The Journal of Antibiotics
Online ISSN : 1881-1469
Print ISSN : 0021-8820
ISSN-L : 0021-8820
Volume 41 , Issue 1
Showing 1-23 articles out of 23 articles from the selected issue
  • MICHAEL N. GWYNN, STEPHEN J. Box, ALLAN G. BROWN, MARTIN L. GILPIN
    1988 Volume 41 Issue 1 Pages 1-6
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    A bacterial soil isolate designated 326-32B produces a new member of the monobactam series of antibiotics, MM 42842, and the bulgecins. Identification studies show isolate 326-32B to be a strain of Pseudomonas cocovenenans which is a species previously noted for the production of toxoflavin. A description of P. cocovenenans does not appear to have been previously published and the identity of strain 326-32B was established by means of a direct comparison with the deposited organism P. cocovenenans NCIB 9450.
    The properties of strain 326-32B, and P. cocovenenans NCIB 9450 were compared with those of the monobactam and bulgecin producing organisms Pseudomonas acidophila ATCG 31363 and Pseudomonas mesoacidophila ATCC 31433. The four organisms were found to share certain properties, including the ability to grow at pH 4.0.
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  • STEPHEN J. Box, ALLAN G. BROWN, MARTIN L. GILPIN, MICHAEL N. GWYNN, SI ...
    1988 Volume 41 Issue 1 Pages 7-12
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    A new member of the monobactam family of β-lactam antibiotics, designated MM 42842, has been detected in a culture of Pseudomonas cocovenenans. The production, isolation and some properties of the antibiotic are described. Structural studies show MM 42842 to be closely related to the previously described antibiotic sulfazecin.
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  • RAYMOND COOPER, ANN C. HORAN, FRANK GENTILE, VINCENT GULLO, DAVID LOEB ...
    1988 Volume 41 Issue 1 Pages 13-19
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    A new antifungal compound, Sch 37137, was isolated from the cultured broth of a Micromonospora sp., SCC 1792. Sch 37137 is structurally related to A 19009, a dipeptide previously discovered from a Streptomyces sp. The compound was weakly active against species of Candida and dermatophytes (mean MICs ≥128μg/ml) in Sabouraud dextrose, yeastnitrogen and modified Eagles minimum essential media; however activity against Candida sp. (mean MICs ≥12μg/ml) and dermatophytes (mean MICs ≥0.8μg/ml) significantly improved in MA medium.
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  • VINCENT GULLO, MICHAEL CONOVER, RAYMOND COOPER, CLAIRE FEDERBUSH, ANN ...
    1988 Volume 41 Issue 1 Pages 20-24
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    A novel anti-inflammatory compound, Sch 36605, belonging to the blasticidin family of nucleoside compounds was isolated from the fermentation filtrate of a Streptomyces sp. Sch 36605, as well as blasticidin S, demonstrated anti-inflammatory activity in the reverse passive Arthus reaction and the adjuvant arthritic rat at doses ranging between 1-10mg/kg and 0.3-6.0 mg/kg, respectively. A minor component, Sch 36606, co-produced in the fermentation was isolated and identified as a known compound in the blasticidin family of compounds.
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  • TAKESHI ANDO, YASUHISA TSURUMI, NOBUTAKA OHATA, ITSUO UCHIDA, KEIZO YO ...
    1988 Volume 41 Issue 1 Pages 25-30
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    Vinigrol, produced by a fungal strain identified as Virgaria nigra, was extracted from the cultured mycelium, purified by solvent extraction followed by chromatography on silica gel and then isolated as crystals (C20H34O3, mp 108°C). Vinigrol decreased arterial blood pressure of anesthetized normotensive rats dose-dependently when administered intravenously. Vinigrol inhibited platelet activating factor and epinephrine induced platelet aggregation.
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  • TAKESHI ANDO, KEIZO YOSHIDA, MASAKUNI OKUHARA
    1988 Volume 41 Issue 1 Pages 31-35
    Published: January 25, 1988
    Released: April 19, 2006
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    Vinigrol, a novel diterpene produced by Virgaria nigra, was tested orally in conscious spontaneously hypertensive rats (SHR) to confirm its antihypertensive activity. Vinigrol (2 mg/kg, po) decreased the mean arterial blood pressure of SHR by approximately 15% for at least 6 hours.
    Vinigrol induced contraction of rat aortic smooth muscle preparation at 1.5×10-7M, the contraction was blocked by nilvadipine, a Ca2+ entry blocker, but was not inhibited by prazosin or yohimbine.
    Radio-receptor binding assay of α adrenoceptors of rat brain membrane revealed that vinigrol had no affinity for these receptors.
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  • GREGORY M. BRILL, JAMES B. MCALPINE, DAVID WHITTERN
    1988 Volume 41 Issue 1 Pages 36-44
    Published: January 25, 1988
    Released: April 19, 2006
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    Tirandalydigin a structurally unique hybrid of the tirandamycin-streptolydigin families of tetramic acid antibiotics has been isolated from the fermentation beers of Streptomyces sp. AB-1006A-9. The structure of this anti-anaerobic antibiotic has been characterized based upon NMR, UV and mass spectrometric data.
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  • MITSUO KOENUMA, NAOMI UCHIDA, KENJI YAMAGUCHI, YOSHIMI KAWAMURA, KOICH ...
    1988 Volume 41 Issue 1 Pages 45-52
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    A new antibiotic complex was isolated from the fermentation broth of Streptomyces aburaviensis PA-39856. The individual factors, demethylolivomycins A, B and demethylchromomycins A2, A3 were separated and purified by preparative HLC. These antibiotics possess high activities against Gram-positive bacteria and P388 leukemia in mice.
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  • YOHKO YOSHIMURA, MITSUO KOENUMA, KOICHI MATSUMOTO, KAZUO TORI, YOSHIHI ...
    1988 Volume 41 Issue 1 Pages 53-67
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    Detailed studies on the 13C and 1H NMR spectra of chromomycins A2 and A3, olivomycins A and B, and their derivatives clarified the assignment of many signals which had been unassigned or erroneously reported in the literatures. The revised assignments for chromomycin A3 and olivomycin A include the assignment of a key 13C signal used to discuss the saccharide linkage in question. Structure analyses based on the revised assignments support the α, 1→3-bond between components of the disaccharide moiety in the molecules. Some general information useful for structure analysis of saccharides is also reported.
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  • MITSUO KOENUMA, YOHKO YOSHIMURA, KOICHI MATSUMOTO, YOSHIHIRO TERUI
    1988 Volume 41 Issue 1 Pages 68-72
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    Structure determination using NMR spectroscopy of new aureolic acid analogues, demethylchromomycins A2 and A3 and demethylolivomycins A and B produced by Streptomyces aburaviensis PA-39856, is described.
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  • CHANG HAN KIM, TOYOSHIGE ENDO, HIROSHI YONEHARA
    1988 Volume 41 Issue 1 Pages 73-80
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    In mikamycin B fermentation, some procedures were examined to remove the participation of mikamycin B lactonase, which reduces mikamycin B titers. Addition of enzyme inhibitors and control of pH resulted in the elimination of the enzyme activity, and in the stimulation of antibiotic production.
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  • TADASHI FUJII, KENICHI SATO, EISAKU YOKOTA, TETSURO MAEJIMA, MATSUHISA ...
    1988 Volume 41 Issue 1 Pages 81-85
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    A broad substrate-spectrum β-lactamase was purified from Flavobacterium meningosepticum GN14059. The purified enzyme gave a single protein band on SDS-polyacrylamide gel electrophoresis. The molecular weight was estimated to be about 30, 000 and the isoelectric point was 5.1.
    The enzyme hydrolyzed various β-lactam antibiotics including oxyiminocephalosporins and aztreonam. Relative rates, with cephaloridine as 100, were cephalothin 200, cefazolin 48, cefuroxime 153, cefotaxime 51, ceftazidime 20, ampicillin 26, carbenicillin 19, and aztreonam 20.
    The enzyme activity was inhibited by clavulanic acid, sulbactam, imipenem and cephamycins.
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  • MASAKI HIRAOKA, SHINJI MASUYOSHI, SUSUMU MITSUHASHI, Kozo TOMATSU, MAT ...
    1988 Volume 41 Issue 1 Pages 86-93
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    Cephalosporinases of Enterobacter cloacae and Citrobacter freundii were responsible for resistance to newer cephalosporins such as cefotaxime and ceftazidime but not BMY-28142. Interaction of these cephalosporins including hydrolysis, binding, inhibition, and inactivation with Cephalosporinases from E. cloacae GN7471 and C. freundii GN7391 were studied. BMY-28142 at 0.1 μM was much more stable against the both enzymes than cephalothin, but more hydrolyzable than cefotaxime and ceftazidime at higher concentration such as 100 μM. Because of low affinity for the enzymes, i.e. large Km and ki, the calculated hydrolysis rate of BMY-28142 at 0.1 μM was smaller than those of cefotaxime and ceftazidime, that explained the difference in activity against cephalosporinase-producing strains between BMY-28142 and cefotaxime or ceftazidime. The effects of cephalosporinase production on susceptibility of Escherichia coli omp mutants were examined using a plasmid having cephalosporinase gene of C. freundii GN346. Decrease in susceptibility of E. coli by cephalosporinase production was larger in the strain lacking outer membrane proteins (Omp) F and C, and smaller in the strain producing OmpF constitutively.
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  • KUNIMOTO HOTTA, JUN ISHIKAWA, MASARU ICHIHARA, HIROSHI NAGANAWA, SATOS ...
    1988 Volume 41 Issue 1 Pages 94-103
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    The genetic and biochemical basis of a 200-fold increase in kanamycin (KM)-resistance shown in Streptomyces griseus SS-1198PR generated by protoplast regeneration was investigated. A 15-kb Bel I-DNA segment responsible for the KM-resistance was cloned into pIJ61 with Streptomyces lividans TK21 as host. The KM-resistance segment was then subcloned into pIJ702 as a 1.8-kb BamH I-Bgl II fragment with a BamH I site essential for the KM-resistance. Both S. lividans TK21 containing the cloned segments and S. griseus SS-1198PR showed multiple resistance to KM, dibekacin and gentamicin C complex. Cell free extracts from these strains inactivated the antibiotics in the presence of acetyl CoA in agreement with their resistance pattern. The structure of the inactivated KM-A was determined as 3-N-acetyl-KM-A indicating acetylation by an aminoglycoside acetyltransferase, AAC(3). jThe substrate range of the enzyme was unique and was designated AAC(3)-V. No genetic linkage was found between the cloned 15kb Bcl I segment and the separately cloned streptomycin resistance gene (str) segment (3.8 kb Sph I fragment). The str genes cloned from both the parent (SS-1198) and the strain SS-1198PR were identical in their size, restriction site and function. In addition, these strains showed no significant difference in the total DNA digestion pattern. These results indicate that protoplast regeneration may cause a critical change in a specific region of DNA resulting in a high activity of an AAC(3) with a novel substrate range.
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  • JUN ISHIKAWA, YASUMASA KOYAMA, SATOSHI MIZUNO, KUNIMOTO HOTTA
    1988 Volume 41 Issue 1 Pages 104-112
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    Genetic mechanisms involved in the kanamycin (KM)-hyper-resistance of Streptomyces griseus SS-1198PR and NP1-1PR generated by protoplast regeneration were investigated. Southern hybridization of Sph I-digested genomic DNA with a KM-resistance gene (kan) probe revealed that the strain SS-1198PR and its KM-sensitive parent (SS-1198) had the same copy number of a 4.2-kb Sph I fragment hybridizing to the kan probe, while the kan gene of the strain NP1-1PR was located on a highly amplified DNA sequence (100, 0 copies/chromosome) consisting of the 6.7 kb amplifiable unit with Sph I site at the junction site region. There was no difference in the restriction endonuclease cleavage map of the kan gene region of the Sph I fragments from the three strains. However, the level (50 μg/ml) of KM-resistance conferred by the cloned NP1-1PR kan gene was much lower than that (1, 000 μg/ml) conferred by the cloned SS-1198PR kan gene in Streptomyces lividans TK21 although the strain TK21 harboring these kan genes produced an aminoglycoside acetyltransferase, AAC(3)-V, with the same substrate specificity. It seemed, therefore, likely that a mutational alteration of the kan gene and a DNA amplification involving the kan region played major roles for the KM-hyper-resistance depending on AAC(3)-V in the strains SS-1198PR and NP1-1PR, respectively.
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  • ICHIRO ARAMORI, HITOSHI KOJO, MINORU NISHIDA, SACHIKO GOTO, SHOGO KUWA ...
    1988 Volume 41 Issue 1 Pages 113-122
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
    A small number of highly cephem-resistant strains was found in extensive susceptibility testing of clinical isolates of Escherichia coli to the new cephalosporin derivatives. The cephem-resistance of these clinical isolates appeared to be due to the increased cephalosporinase activities. To clarify the mechanism of the resistance, we cloned the cephalosporinase genes from two typical cephem-resistant clinical isolates as well as from an E. coli K-12 strain. The following two lines of evidence indicated that the cephem-resistance resulted from hyper production of the cephalosporinase due to the up-mutation of the regulatory sequence of the cephalosporinase gene.
    1) Reciprocal exchange of the regulatory sequence including a short segment of N-terminal coding sequence and the rest of the coding sequence between the cephalosporinase genes from E. coli K-12 and the cephem-resistant clinical isolate showed that the higher cephalosporinase activity was accompanied by the regulatory sequence of the cephalosporinase gene from the clinical isolate.
    2) The promoter activities of the cephalosporinase genes were determined by cloning the regulatory sequences into a promoter analysis vector. The promoter activities of the cephalosporinase genes from the clinical isolates were 23 - 33-fold higher than that of the cephalosporinase gene from E. coli K-12.
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  • RAYMOND COOPER, MICHAEL CONOVER, MAHESH PATEL
    1988 Volume 41 Issue 1 Pages 123-125
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
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  • JÜRGEN ROHR, AXEL ZEECK, HEINZ G. FLOSS
    1988 Volume 41 Issue 1 Pages 126-129
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
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  • PAUL G. WILLIARD, JAE KYUNG SOHNG, DAVID E. CANE
    1988 Volume 41 Issue 1 Pages 130-133
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
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  • YUHPYNG L. CHEN, KIRK HEDBERG, JOHN F. BARRETT, JAMES A. RETSEMA
    1988 Volume 41 Issue 1 Pages 134-138
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
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  • LEONE DALL'ASTA, ANDREA COMINI, EUGENIC GAREGNANI, DARIO ALBERTI, GERM ...
    1988 Volume 41 Issue 1 Pages 139-141
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
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  • J. F. FIERRO, C. HARDISSON, J. A. SALAS
    1988 Volume 41 Issue 1 Pages 142-144
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
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  • KYUICHI NEMOTO, YUMI SUGAWARA, TOMOHISA TAKITA, TERUYA NAKAMURA, TOMIO ...
    1988 Volume 41 Issue 1 Pages 145-147
    Published: January 25, 1988
    Released: April 19, 2006
    JOURNALS FREE ACCESS
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