Taurine, required by the fetus for nutrition and neurological development, is inadequately synthesized by the fetus and substantial quantities of the amino acid are supplied by the mother. Maternal to fetal unidirectional taurine transport was studied inin vitroperfused human placentae from normal term deliveries. To determine whether the placenta can achieve and maintain a chemical gradient for taurine, recirculating equimolar maternal and fetal perfusions were performed. The ratio of fetal/maternal taurine concentration increased over 75 min and was maintained at 1.38 ± 0.14 (SEM) through 2.25 h (n=6). To determine the rate of taurine transport against a concentration gradient, flux was determined with maternal taurine constant at 50 μM whereas the fetal taurine concentration varied from 0 to 500 μM in a nonrecirculating system (n=5). Despite increasing the chemical gradient tenfold, taurine was transported at a constant rate of 1.75 ± 0.75 (SEM) nmol/min/g. Nonrecirculating perfusions were performed with B-alanine (»=13) and hypotaurine (w=10), both B-carrier competitors, and no inhibition of taurine transport could be detected, taurine flux being 104.1 ± 6.0% (SEM) of baseline in the presence of Balanine and 106.0 ± 7.0% (SEM) with hypotaurine. Finally, ouabain inhibited transport (n=3) by 58.1 ± 5.4% (SEM). We conclude that taurine is transported in the human placenta by an active carrier mechanism.