Taurine is an essential amino acid during fetal life and appears to be vital for the growth of the fetus and for the development of the CNS. In intrauterine growth restriction (IUGR), fetal plasma concentrations of taurine are reduced, and we tested the hypothesis that this is caused by altered placental transport of taurine. Syncytiotrophoblast microvillous membrane (MVM) and basal membrane (BM) vesicles were isolated from control (fetal weight, 3068+/-191 g; gestational age, 37.0+/-0.7 wk; n=13) and IUGR pregnancies (fetal weight, 1724+/-118 g; gestational age, 35.8+/-0.7 wk; n=11). Uptake of [3H]taurine (0.5 microM) was studied at 22 degrees C using rapid filtration techniques. Sodium stimulated taurine uptake 35-fold in MVM, confirming Na+-dependent transport in this membrane. A Na+-dependent taurine transport could also be demonstrated in BM; however, the activity was only 6% of that in MVM. Na+-independent transport activities were similar in MVM and BM. In IUGR, MVM Na+-dependent taurine transport was reduced by 34% (p < 0.05), whereas Na+-independent uptake was unaltered. In contrast to MVM, Na+-dependent taurine uptake in BM was unaffected by IUGR, whereas Na+-independent transport was decreased by 33% (p < 0.05). The highly polarized distribution of the Na+/taurine cotransporter to the MVM in conjunction with similar Na+-independent transport rates for taurine in MVM and BM provides the basis for net taurine flux from the mother to the fetus. These data suggest that the low plasma concentrations of taurine in IUGR fetuses are caused by a reduced activity of placental taurine transporters.
