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   <subfield code="a">The riminophenazines, clofazimine and B669, inhibit potassium transport in Gram-positive bacteria by a lysophospholipid-dependent mechanism</subfield>
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   <subfield code="c">[Engela E. De Bruyn, Helen C. Steel, Constance E. J. Van Rensburg, Ronald Anderson]</subfield>
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   <subfield code="a">The effects of the riminophenazine antimicrobial agents clofazimine and B669 as well as those of lysophosphatidylcholine (LPC), on microbial K+-transporting systems were investigated in a range of Gram-positive and Gram-negative bacteria using 42K and 36Rubidium (26Rb) as tracers. Exposing the Gram-positive bacteria to 0.1-10 mg/L of the drugs resulted in a dose-related inhibition of uptake of both radiolabelled cations due primarily to the inhibition of their influx which was prevented by pretreating the microorganisms with 25 mg/L α-tocopherol (vitamin E) which forms a complex with lysophospholipids. In contrast, Gram-negative bacteria were resistant to riminophenazine-mediated inhibition of K+-transport, with only one of four well-characterised K+-transport system mutants of Escherichia coli, namely Kup, being affected by the antimicrobial agents. The selective antimicrobial activity of riminophenazines against Gram-positive bacteria is probably achieved by lysophospholipid-mediated inactivation of K+-transport, while Gram-negative microorganisms possess several K+-transport systems which are either inaccessible and/or insensitive to lysophospholipids. Thus, K+-transport systems may represent novel targets for antimicrobial agents.</subfield>
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