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Y Shirasu

Publications and source records attributed to Y Shirasu.

At least 91 records · Page 5Linked to original sources
PubMed1983

Analysis of the antimutagenic effect of cinnamaldehyde on chemically induced mutagenesis in Escherichia coli.

The antimutagenic effect of cinnamaldehyde on mutagenesis was investigated using ten kinds of chemical mutagen in Escherichia coli WP2s (uvr A-). In addition, the frequency of mutation induction by each mutagen in an SOS repair deficient (umuC-) strain was compared with that in a wild-type (umuC+) strain. Cinnamaldehyde greatly suppressed the umuC-dependent mutagenesis induced by 4-nitroquinoline 1-oxide (4-NQO), furylfuramide or captan. However, cinnamaldehyde was less effective against the umuC-independent mutagenesis by alkylating agents such as N-methyl-N'-nitro-N-nitrosoguanidine and ethylmethanesulfonate. On the other hand, no inhibitory effect of cinnamaldehyde was observed on prophage induction or tif-mediated filamentous growth. These results suggest that a cinnamaldehyde does not prevent the induction of the SOS functions. Despite the decrease in the number of revertants, a remarkable increase was observed in the survival of 4-NQO-treated WP2s cells after exposure to cinnamaldehyde. The reactivation of survival suggests the promotion of some DNA repair system by cinnamaldehyde. This enhancement of survival was also observed in uvr B, polA, recF or umuC mutants and less in lexA or recB, C mutants. However, it was not observed in recA mutants. Therefore, we assume that cinnamaldehyde may enhance an error-free recombinational repair system by acting on recA-enzyme activity.

4-Nitroquinoline-1-oxide↗
PubMed1983

Antimutagenic effects of cinnamaldehyde on chemical mutagenesis in Escherichia coli.

Antimutagenic effects of cinnamaldehyde on mutagenesis by chemical agents were investigated in Escherichia coli WP2 uvrA- trpE-. Cinnamaldehyde, when added to agar medium, greatly reduced the number of Trp+ revertants induced by 4-nitroquinoline 1-oxide (4-NQO) without any decrease of cell viability. This antimutagenic effect could not be explained by inactivation of 4-NQO caused by direct interaction with cinnamaldehyde. Mutagenesis by furylfuramide (AF-2) was also suppressed significantly. Mutations induced by methyl methanesulfonate (MMS) and ethyl methanesulfonate (EMS) were slightly inhibited. However, cinnamaldehyde was not at all effective on the mutagenesis of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Two derivatives of cinnamaldehyde, cinnamyl alcohol and trans-cinnamic acid, did not have as strong antimutagenic effects on 4-NQO mutagenesis as cinnamaldehyde had. Because cinnamaldehyde showed marked antimutagenic effects against mutations induced by UV-mimic mutagens but not those induced by MNNG or EMS, it seems that cinnamaldehyde might act by interfering with an inducible error-prone DNA repair pathway.

4-Nitroquinoline-1-oxide↗
PubMed1983

Further mutagenicity studies on pesticides in bacterial reversion assay systems.

A total of 228 pesticides (88 insecticides, 60 fungicides, 62 herbicides, 12 plant-growth regulators, 3 metabolites and 3 other compounds) was tested for mutagenicity in bacterial reversion-assay systems with 5 strains (TA100, TA98, TA1535, TA1537 and TA1538) of Salmonella typhimurium and a strain (WP2 hcr) of Escherichia coli. 50 pesticides (25 insecticides, 20 fungicides, 3 herbicides, 1 plant-growth regulator and 1 other compound) were found to be mutagenic. 5 of them required metabolic activation (S9 mix) for their activities. Among various chemical groups, organic phosphates, halogenated alkanes and dithiocarbamates showed higher ratios of mutagens. Although 22 of the pesticides tested have been reported to be carcinogenic, 7 of them, i.e., captain, DBCP, EDB, EDC, ETU, HEH and nitrofen, were detected as mutagens in the present assay. Most of the other 15 non-mutagenic carcinogens were organochlorine pesticides such as alpha-BHC, chlorobenzilate, p,p'-DDT, dieldrin and quintozene.

Carcinogens↗
PubMed1982

Dominant lethal studies in rats with 1,2-dibromo-3-chloropropane and its structurally related compounds.

Dominant lethal studies were conducted in SD male rats with 5 halogenated 3-carbon compounds that are structurally similar to a known mutagen 1,2-dibromo-3-chloropropane (DBCP). 1,2,3-Tribromopropane induced dominant lethal mutation especially in the early spermatid stage. This finding was almost the same as that obtained after DBCP treatment. The estimated dominant lethal mutation index of a group treated with 1,2-dibromopropane was marginal at week 1 of testing. On the other hand, bromopropane, 1,2,3-trichloropropane and 1-chloropropane produced negative responses for induction of dominant lethals.

Animals↗
PubMed1982

Induction of sex-linked recessive lethal mutations in Drosophila melanogaster males by gaseous 1,2-dibromo-3-chloropropane (DBCP).

Acute exposure to gaseous 1,2-dibromo-3-chloropropane (DBCP) caused sex-linked recessive lethal mutations in Drosophila melanogaster males. Brood pattern analysis showed that spermatids and spermatocytes were more sensitive to the lethal-mutation induction by DBCP than were spermatogonia. The mutation induction was not observed in the stage of spermatozoa.

Animals↗
PubMed1981

Correlation between the molecular structure of N-alkylureas and N-alkylthioureas and their teratogenic properties.

Eleven urea compounds were administered individually as a single oral dose to rats either on day 12 or 14 and to mice on day 10 of pregnancy. 1-Methylurea and 1-ethylurea were not teratogenic in either of the animal species. Administration of 1-methylthiourea and 1-ethylthiourea, however, resulted in high incidences of malformations in the rat but not in the mouse fetuses. The types of malformation were similar to those produced by the known teratogen ethylenethiourea. Methylated ureas such as 1,3-dimethylurea, 1,3-dimethylthiourea, 1,1,3,3-tetramethylurea, and 1,1,3,3-tetramethylthiourea were fetotoxic and produced malformations in the tail, palate, or extremities of the surviving rat and/or mouse fetuses. These findings suggest that the teratogenic properties of N-alkylureas can be categorized into two groups, i.e., mono-alkylated thioureas and methylated ureas or thioureas.

Abnormalities, Drug-Induced↗
PubMed1981

Carcinogenicity of methylmercury chloride in ICR mice: preliminary note on renal carcinogenesis.

ICR mice (60/group) were fed diets containing methylmercury chloride (MMC) in 0, 15 or 30 ppm for 78 weeks. The majority of mice in the 30-ppm group died due to the neurotoxicity by week 26. The first renal mass was grossly seen in a male of the 15-ppm group at week 58. Histopathology on kidney tissue from all animals surviving after 53 weeks revealed renal tumors in 13 of 16 males of the 15-ppm group in contrast with 1 of 37 males of the control. No renal tumors were seen in the female treated groups and/or control groups.

Animals↗
PubMed1981

An ultrastructural study of spinal nerve roots and dorsal root ganglia in aging rats with spontaneous radiculoneuropathy.

The spinal nerve roots and dorsal ganglia of 104- to 135-week-old rats with spontaneous radiculoneuropathy were examined by light and electron microscopy. Demyelination was common in myelinated fibers of various diameters of both ventral and dorsal roots. The most striking alteration was wide distention of myelin sheaths, which extended throughout the entire internode. The spaces formed between separated lamellae frequently were invaded by macrophages. Subsequent vesicular degeneration of myelin seemed to be mediated by invading macrophages. These processes caused complete myelin destruction, but most axons showed no degenerative changes except for obvious reduction in diameter. Occasionally, there were clumping and partial degradation of neurofilaments and ruptured axolemma in the severely demyelinated axons. A few fibers also were undergoing wallerian-type degeneration, perhaps secondary to the severe demyelinative changes. Remyelinating fibers in various phases of repair were coexistent with markedly demyelinated ones. Demyelinative changes described above also developed within some of these remyelinated internodes. There were no remarkable changes in neurons of the dorsal root ganglia, though accumulation of lipofuscin was common. Our findings suggest that the changes in the nerve roots are essentially a primary segmental demyelination in aging rats with radiculoneuropathy.

Aging↗
PubMed1980

Teratogenic effects of combined administration of ethylenethiourea and nitrite in mice.

Teratogenic potential of ethylenethiourea (ETU) was investigated in SLC-ICR mice after its reaction with sodium nitrite. ETU was given orally in doses of 400 mg/kg on various days of pregnancy in combination with 200 mg/kg NaNO2 at varied intervals. When NaNO2 was given to females immediately after their treatment with ETU on day 6 or 8 of pregnancy, fetal survival was significantly decreased. Various types of malformations were observed in the living fetuses from mothers treated on day 6, 8, or 10 of pregnancy, but not on day 12. The teratogenicity disappeared when NaNO2 was given 2 h after the treatment with ETU.

Abnormalities, Drug-Induced↗