Permeability pathways for non-electrolytes through Bufo bufo gall-bladder.
Amphotericin B treatment increases the thiourea, D-xylose and mannitol fluxes and lowers those of urea, N-methyl-urea, acetamide, formamide, and N-N'-dimethyl-thiourea. The degree of flux inhibition is related to the cellular permeability of these compounds. Most probably Amphotericin B increases the permeability of all those molecules across the luminal plasma membrane, but simultaneously elicits a cellular swelling, which reduces the diffusion across the lateral plasma membranes. This effect masks the polyene effect especially for molecules showing a mainly cellular permeation pathway such as amides and lipid soluble molecules.
D000081:Acetamides / Q000378:metabolism; D000666:Amphotericin B / Q000494:pharmacology; D000818:Animals; D002023:Bufo bufo; D002463:Cell Membrane Permeability / Q000187:drug effects; D005260:Female; D005559:Formamides / Q000378:metabolism; D005704:Gallbladder / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D008353:Mannitol / Q000378:metabolism; D008968:Molecular Conformation; D009092:Mucous Membrane / Q000378:metabolism; D012704:Serous Membrane / Q000378:metabolism; D014508:Urea / Q000031:analogs & derivatives / Q000378:metabolism; D014994:Xylose / Q000378:metabolism
D000081:Acetamides; D005559:Formamides; D008353:Mannitol; D000666:Amphotericin B; D014508:Urea; D014994:Xylose