Human PL and pGH are both involved in maternal adaptation to pregnancy and in the control of fetal growth. Very few studies have focused on the effect of FA on the production and secretion of hormones in general, and none have specifically concerned pregnancy hormones. Rat and mice exposed to FA present reduced testosterone levels, Mirtazapine suggesting an adverse effect of FA on hormone synthesis. However, no cellular or biochemical studies have been performed to decipher the underlying mechanism. Here, we clearly demonstrated for the first time that FA Vanoxerine exposure of human trophoblasts reduces pregnancy peptide hormone synthesis and secretion. A similar adverse effect was observed on hCG secretion after H2O2 treatment. Interestingly, we found that hormone secretion was restored by an antioxidant. We thus postulated that the oxidative stress induced by FA exposure, and particularly the H2O2 produced by FA metabolism, may trigger the adverse effects of FA on pregnancy hormone production. This is supported by are cent study in which H2O2 exposure affected hCG secretion by Be Wo cells. In keeping with previous studies, we found that oxsr1 gene and protein expression in FA-exposed trophoblasts was increased, high lighting the induction of intracellular oxidative stress. Oxidative stress or a redox imbalance due to FA exposure could be responsible for abnormal trophoblast functions. For instance, trisomy 21 trophoblasts present SOD1 upregulation and unbalanced redox status, owing to the location of sod1 on chromosome 21. This redox imbalance is associated with defective cell differentiation and hormone secretion. It has been reported that exposure of pregnant women to FA is associated with spontaneous abortions and low birth weight, in keeping with our observation of syncytial dysfunction leading to abnormal trophoblast differentiation and regeneration and defective pregnancy hormone secretion. FA also increased GPx and GSR gene expression, reflecting excessive consumption of glutathione due to oxidative stress.In this context of FA exposure, both denovo synthesis and recycling fGSH are required to ensure the catalytic cycle of GPx, along with FA oxidation to formic acid.