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Biomedical subjects

K Kohda

Publications and source records attributed to K Kohda.

At least 127 records · Page 7Linked to original sources
PubMed1988

[A case of acute adult T-cell leukemia with long-term remission by cisplatin therapy].

A 37-year-old man was admitted because of general malaise, slight fever, pain in the knee joint and lower extremities, polydypsia, polyuria and skin lesion in September, 1985. The white blood cell count was 16,920/cmm with 41% of abnormal lymphoid cells with convoluted nuclei, which were compatible with adult T-cell leukemia (ATL). The serum calcium level was 15.1 mg/dl, serum LDH 307 IU/l, and the titer of anti-ATLA antibody in serum x 160. The cell surface phenotype of abnormal lymphocyte was OKT-3+, OKT-4+ and OKT-8-. Therefore the diagnosis of acute ATL was made. He was treated with cisplatin because VEPA therapy was not effective. About five months after the start of chemotherapy, he entered remission with almost complete disappearance of abnormal lymphocyte. The remission continued over twenty-nine months with maintenance therapy by cisplatin alone. The clinical course of this patient suggests that cisplatin could be applied to a case of ATL which is refractory to the conventional treatment.

Adult↗
PubMed1987

Formation of 8-hydroxyguanine residues in DNA treated with 4-hydroxyaminoquinoline 1-oxide and its related compounds in the presence of seryl-AMP.

The mechanism whereby treatment of DNA with 4-hydroxyaminoquinoline 1-oxide (4HAQO) in the presence of seryl-AMP leads to the formation of 8-hydroxyguanine (8-OH-Gua) residues in DNA (Kohda et al., this journal, 139, 626, 1986) has been studied. In the survey of other N-arylhydroxylamines, only 4HAQO analogues which could bind to DNA produced 8-OH-Gua. The amount of 8-OH-Gua varied depending on the structure of 4HAQO analogues and that of DNA. The formation of 8-OH-Gua was not inhibited by active oxygen scavengers. Possible mechanisms are discussed.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1987

Temperature-dependence of cytotoxicity of several genotoxicants in Chinese hamster V79 cells: bleomycin, paraquat, and some N-alkyl-N-nitrosoureas.

Chinese hamster V79 cultured cells were treated with bleomycin (BLM), paraquat (PQ), N-methyl-N-nitrosourea (MNU), and ACNU (an anti-cancer agent) at 30-43 degrees C. The survival fractions normalized by those released from heat-death were plotted vs. the integrated doses of the chemical. Arrhenius analysis of the cell inactivation by the chemical was made. The results revealed that BLM and PQ exerted synergistic cytotoxicity with hyperthermia, whereas MNU and ACNU exerted temperature-dependent cytotoxicities obeying the Arrhenius law.

Animals↗
PubMed1987

Inhibitory effect of heavy water on mutability of chemically injured Escherichia coli cells.

After E. coli cells (WP2 and WP2uvrA) were treated with chemical mutagens (methyl methanesulfonate, MMS; N-methyl-N-nitrosourea, MNU; 4-nitroquinoline 1-oxide, 4NQO) in 1/15 M phosphate buffer, the mutability of the treated cells plated on a D2O-agar plate was compared with that plated on an ordinary H2O-agar plate. The mutation frequency decreased more or less on the D2O-agar plate. The D2O-substitution effects, as termed by the relative mutation frequencies (MFD2O/MFH2O), are 0.92 for MMS, 0.29 for MNU, and 0.42 for 4NQO in WP2, and 0.68 for MMS, 0.49 for MNU, and 0.16 for 4NQO in WP2uvrA. The D2O effect seemed to be partly related to the function of the uvrA gene-associated products. The pH dependence of mutability was discussed in connection with the D2O-substitution effect.

4-Nitroquinoline-1-oxide↗
PubMed1986

Formation of 8-hydroxyguanine residues in cellular DNA exposed to the carcinogen 4-nitroquinoline 1-oxide.

8-Hydroxyguanine (8-OH-Gua) residues were formed in DNA of Ehrlich ascites cells exposed to the carcinogen 4-nitroquinoline 1-oxide. Formation of 8-OH-Gua was confirmed by chemical treatment of calf thymus DNA with the proximate metabolite of this carcinogen, 4-hydroxyaminoquinoline 1-oxide, together with seryl-adenosine monophosphate. The ratio of the rates of formations of 8-OH-Gua and the quinoline-bound adducts was about 0.2-0.3. A conceivable mechanism of formation of 8-OH-Gua is proposed.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1986

Ornithine decarboxylase activity and DNA synthesis in rats after long term treatment with butylated hydroxyanisole, sodium saccharin or phenobarbital.

Ornithine decarboxylase (ODC) activity and DNA synthesis were measured in the forestomach, urinary bladder and liver of rats given diet containing 2% butylated hydroxyanisole (BHA), 5% sodium saccharin (SS) or 0.05% phenobarbital (PB) for 21 weeks. ODC activity was not increased significantly in any of these organs in any of the groups, but the labeling index (LI) of the forestomach epithelium was increased by BHA and PB, and that of the urinary bladder epithelium by SS. PB did not increase the LI of the liver. These results do not indicate any relation between the effects of promoters, and the ODC activity or DNA synthesis in non-initiated target organs.

Animals↗
PubMed1986

Aminations of guanosine and deoxyguanosine with hydroxylamine-O-sulfonic acid and 2,4-dinitrophenoxyamine. Dependence on the reaction medium.

Amination of guanosine (Guo) with 2,4-dinitrophenoxyamine in aqueous DMF gave 7-amino-Guo, which was readily converted to 8,5'-O-cyclo-Guo, and 8-hydroxy-Guo. Deoxyguanosine (dG) gave only deglycosylated 7-amino-G under the same reaction condition. Aminations of Guo and dG with hydroxylamine-O-sulfonic acid above pH 9 gave the corresponding 1-amino derivatives, whereas those in acidic media at pH 2-4 gave 8-amino-Guo and 7-amino-G as the main products, respectively. Amination of Guo in neutral media gave 1-amino-Guo and decomposed products of 7-amino-Guo. The mechanisms of these amination reactions are described.

Deoxyguanosine↗
PubMed1985

Studies on chemical carcinogens and mutagens. XXIX. Mutagenic N-trimethylsilylmethyl-N-nitrosourea as a biological alkylating agent equivalent to N-methyl-N-nitrosourea (MNU).

N-Trimethylsilylmethyl-N-nitrosourea (TMS-MNU), a silicon analogue of N-neopentyl-N-nitrosourea (neoPNU), was assayed for mutagenicity and/or cytotoxicity on a series of E. coli B tester strains, S. typhimurium TA100, Chinese hamster V79, and cultured murine leukemia L1210 cells. All the biological activities demonstrated in this study reveal that this nitrosourea is a biological methylating agent equivalent to N-methyl-N-nitrosourea (MNU) but definitely distinguished from all the other alkylnitrosoureas examined so far, including neoPNU (the carbon analogue of TMS-MNU). The proposed molecular mechanism is that trimethylsilylmethanediazohydroxide is produced by hydrolytic activation of TMS-MNU and undergoes a nucleophilic cleavage of the Si--CH2 chemical bond at a high rate to form methanediazohydroxide (the reactive intermediate of MNU) which, in turn, methylates the informational biopolymer leading to mutagenesis.

Animals↗
PubMed1984

Automated enzymatic determination of serum and urine creatine using the Abbott ABA-200.

A new enzymatic method is described for the determination of creatine in serum and urine with Abbott ABA-200. The measurement is accomplished by transforming creatine to formic acid in a reaction catalyzed by creatinase (creatine amidinohydrolase), sarcosine oxidase and formaldehyde dehydrogenase (see Figure 1). The assay takes less than 20 minutes. The standard response is linear for creatine concentrations up to 10 mg/dL (serum) and 80 mg/dL (urine). The coefficients of variation at 0.69 mg/dL (serum) and 4.93 mg/dL (urine) for within-day determination were less than 4% and, for between-day determination, were less than 5%. Results obtained by this procedure on one hundred serum and urine samples conformed well with a manual enzymatic method and the Folin method. The method is useful for the automated measurement of creatine in serum and urine.

Aldehyde Oxidoreductases↗