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T Onoda

Publications and source records attributed to T Onoda.

At least 37 records · Page 2Linked to original sources
PubMed1989

Effect of protonophore on growth of Escherichia coli.

When 20 microM of carbonyl cyanide-m-chlorophenyl hydrazone (CCCP) were added to a M medium containing glucose as an energy source at pH 7.6, the Escherichia coli K12 strain 3301 was able to grow, whereas on the medium containing NaCl above 200 mM, the growth was remarkably suppressed by the addition of 20 microM CCCP. Furthermore, when glucose was replaced by either glycerol or lactate as an energy source, no growth occurred in the presence of 20 microM of CCCP. When glycerol was used as a substrate, O2 consumption by whole cells was observed in the presence of 20 microM of CCCP, but not in the case of lactate. We found that 14C-lactate uptake was completely inhibited by the addition of 20 microM of CCCP. The cells, which were incubated for 24 h on a M medium containing glucose in the presence of 20 microM of CCCP produced many more organic acids (mainly, acetate and lactate) than was the case in its absence. It appears that the influx process of external lactate when this was added as an energy source, was completely inhibited by addition of CCCP (20 microM), but the efflux process of lactate that was produced by glycolysis, was not influenced by this protonophore. On the other hand, it is suggested that on the hyposalts medium, a proton motive force (pmf) is not necessary for the growth of the strain 3301, whereas pmf is necessary for growth to occur.

Carbonyl Cyanide m-Chlorophenyl Hydrazone↗
PubMed1988

Effects of Ca2+ and a protonophore on growth of an Escherichia coli L-form.

The influence of Ca2+ ions on the growth of an L-form (NC7) derived from Escherichia coli K12 was investigated. In a medium containing NaCl as osmotic stabilizer 1 mM-Ca2+ was required for optimal growth of the L-form, while with KCl as osmotic stabilizer, in a medium containing 0.1 or 1.0 mM-Ca2+, optimium growth was observed at 32 and 37 degrees C, respectively. When the L-form, growing exponentially at 32 degrees C in medium containing KCl and 0.1 mM-Ca2+, was shifted to 37 degrees C growth was strikingly suppressed. In contrast, the suppression of growth in the presence of 1.0 mM-Ca2+ at 32 degrees C was relieved when the culture was shifted to 37 degrees C. When the protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP), at a final concentration of 10 microM, was added to a medium containing NaCl and sucrose as osmotic stabilizers, together with 10 mM-glucose, the parent strain could grow exponentially. In contrast, growth of the L-form was completely stopped by 10 microM-CCCP under the same conditions. In the presence of 20 microM-CCCP, the L-form accumulated more than twice as much 45Ca as in the absence of the protonophore. Thus, it is suggested that growth of the L-form NC7 is coupled to the protonmotive force. Possible mechanisms for the coupling of calcium to growth of the L-form are discussed.

Calcium↗
PubMed1987

Morphology, growth and reversion in a stable L-form of Escherichia coli K12.

An L-form isolated from Escherichia coli K12 by sequential treatment with N-methyl-N'-nitro-N-nitrosoguanidine and lysozyme was adapted to grow in hyperosmolar liquid cultures. It was stable in the absence of antibiotic when cultured in brain heart infusion (BHI) broth containing NaCl and CaCl2, the optimal concentrations being 0.34 M and 1 mM, respectively. No growth of the L-form was observed when CaCl2 was not added to BHI medium containing 0.34 M-NaCl. On the other hand, when KCl replaced NaCl as the osmotic stabilizer, growth of the L-form was repressed in the presence of CaCl2. Electron microscopy of the L-form confirmed the absence of a cell wall. A revertant strain derived from the L-form grew as a stable bacillary form in BHI medium without osmotic stabilizer. The growth characteristics of the revertant strain resembled those of the parent strain. The revertant strain produced L-forms in the presence of NaCl.

Culture Media↗
PubMed1985

Antitumor activity of D-mannosamine in vitro: cytotoxic effect produced by mannosamine in combination with free fatty acids on human leukemia T-cell lines.

Cytotoxic effects of mannosamine and free fatty acids on human malignant T-lymphoid cell lines derived from patients with T-cell leukemia were investigated. The combination of mannosamine and an unsaturated fatty acid (oleate or linoleate) produced more striking cytotoxic effects on malignant lymphoid cells than on normal human lymphocytes. The amino sugars glucosamine or mannosamine in the combination caused a synergistic cytotoxic effect, while the other carbohydrates (N-acetylmannosamine, N-acetylglucosamine, or mannose) had little effect. On the other hand, the effect of saturated fatty acids (palmitate or stearate) in the same system was nil. An unsaturated fatty acid (oleate) caused an increase in lipid fluidity of the surface membrane in MOLT-4 lymphoid cells, which possess higher lipid fluidity in combination with mannosamine, while saturated fatty acids had no effect on the fluidity properties of the membrane lipids (even in the presence of mannosamine). The relationship between mannosamine and unsaturated fatty acids in cytolysis was discussed.

Carbohydrates↗
PubMed1982

Antitumor activity of D-mannosamine in vitro: different sensitivities among human leukemia cell lines possessing T-cell properties.

D-Mannosamine is toxic to human malignant T-lymphoid cell lines derived from patients with T-cell leukemia. We observed heterogeneity of mannosamine susceptibility among those cell lines. The leukemic T-cell lines, subgrouped according to the degree of mannosamine inhibition on nucleic acid biosyntheses, were: Subgroup 1, HPB-MLT cells; Subgroup 2, CCRF-HSB-2 and HPB-ALL cells; and Subgroup 3, MOLT-4 cells. The most sensitive line, HPB-MLT, originated from the patient with adult T-cell leukemia. The cytotoxicity of mannosamine was potentiated by a fatty acid, sodium oleate, at concentrations that were noncytolytic, and the interaction between the two drugs was synergistic. These results would suggest that mannosamine induces changes in the membrane structure of the leukemia cells. Thus, the primary target of the tumoricidal activity of mannosamine may also be the cellular membranes.

Adult↗