The resulting changes in placental development are reflected by significant reduction in fetal weights. These data suggest that alcohol exposure as well as acetaldehyde can adversely affect placental growth throughout pregnancy. SGHPL-4 cells were derived from transformed first trimester extravillous cytotrophoblasts and have retained invasive characteristics. A strong trend towards inhibition of migration was observed through a PF-04217903 956905-27-4 matrigel barrier after ethanol and acetaldehyde exposure; limitations of access to cells for this study precluded more experiments to confirm a statistically significant effect. However, other studies using immortalised extravillous cytotrophoblast cells have shown that motility can be inhibited at approximately 17 mM of alcohol over 48 hours. In rat, ethanol exposure reduces the number of invasive trophoblast giant cells and induces cell death in the spongiotrophoblast layer. Proficient extravillous cytotrophoblast invasion in the early first trimester plays a critical role in transforming maternal arteries, supporting a stable low pressure supply of nutrients and gases. Defective invasion of extravillous cytotrophoblasts with reduced arterial remodelling is associated with a range of pregnancy pathologies including FGR. Further work will be needed to assess the impact of alcohol consumption on invasion and vascular remodelling in the first trimester placental bed. The placental system b amino acid transporter is responsible for providing the fetus with taurine, a sulphur-amino acid with antioxidant properties that may be neuroprotective during fetal development. This study demonstrates detrimental effects of clinically relevant ethanol concentrations on the taurine transporter in both BeWo, an epithelioid trophoblast cell line of lower invasive potential, and explants of first trimester placenta. Even at the lowest concentration used, equivalent to an approximate a blood alcohol concentration of 0.05, is able to disrupt normal taurine transporter function. In humans, taurine is maternally derived during pregnancy as fetal production is insufficient to support development. Maternal taurine deprivation in animal models demonstrates decreased fertility and increased incidence of fetal resorption and stillbirth in feline and rodent models. Surviving neonates have lower birth weight, decreased brain weight and experience slower growth. In the complete absence of taurine transporters, knockout mice are significantly growth restricted at birth, and have visual, auditory, and muscular alterations in adulthood compared to their wild types. Reduced placental taurine concentrations have been correlated with FGR, where system b activity is significantly restricted in placentas of FGR fetuses compared to normal pregnancies. This reduction in placental system b activity is observable even in pregnancies with higher risk of FGR. At 40 mM alcohol, the inhibition of taurine transporter function is potentially exposing the fetus to periods of significant deprivation.