Introduction Infants born with fetal alcohol spectrum disorder (FASD) are the result of high alcohol exposure during pregnancy and have a range of neurological and physical heath problems, including fetal growth restriction. We hypothesised that alcohol exposure in the first trimester, the period critical for normal placental development and organogenesis, negatively affects placental cell turnover and transport of key nutrients for fetal growth and development.

Methods First trimester placental explants (n=7) and BeWo choriocarcinoma cells (n=6) treated with ethanol (0–40 mM) were assessed for apoptosis (M30) and proliferation (Ki67) using immunocytochemistry. Nutrient transport via the system A and system β amino acid transporters was quantified by uptake of radiolabelled methylamino-isobutyric acid (¹⁴C-MeAIB) and taurine (³H-taurine).

Results In first trimester explants, cytotrophoblast proliferation decreased by 40% at 20 mM alcohol (p<0.05). Proliferation of BeWo cells reduced by 5% at 20 mM (p<0.05). Alcohol had no effect on apoptosis. In first trimester explants, there was a trend for reduced taurine uptake at 10 mM (p=0.06) and a significant decrease of at least 20% at 40 mM (p<0.05). System β activity significantly decreased at 10 mM and 40 mM in BeWo cells (p<0.05). System A activity was not affected in first trimester tissue or BeWo cells.

Conclusion Alcohol may adversely affect placental development by reducing cytotrophoblast proliferation and fetal development by reducing uptake of taurine. Taurine is an amino acid believed to be important for neurological development. Alcohol exposure may therefore contribute to the pathogenesis of FASD via two mechanisms, placental development and transport of nutrients important for organogenesis.