Characterization of the Na+-dependent taurine influx in flounder erythrocytes

Abstract

About 92% of the taurine influx in flounder erythrocytes at physiological conditions in vitro (330 mosmol·l-1, 145 mmol·l-1 Na+, 0.30 mmol·l-1 taurine) is Na+-dependent. This influx is highly specific for taurine. The β-amino compounds hypotaurine and β-alanine were the only compounds which mimicked the inhibitory effect of taurine on influx of [14C]taurine, the former more than the latter. Counterexchange of taurine was also mediated by the taurine transporters. Reduction of osmolality per se did not affect the activity of these transporters. Non-linear regression analysis of the influx values revealed the presence of two different influx systems: a system with high affinity and low capacity and another with low affinity and high capacity. However, we cannot exclude the possibility that this influx of taurine was mediated by only one transporter which operated in different modes depending on the extracellular Na+ concentration. On the assumption that the Na+-dependent influx was mediated by two separate systems, the maximal velocity of the low capacity system was 2.55 nmol·g dry weight-1·min-1 at 145 mmol·ll-1 extracellular Na+. This capacity was about 50% lower than that of the high capacity system. The Michaelis constants were 0.013 and 1.34 mmol·l-1, respectively. Reduction of the extracellular Na+ concentration reduced maximal velocity and the affinity to taurine of both transport systems. At 10 mmol·l-1 Na+ or lower concentrations the high capacity system did not seem to operate. The activation method suggested that each taurine molecule transported by the high capacity system was accompanied by two Na+. The stoichiometry of the low capacity system was 1 taurine: 1 Na+. The Hill-coefficient for both transport systems was 1.00.