In addition, intracellular taurine behaves as an osmolyte, regulating the osmotic balance during cellular hydration, which plays an essential role in balancing proliferation and apoptosis. The role of taurine is likely to be important in placental as well as fetal development as siRNA knockdown of system b inhibits differentiation of placental trophoblasts in vitro. Addition of taurine in vitro has also shown to increase rat neural stem cell proliferation and secretion of synapse developmental proteins. When utilised as a dietary supplement after ethanol exposure in animal models, taurine markedly reduces the rate of abnormal neuronal migration and decreases the number of brain lesions. Further work is required to investigate whether supplementation can AZ 960 905586-69-8 improve outcomes where high levels of alcohol exposure are known to have occurred. Acetaldehyde, on the other hand, did not affect taurine transporter activity. Acetaldehyde has been suggested to enhance toxicity of ethanol and be the more toxic teratogen. Other studies have shown acetaldehyde to have a detrimental effect on aamino isobutyric acid uptake in both human and sheep models, but at concentrations over a 1000 fold more than the concentrations used in this study. These pharmacological concentrations of acetaldehyde would not be found in a biological system as the metabolism of acetaldehyde plateaus at 26.5 mM for an average population and 42.3 mM for chronic alcoholics. The system A amino acid transporter is a sodium-dependent transport system of small neutral amino acids that has shown to be associated with FGR, a key feature of FASD. In contrast to the taurine transporter, no effects of ethanol on the activity of system A amino acid transport in either BeWo cells or in first trimester placental explants were observed, in agreement with previous work, with in vitro models, using placental explants exposed to 60 mM ethanol. Acetaldehyde, applied at concentrations much lower than in other studies induced a small increase in 14C-MeAIB uptake in placental explants, but not in BeWo cells. This observation may reflect a compensatory increase in response to an adverse environment as seen in other physiological systems when exposed to a chemical stimulus, as first trimester explants retain their phenotype in culture. There is a potential capacity for functional compensation in first trimester tissue, but not in cells, because of the diversity of cell types. As a trophoblast cell layer model, BeWo cells are commonly used to assess membrane transport as they express similar functional transport receptors and retain the trophoblastic property of fusion into a multinucleated layer. Detrimental effects have been described at pharmacological concentrations of acetaldehyde on system A transport of the amino acid, valine, in rat placental explants and on the neutral system A transport of lithiumdependant L-alanine in human term explants. This indicates that acetaldehyde may have selective effects on different amino acid transporters.