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* Centro de Ciencias Físicas, UNAM, 62251 Cuernavaca, Morelos, México;
Facultad de Ciencias, UAEM, Cuernavaca, Morelos, México; and
Instituto de Fisiología Celular, UNAM, Ciudad Universitaria, México, Distrito Federal, México
Correspondence: Address reprint requests to Iván Ortega-Blake, Fax: +52-7-317-3077; E-mail: ivan{at}fis.unam.mx.
Amphotericin B is an antibiotic that forms ion channels in the membrane of a host cell. The change in permeability produced by these channels is greatly improved by sterols; nevertheless, the single channel conductivity remains invariant. Hence, it is proposed that sterols do not act directly, but rather through the modulation of the membrane phase. We look at the formation of these channels in the bacterial membrane to determine the mechanism of its known antibiotic resistance. We found that channels can indeed be formed in this membrane, but a substantial amount of amphotericin B is required. We also study the effects of the antibiotic concentration needed for channel expression as well as the dynamics of channels affected by both sterol and temperature in phosphatidylcholine membranes. The results support the idea that membrane structure is a determining factor in the action of the antibiotic.
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