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K Isomura

Publications and source records attributed to K Isomura.

At least 19 recordsLinked to original sources
PubMed1984

Induction of mutations and chromosome aberrations in lung cells following in vivo exposure of rats to nitrogen oxides.

In order to investigate the mutagenic effects of nitrogen oxides ( NOx ), induced mutations and chromosome aberrations were examined using primary lung cells obtained from rats exposed in vivo to NO2 and NO. Rats were exposed to nitrogen oxide gases at concentrations of 8-27 ppm for 3 h in a stainless steel chamber. Over the range 15-27 ppm, NO2 significantly increased mutation to ouabain resistance. Over a similar dose range, NO significantly increased mutation only at the highest concentration (27 ppm). Following NO2 exposure, chromosome aberrations (mainly chromatid type) were induced in chromatid breaks, 2.5-11.6-fold over the control at 8 and 27 ppm, respectively.

Animals↗
PubMed1978

Induction and isolation of frameshift mutants in cultured Chinese hamster DON cells.

Induction, isolation and characterization of frameshift mutants were studied by using a Chinese hamster Don (CHD) cell line. ICR-191, known to be a potent frameshift mutagen, was used for the induction of frameshift mutations. The drug (10(-5) M), as well as N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and ethyl methanesulfonate (EMS), increased significantly the frequency of forward mutations from 8-azaguanine (8-AG) sensitivity (8-AGs) to resistance (8-AGr) over the untreated control to an extent of about 100-fold. 21 8-AGr mutants were isolated from the AP-01 (a sub-line of CHD) cells after treatment with appropriate concentrations of ICR-191 (10(-5) and 1.36 X 10(-5) M), and subsequently several reclonal mutants were tested for their ability to revert to 8-AG susceptibility after treatment with the three mutagens and a carcinogen, 2-nitrofluorene (2-NF), known to be a frameshift mutagen. Among the 8-AGr mutants tested, clone ICR-014 or ICR-172 showed a significant increase in reversion frequency over the control level only after treatment with ICR-191 or 2-NF, respectively; but not with the other two mutagens. These results suggest that each of these two kinds of mutant has a different frameshift mutation in one of the loci controlling 8-AG resistibility. It was also found that the hypoxanthine--guanine phosphoribosyl transferase (HGPRT) activities in clones ICR-014 and ICR-172 were 1.9 and 34% of that of the original AP-01 cells, respectively.

Acridines↗