The transfer rate across the barrier is determined by the physicochemical properties of the molecule, such as lipid solubility, polarity, molecular weight, protein binding, and ionisation. The addition to the maternal circulation of a marker that undergoes only passive diffusion, such as antipyrine, can be used to measure tissue integrity/membrane permeability. Since ATP does not bind to proteins and does not accumulate in placental tissue, its transfer rate depends only on the fetal and maternal flows. Hence, a clearance index close to 1 demonstrates passive diffusion without placental accumulation. The kinetics of FA transfer during the perfusion procedure was similar to that of antipyrine, with a clearance index of 0.47. FA can be metabolized and react with many biomolecules, such as proteins, nucleic acids and amino acids, and cause DNA-protein crosslinks and thereby accumulate in placental and fetal tissues. We observed accumulation of FA or its metabolites during a 90min period. Our data are in agreement with those of Katakura et al., who reported that FA-injected pregnant mice displayed accumulation after 5min in both the placenta and the fetuses. This accumulation in human placenta could explain the adverse effects of FA exposure on human primary trophoblasts observed here, namely syncytiotrophoblasth or monaldys function and altered regeneration. The Nepicastat endocrine activity of the human placenta is necessary to maintain pregnancy and to ensure fetal growth and development. Placental environments containing toxics and pollutants have been reported to disrupt the endocrine activity of the human placenta. Changes in syncytiotrophoblast mass, formation, regeneration nor Vildagliptin functioning can lead to abnormal endocrine production and provoke abnormal fetal development and miscarriage. The production and secretion of hCG is necessary at the beginning of pregnancy to induce progesterone synthesis by the ovarian corpus luteum, which leads to myometrium relaxation. Human CG also acts in a paracrine and autocrine manner to trigger villous trophoblast differentiation and turnover throughout pregnancy.