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T Kada

Publications and source records attributed to T Kada.

At least 19 recordsLinked to original sources
PubMed1992

An inhibitor of potentially lethal damage (PLD) repair reduces the frequency of gamma-ray-induced mutations in cultured Chinese hamster V79 cells.

Cordycepin (3'-deoxyadenosine, 3'-dA) is an RNA antimetabolite and a radiosensitizer in cultured mammalian cells. In the present paper, the effects of 3'-dA on gamma-ray-induced lethality and 6-thioguanine (6TG)-resistant mutations in cultured Chinese hamster V79 cells were examined. 3'-dA had the effect of sensitizing the lethality induced by gamma-rays. The potentially lethal damage (PLD) repair produced by post-incubation of cells in Hanks' solution after gamma-irradiation was almost completely suppressed by 5 x 10(-5) M 3'-dA. When cells were irradiated with 10 Gy gamma-rays and incubated with 3'-dA for 5 h, the frequency of 6TG-resistant mutations induced by gamma-rays decreased to one-sixth of that of irradiated cells incubated without 3'-dA. The decrease in the frequency of gamma-ray-induced mutations was dependent on the length of incubation time with 3'-dA. It is suggested that the inhibition of PLD repair by 3'-dA may be that of error-prone repair.

Animals↗
PubMed1990

Antimutagenic action of cobaltous chloride on radiation-induced mutations in cultured Chinese hamster cells.

The effects of cobaltous chloride on 8-azaguanine (8AG)-resistant mutations induced by gamma-rays or ultraviolet (UV) light in cultured Chinese hamster V79 cells were examined. Cobaltous chloride alone had no significant effects on survival and mutations of V79 cells at concentrations less than 1 x 10(-5) M. Cobaltous chloride at a concentration of 3 x 10(-6) M had a marked effect in reducing 8AG-resistant mutations induced by gamma-rays of 2-6 Gy, when cells were incubated for 6-7 days in the presence of cobaltous chloride after gamma-ray irradiation (posttreatment). The pretreatment of cells with cobaltous chloride for 6 days before gamma-ray irradiation reduced 8AG-resistant mutations induced by gamma-rays. Pre- or post-treatment with cobaltous chloride had no such effect on UV-induced mutations, however. The difference in responsiveness to cobaltous chloride between bacterial and mammalian cell systems is discussed.

Animals↗
PubMed1989

Crude tea extracts decrease the mutagenic activity of N-methyl-N'-nitro-N-nitrosoguanidine in vitro and in intragastric tract of rats.

The effects of tea extracts and their ingredients, catechins and L-ascorbic acid (AsA), on the mutagenicity of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were examined in vitro and in the stomachs of rats using E. coli WP2 and S. typhimurium TA100. The extracts of green tea and black tea leaves decreased the mutagenic activity of MNNG to E. coli WP2 in vitro in a desmutagenic manner. Catechins such as (-)-epigallocatechin from green tea leaves and the low-molecular-weight tannin fraction isolated from black tea extract with HP-20 resin also exhibited inhibitory effects against the mutagenic activity of MNNG. A desmutagenic effect of AsA on MNNG-induced mutagenicity was observed depending on the dose, though it was complicated. The effects were also demonstrated in the stomachs of rats by assaying the bacterial mutagenic in vitro; the tea extracts previously given orally to rats reduced the mutagenic activity of MNNG remarkably, though simultaneous administration showed less effect. The effectiveness of tea extracts for the decrease of MNNG-induced mutagenesis in vitro and in vivo suggests that the habitual drinking of tea may reduce the tumor-initiating potency of MNNG-type nitrosoureido compounds if they are formed in the stomach.

Animals↗
PubMed1988

Adsorption of mutagens by refined corn bran.

Refined corn bran (RCB), a dietary fiber derived from the mechanical refining of corn hulls, effectively adsorbed various environmental mutagens. When RCB was added at a concentration of 10 mg/ml to an aqueous solution of dinitropyrene (DNP), 91.6% of the mutagenicity towards Salmonella tester strain TA98 disappeared. Under similar conditions decreases in mutagenicity of DNP using wheat bran and cellulose powder were 58.4% and 43.0%, respectively. The adsorption of DNP to the fibers appeared irreversible since little mutagenicity was recovered by washing the treated fibers with aqueous buffer solutions of various pHs. Even with an organic solvent (methanol: ammonium hydroxide 50:1), only 2/3 of the mutagenicity of DNP was recovered. RCB could similarly adsorb mutagenic heterocyclic amines such as IQ, Trp-P-1, Trp-P-2, Glu-P-1, and Glu-P-2.

Adsorption↗
PubMed1986

Evaluation of the mouse mutant "wasted" as an animal model for ataxia telangiectasia. I. Age-dependent and tissue-specific effects.

The wasted mouse, an animal model proposed for the genetically transmitted human disease ataxia telangiectasia (AT), was examined for its biological, cytogenetic and biochemical properties. In affected homozygotes, a marked age-dependent decrease in the ratio of spleen and thymus to body weight, and a slight but significant decrease in the liver to body weight ratio were observed while no such change was found in the kidney. An age-dependent increase was observed in the frequency of both spontaneous and gamma-ray-induced chromosomal aberrations in bone marrow cells of wasted mice. In littermate control mice, neither of these alterations was observed in an age-dependent manner. The activity of a primer activating enzyme, which has been reported to be deficient in AT cells, also decreased with age in spleen cells, but not in liver cells of affected mice. However, alterations in apurinic DNA endonuclease activity were not detected in the developmental stages examined. These data indicate that this mouse mutant may serve as a useful animal model for studying the relationships between DNA repair and lymphoid tissue differentiation.

Aging↗
PubMed1986

Antimutagenic effects of 5-fluorouracil and 5-fluorodeoxyuridine on UV-induced mutagenesis in Escherichia coli.

Inhibitors of UV induction of the SOS function were screened. A log phase culture of E. coli PQ37 (sulA::lacZ, rfa, uvrA, Phoc) was irradiated with UV and then immediately subjected to culture for 2 h in a liquid LB medium containing each test compound. Expression of the SOS gene (sulA) was assayed by monitoring the levels of beta-galactosidase. In order to examine the inhibitory effects of test compounds on protein synthesis, the levels of the constitutive alkaline phosphatase were assayed in parallel. The total number of compounds tested was 233, including 44 food and feed additives, 23 naturally occurring compounds and derivatives, 21 antibiotics, 61 pesticides, 33 inorganics and 51 other chemicals. As a result, 5-fluorouracil and 5-fluorodeoxyuridine were found to inhibit considerably the UV induction of the SOS gene without any inhibition of protein synthesis. Mutagenesis induced by UV irradiation was depressed by the addition of either compound at non-toxic concentrations.

Alkaline Phosphatase↗
PubMed1986

The pyrogallol related compounds reduce UV-induced mutations in Escherichia coli B/r WP2.

Plant components with bio-antimutagenic activity were screened on UVC (254 nm)-induced mutagenesis using E. coli B/r WP2. The components with a pyrogallol moiety including gallic acid, (-)-epicatechin gallate (ECG), (-)-epigallocatechin (EGC) and (-)-epigallocatechin gallate (EGCG) reduced the mutation induction, but other components such as caffeic acid, chlorogenic acid and quercetin did not. The above compounds with a pyrogallol moiety were also effective on UVAB (295-400 nm)-induced mutagenesis, while they showed little effect on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced mutagenesis. As this bio-antimutagenic effect was not seen in the DNA excision-repair-deficient strains WP2s and ZA159, the activity by the above plant components might be based on the promotion of the excision-repair system in E. coli B/r WP2.

Escherichia coli↗
PubMed1986

Inhibitory effects of flavourings on mutagenesis induced by chemicals in bacteria.

The antimutagenic potential of twenty-five flavourings was tested against the activity of several kinds of chemical mutagens in Escherichia coli and Salmonella typhimurium. Anisaldehyde, ethylvanillin and vanillin showed marked antimutagenic effects on mutagenesis induced by 4-nitroquinoline 1-oxide, furylfuramide (AF-2), captan or methylglyoxal in E. coli WP2s. However, they were not effective against mutations provoked by 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) or 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) in S. typhimurium TA98. Despite the decrease in the number of mutants, a remarkable increase was observed in the survival of mutagen-treated WP2s cells after exposure to these flavourings. We assume that these compounds may act as bio-antimutagens by enhancing an error-free recombinational repair system, because this reactivation of survival was strictly dependent on the recA gene function but not on the lexA and uvrA gene functions.

Benzaldehydes↗
PubMed1986

Antimutagenic properties of lactic acid-cultured milk on chemical and fecal mutagens.

The antimutagenic properties of milk cultured with Lactobacillus bulgaricus and Streptococcus thermophilus were examined using streptomycin-dependent strains of Salmonella in an in vitro assay system. The mutagens utilized for testing included 2-(2-furyl)-3-(5-nitro-2-furyl) acrylamide, 4-nitroquinoline-N-oxide, and fecal mutagenic extracts from cats, monkeys, dogs, and other mammals. Both types of cultured milk exhibited antimutagenic activity on all mutagens used. Antimutagenic activities of the cultured milks with 2-(2-furyl)-3-(5-nitro-2-furyl) acrylamide and 4-nitroquinoline-N-oxide increased with incubation time but were thermolabile beyond 55 degrees C for 10 min.

4-Nitroquinoline-1-oxide↗
PubMed1986

Effect of DNA-damaging agents on isolated spleen cells and lung fibroblasts from the mouse mutant "wasted," a putative animal model for ataxia-telangiectasia.

Spleen cells from control and wasted (wst) mice, a putative animal model for the human genetic disease ataxia-telangiectasia, were tested for inhibition of replicative (semiconservative) DNA synthesis after treatments with bleomycin, gamma-irradiation, 4-nitroquinoline 1-oxide, and ultraviolet irradiation. The wasted cells were found to be more resistant than control cells to the first three treatments, but equally sensitive to ultraviolet light. Bleomycin-stimulated repair synthesis in spleen cells was also studied by the CsCl/bromodeoxyuridine method and found to be similar in cells from wasted and control animals. Similarly, no differences in sensitivity to killing by gamma-rays, as manifested by relative cloning efficiencies, were demonstrated between primary lung fibroblasts from mutant and control mice. We concluded that observed defects in DNA repair in wasted cells are not identical to those reported in human cells from ataxia-telangiectasia patients.

4-Nitroquinoline-1-oxide↗