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Determination of the Transport Rate of Xenobiotics and Nanomaterials Across the Placenta using the ex vivo Human Placental Perfusion Model
Published on: June 18, 2013
[Transfer and metabolism of thyroid gland hormones in the placenta]
1Klinischen Forschergruppe Zelldifferenzierung und Lokale Regulationssyteme, Universität Würzburg, Deutschland.
The human placenta is an important link in the maternal-fetal communication network for thyroid hormones which are essential for the normal development and differentiation of the fetus. The placenta transports and metabolizes maternal thyroid hormones. There is also evidence for transfer of fetal thyroid hormones or their metabolites into the maternal circulation. The placenta mainly expresses 5-deiodinase activity (Type III), which inactivates T4 and other iodothyronines and thus limits the transfer of maternal active thyroid hormones to the fetus in the late pregnancy. Type II 5'-deiodinase is also active in the placenta and locally provides active T3 from the maternal prohormone T4 for placental metabolic functions. The placental expression of type I 5'-deiodinase, which also activates T4 to T3, is still controversial. Placental cells express high affinity, stereo-specific, energy-dependent uptake systems for T4 and T3. Placental membranes are also involved in 4'-OH-sulfation reactions of iodothyronines. The biological role of these sulfoconjugates is unclear at the moment. However, these sulfated metabolites might be useful for non-invasive prenatal diagnostics of fetal thyroid function which is autonomously regulated. In contrast to most textbook descriptions we need to be aware that a significant transfer of thyroid hormone occurs from the mother via the placenta to the fetal compartment especially during the first two trimesters but also later on in pregnancy.
The human placenta is an important link in the maternal-fetal communication network for thyroid hormones which are essential for the normal development and differentiation of the fetus. The placenta transports and metabolizes maternal thyroid hormones. There is also evidence for transfer of fetal thyroid hormones or their metabolites into the maternal circulation. The placenta mainly expresses 5-deiodinase activity (Type III), which inactivates T4 and other iodothyronines and thus limits the transfer of maternal active thyroid hormones to the fetus in the late pregnancy. Type II 5'-deiodinase is also active in the placenta and locally provides active T3 from the maternal prohormone T4 for placental metabolic functions. The placental expression of type I 5'-deiodinase, which also activates T4 to T3, is still controversial. Placental cells express high affinity, stereo-specific, energy-dependent uptake systems for T4 and T3. Placental membranes are also involved in 4'-OH-sulfation reactions of iodothyronines. The biological role of these sulfoconjugates is unclear at the moment. However, these sulfated metabolites might be useful for non-invasive prenatal diagnostics of fetal thyroid function which is autonomously regulated. In contrast to most textbook descriptions we need to be aware that a significant transfer of thyroid hormone occurs from the mother via the placenta to the fetal compartment especially during the first two trimesters but also later on in pregnancy.
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