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Biomedical subjects

A Someya

Publications and source records attributed to A Someya.

7 recordsLinked to original sources
PubMed1979

Morphological changes of Escherichia coli induced by bicyclomycin.

Electron microscopic studies with Escherichia coli revealed that bicyclomycin inhibits septum formation and converts the cells to filamentous forms. The antibiotic induced high undulation and numerous blebs of the outer membrane. Sometimes cytoplasmic contents leaked into the lumen of the bleb through a disrupted region of the membrane. Breakage of the outer membrane or blebs led to cell lysis. Electron-dense masses of amorphous material and vesicles were found in the cytoplasm.

Anti-Bacterial Agents↗
PubMed1979

Interaction of aminoglycosides and other antibiotics with actin.

Skeletal muscle actin was found by centrifugation, turbidity, and viscosity measurements to form polymers upon addition of aminoglycosides, viomycin, polymyxin B, and tetracycline. A linear relationship was observed between the amount of actin polymerization and the number of primary amino groups on the aminoglycoside antibiotics except kanamycin. Of the antibiotics studied, neomycin was most efficient in actin polymerization. Polymerization of actin was not significantly induced by kasugamycin, chloramphenicol, erythromycin, benzylpenicillin, angustmycin A, formycin, actinomycin D, and mitomycin C. Aminoglycosides and viomycin were demonstrated to inhibit the acto-HMM Mg(2+)-ATPase reaction but did not significantly affect HMM Mg(2+)-ATPase activity. It was found by equilibrium dialysis that [(3)H]dihydrostreptomycin bound to actin.

Actins↗
PubMed1979

Active groups of bicyclomycin and the reaction with thiols.

The binding of [14C]bicyclomycin to whole cells of E. coli and to the inner membrane proteins was inhibited by dithiothreitol and 2-mercaptoethanol. The reactivity of the drug with the sulfhydryl group was further studied, using methanethiol as a model compound. The kinetics revealed that the reaction was of pseudo-first-order in excess of thiolate anion. Analysis with gas chromatography-mass spectrometry showed that the main product was an adduct of thiol with bicyclomycin in an equal molar ratio. The structure of the adduct was determined by 1H-NMR spectrometry, showing that thiolate attacked the olefinic double bond of the antibiotic. 3'-Acyl derivatives of bicyclomycin did not significantly affect the binding of [14C] bicyclomycin to inner membrane proteins of E. coli. The results suggested that 4,5-double bond hydrocarbons and 3'-hydroxy group of bicyclomycin participate in the binding to E. coli inner membrane proteins, which are presumably the receptors of the antibiotic. The olefinic double bond seems to be the active center of bicyclomycin, reacting with the sulfhydryl group of the receptor protein, although the whole molecular is needed for the activity.

Anti-Bacterial Agents↗
PubMed1979

DNA strand scission induced by adriamycin and aclacinomycin A.

The binding of adriamycin and aclacinomycin A with PM2 DNA, and the consequent cleavage of DNA have been demonstrated by agarose gel electrophoresis, using an ethidium bromide assay. Adriamycin was observed to induce a single strand scission of DNA in the presence of a reducing agent, but aclacinomycin A caused much less degree of DNA breaks. The DNA cleavage was enhanced by Cu2+ and Fe2+, but not significantly by Ni2+, Zn2+, Mg2+ and Ca2+, suggesting that reduction and auto-oxidation of the quinone moiety and H2O2 production participate in the DNA-cutting effect. The DNA degradation was dependent upon concentrations of the anthracyclines and CuCl2. The degree of DNA cleavage at 0.04 mM adriamycin was similar to that at 0.4 mM aclacinomycin A in the presence of 1 mM NADPH and 0.4 mM CuCl2. DNA was degraded to small fragments at 0.4 mM adriamycin and 0.2 mM CuCl2. The anthracycline-induced DNA cleavage was stimulated by H2O2, but partially inhibited by potassium iodide, superoxide dismutase, catalase and nitrogen gas atmosphere. The results suggested that both free radical of anthracycline quinones and hydroxyl radical directly react with DNA strands.

Antibiotics, Antineoplastic↗