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Y Shirasu

Publications and source records attributed to Y Shirasu.

At least 109 records · Page 6Linked to original sources
PubMed1980

Detection of mutagenicity of procarbazine by the host-mediated assay with polychlorinated biphenyl (aroclor 1254) as enzyme inducer.

Procarbazine [N-isoppropyl-alpha-(2-methylhydrazino)-p-toluamide] was tested for mutagenicity with Salmonella typhimurium G46 in the host-mediated assay by using male BALB/c mice pretreated orally with polychlorinated biphenyl (PCB, Aroclor 1254). Procarbazine was weakly mutagenic without PCB pretreatment, but the pretreatment greatly enhanced the mutagenicity of this compound. The administration of 500 mg PCB/kg 1 day before procarbazine dosage was suitable for the detection of the mutagenicity. Among PCB, 3-methylcholanthrene (3-MC) and phenobarbital sodium (PB), the former 2 inducers showed much stronger enhancing effects than PB. The pretreatment with 3-MC in combination with PB did not cause further enhancement compared with 3-MC alone.

Animals↗
PubMed1980

Sister-chromatid exchanges and chromosomal aberrations in cultured Chinese hamster cells treated with pesticides positive in microbial reversion assays.

The induction of sister-chromatid exchanges (SCEs), chromosomal aberrations and polyploids was investigated in cultured Chinese hamster cells treated with pesticides or a related compound positive in microbial reversion assays. The chemicals tested were captan, captafol, 1,2-dibromoethane (EDB), 1,2-dibromo-3-chloropropane (DBCP), 5-nitro-1-naphrhonitrile (NNN), p-dimethylaminobenzenediazo sodium sulfonate (DAPA), 2-hydrazinoethanol (HEH), vamidothion, dichlorovos (DDVP), N-nitroso-ethylenethiourea (N-nitroso-ETU), and 2,4-dinitrophenyl thiocyanate (NBT). A significant and dose-dependent increase in the frequency of SCEs and chromosomal aberrations was observed in the cell cultures treated with captan, captafol, EDB, DBCP, HEH, DDVP, vamidothion, DAPA or N-nitroso-ETU or NBT produced a significant increase in the frequency of polyploid cells, whereas the other agents did not. When compared with results from microbial reversion assays, a close correlation was observed between the ability to induce SCEs or chromosomal aberrations and the mutagenic potency in bacteria (r:0.71-0.84).

Aneuploidy↗
PubMed1980

Mutagenicity screening of feed additives in the microbial system.

18 feed additives were tested for DNA-modifying effects by the repair test named "rec-assay" with Bacillus subtillis H17 (rec+) and M45 (rec-), and for mutagenicity with Escherichia coli WP2 hcr and 5 Salmonella typhimurium tester strains with the use of a top-agar overlay method. Carbadox, furazolidone, panazon and zoalene were positive in both assays. The former 3 were mutagenic for TA100, TA98 and WP2 hcr, while zoalene was mutagenic for all strains. These 4 compounds did not require a metabolic activation for their mutagenic activities. Nicarbazin was weakly mutagenic for TA1538 and TA98 with and without S9 mix. Amprolium and caprylohydroxamic acid also showed very weak mutagenicities only for TA100 with S9 mix and for WP2 hcr with and without S9 mix, resp. The mutagenic activities of carbadox, furazolidone and panazon for TA100 were reduced only by the addition of S9 mix, but not by S9 fraction or blood, whereas that of zoalene was decreased by any of the 3 factors.

Animal Feed↗
PubMed1980

Dominant lethal mutation induced in male rats by 1,2-dibromo-3-chloropropane (DBCP).

1,2-Dibromoethane (DBE) and 1,2-dibromo-3-chloropropane (DBCP), soil fumigants, were investigated for their potential mutagenicity by dominant lethal studies in the rat and mouse. Dominant lethal mutation was induced by DBE in neither of the species. DBCP, on the other hand, induced dominant lethals in rats in the post-meiotic stage of spermatogenesis, especially in the early spermatid stage. However, DBCP did not cause dominant lethals in mice.

Animals↗
PubMed1979

Inhibitors for the mutagenicities of colon carcinogens, 1,2-dimethylhydrazine and azoxymethane, in the host-mediated assay.

Inhibitory effects of several chemicals on the mutagenicities of 1,2-dimethylhydrazine (DMH) and azoxymethane (AOM) for Salmonella typhimurium G46 in the host-mediated assay were investigated. They were carbon disulfide (CS2), tetraethylthiuram disulfide (disulfiram, DSF), sodium diethyldithiocarbamate (SDDC), ethylene-bis(dithiocarbamato) manganese (Maneb), pyrazole (PZ), aminoacetonitrile hydrogen sulfate (AAN), and sodium selenite (SE). All the compounds, except for SE, inhibited the mutagenicities of DMH and AOM.

Aminoacetonitrile↗
PubMed1979

Carcinogenicity of N-nitroso-ethylenethiourea in female mice.

The nitrosation product of ethylenethiourea (ETU), N-nitroso-ETU, was tested for tumorigenicity in female ICR mice. Ten weekly oral administrations of this compound (0.66-2.64 mg/dose) caused apparently dose-dependent increases in the number of mice with pulmonary and lymphocytic neoplasms.

Animals↗
PubMed1979

Assay for mutagenicity of bile in Sprague-Dawley rats treated subcutaneously with intestinal carcinogens.

To investigate the mode of action of sc injected intestinal carcinogens, the mutagenicity assay of bile collected from noninbred Sprague-Dawley rats treated sc with carcinogens was conducted in the presence and absence of beta-glucuronidase. The bile samples from rats inoculated with 4-aminobiphenyl were mutagenic for Salmonella typhimurium TA100 only in the presence of beta-glucuronidase, whereas those from the 3,2'-dimethyl-4-aminobiphenyl-treated rats did not require the enzyme for mutagenicity toward strain TA100. On the contrary, the assays with S. typhimurium G46 and TA100 of bile from rats inoculated with 1,2-dimethylhydrazine, azoxymethane, or methylazoxymethanol acetate failed to reveal mutagenicity whether beta-glucuronidase was added or not, though these carcinogens were highly mutagenic for strain G46 in the Salmonella-microsome mutagenicity test and/or in the host-mediated assay.

Animals↗
PubMed1978

Induction of dominant-lethal mutations after administration of ethylenethiourea in combination with nitrite of the n-nitroso-ethylenethiourea in mice.

Mutagenic potentials of ethylenethiourea (ETU) in combination with sodium nitrite or of N-nitroso-ETU, a nitrosation product of ETU in vitro, were investigated in the mouse dominant-lethal test. Simultaneous 5-day p.o. administration of ETU (150 mg/kg) and sodium nitrite (50 mg/kg) caused a significant decrease in the percentage pregnancy and the number of implants in weeks 5 and 6 of testing, although no effects were obtained on these indices when the chemicals were applied separately. However, in the group treated with 30 mg ETU plus 10 mg sodium nitrite per kg no dominant-lethal mutations were induced. 5-day oral administration of 100 mg of N-nitroso-ETU per kg also exhibited similar effects to those observed after treatment with 150 mg ETU plus 50 mg sodium nitrite per kg.

Animals↗
PubMed1978

Cytogenetic and dominant lethal studies on captan.

Possible mutagenic activity of captan was investigated by in vitro and in vivo cytogenetic studies and by the dominant lethal study in mice. In vitro cytogenetic study with cultured human diploid cells revealed a significant increase in the frequency of cells showing stickiness and a severe mitotic inhibition at concentrations of 3.0 and 4.0 microgram of captan per ml. although no chromosomal aberrations were observed. In in vivo cytogenetic study, no chromosomal aberrations were induced in the bone marrow cells of rats treated orally with captan at a single dose of 500, 1000 or 2000 mg/kg or at five consecutive doses of 200, 400 or 800 mg/kg/day. Dominant lethal study also failed to show any mutation induction after treatment of male mice with daily oral dose of 200 or 600 mg of captan per kg bw for five days.

Animals↗
PubMed1978

Detection of mutagenicity of the colon carcinogen 1,2-dimethylhydrazine by the host-mediated assay and its correlation to carcinogenicity.

Mutagenic potential of 1,2-dimethylhydrazine (DMH) was investigated in the host-mediated assay with mice used as hosts. This assay revealed potent mutagenicity of this colon carcinogen for Salmonella typhimurium G46. The mutagenicity of DMH was inhibited by pretreatment of mice with disulfiram. In addition, mouse strain and sex differences influenced the mutation induction by DMH: Mutation induction was significantly lower in C57BL/6 mice than in outbred ICR mice of either sex and was generally higher in male than in females of either C57BL/6 or ICR mice.

Animals↗
PubMed1976

Mutagenicity screening of pesticides in the microbial system.

A survey on the mutation induction capacity was made in the microbial system on 166 pesticides including 57 fungicides, 63 herbicides and 46 insecticides. The screening methods consisted of the rec-assay procedure, a sensitivity test utilizing H17 Rec+ and M45 Rec- strains of Bacillus subtilis, as well as the reversion assays on plates utilizing auxotrophic strains of Escherichia coli (WP2) and Salmonella typhimurium (Ames series). Chemicals inducing reversions were detected only among those showing positive effects in the rec-assay but not among negative samples. In addition to Captafol, Captan, Dexon and NBT of which mutagenicities have been previously reported, Dichlorvos, Folpet, 2-hydrazinoethanol (HEH), 5-nitro-1-naphthonitrile (NNN) and Vamidothion were found to be mutagens in our systems.

Bacillus subtilis↗
PubMed1975

Significance of mutagenicity testing on pesticides.

Our mutagenicity screening studies on pesticides totalling 165 have newly revealed microbial mutagenic activity in the following four compounds: 2,4-dinitrophenyl thiocyanate (NBT), sodium p-dimethylamino-azobenzene diazosulfonate (DAPA), 5-nitro-1-napthonitrile (NNN) and N-(1,1,2,2-tetrachloroethylthio)-4-cyclohexene-1, 2-dicarboximide (Captafol). Significance of mutagenicity testing on pesticides is discussed from the toxicological point of view. No definite relationship has been proven among mutagenicity, carcinogenicity and teratogenicity of pesticides although there are some correlations in these activities of several pesticides. Further studies are needed to clarify the significance of mutagenicity testing in toxicological areas.

Animals↗