Bacterial uptake of aminoglycoside antibiotics.

Taber, Harry; Mueller, J P; Miller, Paul; Arrow, A S

doi:10.1128/mmbr.51.4.439-457.1987

Cited by 308 publications

(227 citation statements)

References 66 publications

(162 reference statements)

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“…The inhibitory activity of these N-oxides (at concentration ratios with respect to streptomycin of the order of 1 : 100) was found to correlate with the potent inhibition of electron transport in both heart-muscle and bacterial cells through the cytochrome bc 1 segment (ubiquinol:cytochrome c oxidoreductase) of the respiratory chain (Lightbown & Jackson, 1954. This is in line with the need for respiration and the transmembrane potential required for bacteria to take up aminoglycoside antibiotics (Hancock, 1962;Damper & Epstein, 1981;Arrow & Taber, 1986;Taber et al, 1987). 2-Heptyl-4-hydroxyquinoline N-oxide (HQNO) acts as a ubiquinone and menaquinone analogue on quinonereactive cytochrome b enzymes in various organisms (Van Ark & Berden, 1977;Smirnova et al, 1995;Rothery & Weiner, 1996).…”

Section: Natural Antimicrobial Quinolonesmentioning

confidence: 64%

Quinolones: from antibiotics to autoinducers

et al. 2011

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Since quinine was first isolated, animals, plants and microorganisms producing a wide variety of quinolone compounds have been discovered, several of which possess medicinally interesting properties ranging from antiallergenic and anticancer to antimicrobial activities. Over the years, these have served in the development of many synthetic drugs, including the successful fluoroquinolone antibiotics. Pseudomonas aeruginosa and related bacteria produce a number of 2-alkyl-4(1H)-quinolones, some of which exhibit antimicrobial activity. However, quinolones such as the Pseudomonas quinolone signal and 2-heptyl-4-hydroxyquinoline act as quorum-sensing signal molecules, controlling the expression of many virulence genes as a function of cell population density. Here, we review selectively this extensive family of bicyclic compounds, from natural and synthetic antimicrobials to signalling molecules, with a special emphasis on the biology of P. aeruginosa. In particular, we review their nomenclature and biochemistry, their multiple properties as membrane-interacting compounds, inhibitors of the cytochrome bc1 complex and iron chelators, as well as the regulation of their biosynthesis and their integration into the intricate quorum-sensing regulatory networks governing virulence and secondary metabolite gene expression.

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Section: Natural Antimicrobial Quinolonesmentioning

confidence: 64%

Quinolones: from antibiotics to autoinducers

et al. 2011

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“…These genes are expected to influence aminoglycoside-induced oxidative stress and/or aminoglycoside uptake. Indeed, aminoglycosides uniquely require the PMF for active cellular uptake (Taber et al, 1987;Allison et al, 2011). In sharp contrast, the efflux of many other antibiotics depends on PMF-dependent pumps (Paulsen et al, 1996).…”

Section: Evidence For Antagonistic Mutational Effects On Membrane Permentioning

confidence: 99%

Bacterial evolution of antibiotic hypersensitivity

Lázár

Palsson

Spohn

et al. 2013

Molecular Systems Biology

294

370

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“…The majority of antimicrobial agents must gain access to the cytoplasm in order to exert their effect. Polycationic agents, such as the aminoglycosides, gain access to the cell through a self-promoted mechanism (Hancock 1981;Taber et al 1987). In self promotion, the agent destabilizes cations associated with the cell envelope causing reorganization of the LPS to facilitate antibiotic entry.…”

Section: Biocide and Antibiotic Resistance Through Permeability Changmentioning

confidence: 99%