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Properties of phallotoxin uptake by basolateral plasma membrane vesicles from rat liver: evidence for a carrier-mediated transport

Summary

The mechanism and driving forces for hepatocellular phallotoxin uptake were studied by a rapid-filtration technique using basolateral liver plasma membrane vesicles (blLPM). An inwardly directed Na+ gradient but not K+-gradient transiently stimulated taurocholate uptake into blLPM 1.4–1.7-fold above the equilibrium value (overshoot), demonstrating functionally intact vesicles. In contrast, overshooting phallotoxin uptake (1.15–1.2-fold intravesicular accumulation above equilibrium value) was observed in the presence of a K+ as well as of a Na+ gradient. Na+ could be replaced by K+ or Li+. In the presence of choline chloride a distinct uptake reduction of 57% was seen. Counter-transport phenomena suggest phallotoxin transport rather than binding. Phallotoxin uptake was inhibited significantly by taurocholate, iodipamide and antamanide, but only slightly by a-amanitin. Creation of a negative intravesicular potential by altered accompanying anions or by valinomycin-induced K+ diffusion potential enhanced the initial uptake rate for phallotoxin, demonstrating rheogenic solute uptake.

These findings provide evidence that hepatocellular uptake of phallotoxin is due to carrier-mediated transport. Hepatic uptake of phallotoxin is assumed to be driven by both a monovalent cation gradient (Na+ or K+) and a transmembranal potential difference.

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Abbreviations

bILPM:

basolateral liver plasma membrane vesicles

DMP:

demethylphalloin

Hepes:

4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid

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Täfler, M., Ziegler, K. & Frimmer, M. Properties of phallotoxin uptake by basolateral plasma membrane vesicles from rat liver: evidence for a carrier-mediated transport. Naunyn-Schmiedeberg's Arch Pharmacol 337, 231–237 (1988). https://doi.org/10.1007/BF00169253

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  • DOI: https://doi.org/10.1007/BF00169253

Key words

  • Plasma membrane vesicles
  • Phallotoxin transport
  • Membrane potential