The role of chloride in taurine transport across the human placental brush-border membrane

Abstract

Taurine, a sulfated ß-amino acid, is conditionally essential during development. A maternal supply of tarine is necessary for normal fetal growth and neurologic development, suggesting the importance of efficient placental transfer. Uptake by the brush-border membrane (BBM) in several other tissues has been shown to be via a selective Na +-dependent carrier mechanism which also has a specific anion requirement. Using BBM vesicles purified from the human placenta, we have confirmed the presence of Na +-dependent, carrier-mediated taurine transport with an apparent K mof 4.00 ± 0.22 μM and a V max of 11.72–0.36 pmol mg 1 protein 20 s 1. Anion dependence was examined under voltage-clamped conditions, in order to minimize the contribution of membrane potential o transport. Uptake was significantly reduced when anions such as thiocyanate, gluconate, or nitrate were substituted for Cl −. In addition, a Cl −-gradient alone (under Na +-equilibrated conditions) could energize uphill transport as evidenced by accelerated uptake (3.13 ± 0.8 pmol mg −1 protein 20 s −1) and an overshoot compared to Na +, Cl −-equilibrated conditions (0.60 ± 0.06 pmol mg −1 protein 20 s −1). A Cl -gradient (Na +-equilibrated) also to Na +, Cl −-equilibrated conditions (0.60 ± 0.06 pmol mg −1 protein 20 s −1). A Cl −-gradient (Na +-equilibrated) also stimulated uptake of [ 3H]taurine against its concentration gradient. Analysis of uptake in the presence of varying concentrations of external Cl − suggested that 1 Cl − ions is involved in Na +/taurine cotransport. We conclude that Na +-dependent taurine uptake in the placental BBM has a selective anion requirement for optimum transport. This process is electrogenic and involves a stoichiometry of 2:1:1 for Na +/Cl −/taurine symport.