Folate and cobalamin uptake by human placenta in complicated pregnancies: Prematurity, preeclampsia and fetal neural tube defects

Abstract

The purpose of the present study was to evaluate whether folate and cobalamin uptakes by microvillous membrane vesicles (MV) from human placenta are affected in pregnancy complications such as prematurity, preeclampsia, and fetal neural tube defects. MMVs were obtained from pooled placental samples from adult women with uncomplicated full-term gestations (n=4), premature delivery (n=3), preeclampsia (n=3), and fetal neural tube defects (n=2). Uptake of cobalamin bound to transcobalamin (TC) was several times higher than the uptake of free cobalamin or cobalamin bound to haptocorrin. TC-cobalamin and folate uptakes by placental MMV were not impaired in preeclampsia, but TC-cobalamin uptake was higher (p<0.001) in prematurity than in term gestations (58±7 vs 33±5 pmol cyano-[57Co]cobalmnin/g MMV protein), whereas folate uptake was unaffected (11.0±1.0 vs 10±0.8 pmol [3H]folic acid/mg MMV protein). In pregnancies affected by fetal neural tube defects, placental folate uptake was similar to that of uncomplicated pregnancies, whereas TC cobalamin uptake was lower (p<0.001; 17±3 pmol cyano-[57Co]cobalamin/g MMV protein). Whether the results obtained for cobalamin uptake in mature placenta is a mere consequence of placental changes in NTD-affected pregnancies or whether it reflects a situation that occurs during the closure of the neural tube in early pregnancy is still unclear. These results suggest that a defect in folate uptake is not involved in NTD etiology, but that the supply of cobalamin to embryonic cells may be impaired, which could affect folate metabolism. (C) 2000 Elsevier Science Inc.