title: [Ionic binding of 3H-gentamicin and short-term bactericidal activity of gentamicin against Pseudomonas aeruginosa isolates differing in lipopolysaccharide structure].
abstract: The clinical isolates of Pseudomonas aeruginosa can be roughly classified into long- and short-lipopolysaccharide (LPS) strains and LPS-deficient strains, based on the silver-stained patterns of their LPSs after SDS-PAGE. The ionic binding of 3H-gentamicin, a polycationic antibiotic, to the negatively charged sites on the surface structures of P. aeruginosa strains, often differing in LPS structure, was the highest in the long-LPS strains followed in descending order by the short-LPS strains and LPS-deficient strains. It was presumed that a clinical isolate of P. aeruginosa No. 45 is lacking in the O-polysaccharide chains and some structures of the core-regions consisting of its LPS-structure after SDS-PAGE. On the other hand, the binding of 3H-gentamicin to this strain was quite. high, i.e., similar to that to of the long-LPS strains. To clarify this finding, P. aeruginosa PAC1R and its LPS-deficient mutants were used as reference strains because the chemical structures of their LPSs containing the repeated units of O-polysaccharides and the neutral sugar contents in the core-regions were previously confirmed. The PAC605 strain of the LPS-mutants of the PAC series, was completely lacking in the repeated units of O-polysaccharide and also lacking in some neutral sugar residues of the core-oligosaccharide region. However, this strain was highly bound to 3H-gentamicin, suggesting that the negatively charged sites on the deep core-oligosaccharide region and/or on lipid A participated in the binding of 3H-gentamicin. This manner of binding may be also applied to P. aeruginosa No. 45. When P. aeruginosa PAC1R, PAC605 and No. 45 strains were each exposed to gentamicin (20 micrograms/ml) for 10 minutes, the viable cell counts of PAC1R decreased to about 70% of the initial count, whereas the viable cell counts of PAC605 and No. 45 strains decreased to 3.6 and 11.0% respectively, indicating the vulnerability of both types of the strains to be enhanced by the bactericidal action of gentamicin with short-term incubation.
authors.affiliation: Chemotherapy Division, Mitsubishi Kagaku Bio Clinical Laboratories, Inc.
authors.forename: T
authors.initials: T
authors.lastname: Saika
authors.forename: M
authors.initials: M
authors.lastname: Hasegawa
authors.forename: I
authors.initials: I
authors.lastname: Kobayashi
authors.forename: M
authors.initials: M
authors.lastname: Nishida
mesh_terms: D000900:Anti-Bacterial Agents / Q000378:metabolism* / Q000494:pharmacology; D005839:Gentamicins / Q000378:metabolism* / Q000494:pharmacology; D009154:Mutation; D011135:Polysaccharides, Bacterial / Q000737:chemistry* / Q000378:metabolism; D011550:Pseudomonas aeruginosa / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*; D014316:Tritium
chemical_list: D000900:Anti-Bacterial Agents; D005839:Gentamicins; D011135:Polysaccharides, Bacterial; D014316:Tritium