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Dive into the research topics where Hideyo Yamaguchi is active.

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Featured researches published by Hideyo Yamaguchi.


Medical Mycology | 1973

Mode of action of clotrimazole

Kazuo Iwata; Hideyo Yamaguchi; Tamio Hiratani

Clotrimazole, a synthetic antifungal agent, was fungicidal to growing cultures of one strain of Candida albicans. Cultures treated with the drug were osmotically stable. It had no effect on the respiratory activity of intact C. albicans cells or their isolated mitochondria with exogenous NADH and succinate as substrates. Studies with radioactive precursors revealed that clotrimazole inhibited synthesis of both protein and RNA by intact cells to a greater extent than that of DNA, lipid and wall polysaccharides. However, even with higher levels of the drug, the effect on endogenous or poly U-directed polypeptide synthesis by cell-free extracts was consistently negative. The minimum fungicidal concentration of the drug caused a marked enhancement of leakage of intracellular phosphorus compounds into the ambient medium with concomitant breakdown of cellular nucleic acids. Acceleration of K-efflux in treated cells also occurred to the corresponding extent. Both of these events began rapidly and extensively aft...


Antimicrobial Agents and Chemotherapy | 1977

Antagonistic Action of Lipid Components of Membranes from Candida albicans and Various Other Lipids on Two Imidazole Antimycotics, Clotrimazole and Miconazole

Hideyo Yamaguchi

The growth-inhibitory activity of two imidazole antimycotics, clotrimazole and miconazole, against Candida albicans was significantly reversed when lipid extracts from protoplast membranes of the same organism were added to the assay medium together with the drugs. Of four major classes of lipids further separated from them, viz., phospholipids, triglycerides, sterol esters, and free sterols, the former two were capable of counteracting both drugs, whereas the latter two were not. However, even with phospholipids or triglycerides, no antagonism was noted when they were saturated by catalytic hydrogenation before use. The antagonistic effect of varying classes of commercial lipids, including phospholipids, acylglycerides, sterols, and fatty acids, was also studied by means of the agar diffusion technique. Significant antagonism to both drugs was observed with: (i) phospholipids with an unsaturated acyl group; (ii) acylglycerides, the ester portion of which consists of unsaturated fatty acid; (iii) ultraviolet-activated sterols; and (iv) unsaturated fatty acids of cis-configuration. By contrast, none of the saturated phospholipids and acylglycerides nor sterols was effective as an antagonist. With the exception only of lauric acid, all of a series of saturated fatty acids and unsaturated trans-fatty acids ranging from C8 to C18 in chain length were either minimally effective or completely ineffective. Essentially, there was no qualitative difference between clotrimazole and miconazole in the response to these various lipids.


Medical Mycology | 1973

Electron microscopic studies on the mechanism of action of clotrimazole on Canada albicans

Kazuo Iwata; Y. Kanda; Hideyo Yamaguchi; Masako Osumi

During investigations on the mechanism of action of clotrimazole, electron microscopy was undertaken. When Candida albicans cells were exposed to a fungistatic concentration (3 × 10-5 M) of the drug, there was no cytological change except the swelling of mitochondria. Exposure to a fungicidal level (1·5 × 10-4 M) produced unusual development and destruction of certain membranous structures. The cell membrane frequently invaginated to form extensive and complex intracytoplasmic membranes varying in size, shape and complexity. Such structures were usually close to vacuoles. Numerous membrane particles occurred between the retracted cell membrane and the cell wall (lomasomes). In contrast, the nuclear membrane as well as the mitochondrial inner membrane deteriorated markedly. Intracytoplasmic vacuoles increased in size and number and, often contained multivesicular structures. Plasmolysis, accompanied by complete disorganization of cytoplasmic structures, appears to be the terminal event. The nature and the ...


Antimicrobial Agents and Chemotherapy | 1979

Effect of Fatty Acyl Group and Sterol Composition on Sensitivity of Lecithin Liposomes to Imidazole Antimycotics

Hideyo Yamaguchi; Kazuo Iwata

The specific affinity for membrane lipids and the membrane selectivity of three imidazole derivatives, clotrimazole, miconazole, and econazole, were studied using various types of liposomes with respect to the lecithin fatty acyl group composition and the liposome content and composition of sterol as membrane models. The sensitivity of liposomes to these drugs was primarily dependent upon the lecithin fatty acyl group composition. With sterol-free liposome systems, each imidazole induced maximum release of trapped glucose as a marker from the unsaturated dioleoyl lecithin liposomes, minimum release from the saturated dipalmitoyl lecithin liposomes, and intermediate release from egg lecithin liposomes. The sensitivity of the dipalmitoyl lecithin liposomes to any imidazole drug was not influenced by the incorporation of cholesterol or ergosterol. On the other hand, clotrimazole-induced permeability changes of liposomes prepared from unsaturated dioleoyl lecithin or egg lecithin were greatly enhanced by the incorporation of ergosterol, whereas they were suppressed by cholesterol incorporation. The sensitivity of liposomes prepared from these unsaturated lecithins to miconazole and econazole was also augmented by ergosterol incorporation, although it was scarcely altered by cholesterol incorporation. Negatively charged liposomes were more sensitive to the three imidazole drugs than positively charged liposomes.


Chemotherapy | 1978

Mode of Action of 6-Cyclohexyl-l-hydroxy-4-methyl-2(1H)-pyridone Ethanolamine Salt (Hoe 296)

Kyoko Sakurai; Takashi Sakaguchi; Hideyo Yamaguchi; Kazuo Iwata

Mode of action studies were made with Hoe 296, a new synthetic antimycotic, mainly in Candida albicans. The specific parameters examined included possible effects on (i) osmotic fragility, (ii) respiration, (iii) uptake and incorporation of radioactive leucine and adenine, and (iv) leakage or efflux of intracellular K+ and other materials. As a result, fungitoxic activity of Hoe 296 appears to be attributed to inhibition of uptake of precursors of macromolecular syntheses from the medium. Uptake and accumulation of leucine in the internal pool of starved cells was more susceptible to the drug than subsequent incorporation into proteins. Hoe 296 was also effective in altering the cell permeability, but greater drug concentrations were required to induce appreciable leakage of cellular constituents, such as 260 nm-absorbing materials, folin-positive substances and potassium ions, from the cells. Osmotic fragility or endogenous respiration was virtually insensitive to the drug. Partial inhibition by relatively high concentrations of Hoe 296 of the respiratory activity of yeast cells or mitochondria therefrom with exogenous substrates can be explained by decreased uptake of the substrates from the medium.


Biochemical and Biophysical Research Communications | 1990

The mechanism of antifungal action of (S)-2-amino-4-oxo-5-hydroxypentanoic acid, RI-331: the inhibition of homoserine dehydrogenase in Saccharomyces cerevisiae.

Hiroshi Yamaki; Mineko Yamaguchi; Hiromi Imamura; Hideo Suzuki; Toshio Nishimura; Hidehiko Saito; Hideyo Yamaguchi

We have explored the mechanism by which an antifungal antibiotic, (S)-2-amino-4-oxo-5-hydroxypentanoic acid, RI-331, preferentially inhibits protein biosynthesis in Saccharomyces cerevisiae, by inhibiting the biosynthesis of the aspartate family of amino acids, methionine, isoleucine and threonine. This inhibition was effected by inhibiting the biosynthesis of their common intermediate precursor homoserine. The target enzyme of RI-331 was homoserine dehydrogenase (EC.1.1.1.3) which is involved in converting aspartate semialdehyde to homoserine in the pathway from aspartate to homoserine. The enzyme is lacking in animals. So the antibiotic is selectively toxic to prototrophic fungi.


Medical Mycology | 1992

Granulocyte-colony stimulating factor facilitates the restoration of resistance to opportunistic fungi in leukopenic mice.

Katsuhisa Uchida; Y. Yamamoto; T.W. Klein; H. Friedman; Hideyo Yamaguchi

Administration of recombinant human granulocyte-colony stimulating factor (G-CSF), which induces hemopoietic precursor cells to proliferate and differentiate into neutrophils, protected leukopenic mice infected with opportunistic fungi. Mice were injected with cyclophosphamide and were then subcutaneously (s.c.) or intravenously (i.v.) administered 15-120 micrograms G-CSF kg-1 day-1 for 3 days. The number of peripheral blood neutrophils in the G-CSF treated mice was significantly increased 48 h after G-CSF administration. All leukopenic mice infected with either Candida albicans, Cryptococcus neoformans or Aspergillus fumigatus were significantly protected by treatment with the G-CSF. Moreover, G-CSF treatment caused a decrease in the number of viable yeasts in kidneys of Candida infected mice. These data suggest that prophylactic therapy with G-CSF may be useful against fungal infections in an immunocompromised host.


Medical Mycology | 1974

Mycelial Development and Chemical Alteration of Candida albicans from Biotin Insufficiency

Hideyo Yamaguchi

A strain of Candida albicans in a chemically defined basal medium supplemented with biotin at optimal (10 ng/ml) and suboptimal (0.1 ng/ml) concentrations for growth developed predominantly into yeast (Y) and mycelial (M) phases, respectively. The M-phase thus grown showed an increase in alkali-insoluble glucan and a decrease in RNA and mannan as compared with Y- cells grown in biotin-optimal medium. Changes in the cell morphology as well as the chemical composition due to biotin insufficiency were almost completely restored by the supplementation of glyceryl mono-oleate to the medium. However, the supplementation of aspartie acid, accentuated both morphological and biochemical properties which were characteristic for biotin-insufficient cells. The correlation of morphology with the composition of major cellular constituents, especially cell wall polysaceharides, is discussed in relation to the casual role of certain biotin-participating metabolic processes in this fungus.


Biochemical and Biophysical Research Communications | 1965

Inhibition of RNA and DNA polymerase reactions by pluramycin A

Nobuo Tanaka; Kazuo Nagai; Hideyo Yamaguchi; Hamao Umezawa

Pluramycin A, isolated from the culture of Streptomyces pluricolorescens by Maeda et al (19561, is a basic antibiotic of orange needle crystals. The antitumor and antibacterial activity was reported by Takeuchi et al (1957). Lein et al (1962) observed phage induction of lysogenic bacteria by pluramycin. We investigated the activity of pluramycin A on macromolecular syntheses and observed that the antibiotic inhibits both protein and nucleic acids syntheses in the intact cells of bacteria. The effects were further investigated, using cell-free systems. The results are described in this communication. Protein synthesis was not significantly affected in bacterial cell-free systems but RNA and DNA polymerase reactions were markedly inhibited by the antibiotic, which was suggested to bind with DNA by the thermal transition curve. Effects on protein synthesis in cell-free systems from E. coli: Pluramycin A was observed to exhibit no significant effects on 14C-leucine incorporation into protein and polyuridylate-directed polyphenylalanine synthesis in cell-free systems obtained from exponentially growing cells of E. coli B. The method employed principally followed the one developed by Nirenberg and Matthaei (1961). The results are summarized in Tables 1 and 2.


Biochemical and Biophysical Research Communications | 1989

Bleomycin hydrolase is a unique thiol aminopeptidase

Chiaki Nishimura; Hideo Suzuki; Nobuo Tanaka; Hideyo Yamaguchi

Bleomycin hydrolase, which hydrolyzes the carboxamide bond in the pyrimidoblamic acid moiety of the bleomycin molecule, also cleaved several p-nitroanilide substrates with a neutral or basic amino acid residue and dipeptide substrates such as L-leucyl-glycine. The activity of bleomycin hydrolase was inhibited by two thiol protease inhibitors, E-64 and leupeptin, as well as by N-ethylmaleimide. These results suggest that bleomycin hydrolase is a thiol aminopeptidase. Magnesium ion, sodium chloride, ethylenediaminetetraacetic acid and 1,2-dihydroxybenzene-3,5-disulfonic acid specifically activated the enzymatic hydrolysis of L-arginine-p-nitroanilide, but did not that of L-leucine-p-nitroanilide. Lineweaver-Burk plots showed that Km values of the enzymatic activity for L-arginine-p-nitroanilide were altered by these reagents, although Vmax values were almost unaltered.

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Kazutoh Takesako

Center for Cell and Gene Therapy

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Masako Osumi

Japan Women's University

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