Abstract
Phloretin, the aglucone derivative of phlorizin, increases cation conductance and decreases anion conductance in lipid bilayer membranes. In this paper we present evidence that phloretin acts almost exclusively by altering the permeability of the membrane interior and not by modifying the partition of the permanent species between the membrane and the bulk aqueous phases. We base our conclusion on an analysis of the current responses to a senylborate, and the cation complex, peptide PV-K+. These results are consistent with the hypothesis that phloretin decreases the intrinsic positive internal membrane potential but does not modify to a great extent the potential energy minima at the membrane interfaces. Phloretin increases the conductance for the nonactin-K+ complex, but above 10(-5) M the steady-state nonactin-K+ voltage-current curve changes from superlinear to sublinear. These results imply that, above 10(-5) M phloretin, the nonactin-5+ transport across the membrane becomes interfacially limited.
MeSH Terms
Anti-Bacterial Agents/metabolism
Biological Transport/drug effects
Electric Conductivity
Ions
Kinetics
Membrane Potentials
Membranes, Artificial
Models, Biological
Peptides/metabolism
Permeability
Phloretin/pharmacology
Potassium/metabolism
Tetraphenylborate/metabolism
Chemicals
Anti-Bacterial Agents
Ions
Membranes, Artificial
Peptides
Tetraphenylborate
Potassium
Phloretin
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Melnik E
Latorre R
Hall J E
Tosteson D C
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