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

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 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 alpha-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.