyl-N'-nitro-N-nitrosoguanidine and methylmethanesulfonate were also tested.
4-Nitroquinoline 1-oxide, 4-hydroxyaminoquinoline 1-oxide, 3-methyl-4-nitropyridine 1-oxide, and 2,3-dimethyl-4-nitropyridine 1-oxide caused wider growth-inhibiting zones with mutants of Escherichia coli, such as the DNA polymerase I-deficient mutant, polA1, and the recombination-deficient mutants, recA13 and recB21, than with the wild strain. These compounds also caused wider growth-inhibiting zones with ultraviolet-sensitive mutants of Saccharomyces cerevisiae and Bacillus subtilis than with the corresponding wild types.
4-Nitropyridine 1-oxide, N-methyl-N'-nitro-N-nitrosoguanidine, and methylmethanesulfonate caused wider growth inhibition zones with the polA1, recA13, and recB21 mutants of E. coli than with the wild strain but similar zones with ultraviolet-sensitive mutants of S. cerevisiae and B. subtilis and the wild strains. The results indicate that different mechanisms are involved in repair of DNA damaged by ultraviolet irradiation or 4-nitroquinoline 1-oxide and its derivatives on the one hand and by 4-nitropyridine 1-oxide, N-methyl-N'-nitro-N-nitrosoguanidine, or methylmethanesulfonate on the other.
1 This work was supported in part by grants from the Ministry of Education and Ministry of Health.
Received 3/28/72. Accepted 7/ 7/72.
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