title: Divergent deiodination of thyroid hormones in the separated parts of the fetal and maternal placenta in pigs.
abstract: Previous work from this laboratory has shown that the thyroid gland of the fetal pig begins to function at about day 46-47 (0.40-0.415 fraction of gestational age). Sera from fetuses contain lower thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) concentrations than maternal sera, except for about 2 weeks before term. The fetal T4 metabolism is dominated by the 5'-monodeiodinating activity (5'-MD). In the present study we measured the iodothyronines content, and the outer (5'-MD) and inner (5-MD) monodeiodinases activity, in homogenates of the placenta. The pig placenta, which is of the epitheliochorial type, was separated into the fetal and the maternal part. The concentrations of T4, T3 and rT3 were lower, and the deiodinating activity of 5'-MD and 5-MD higher, in the fetal than in the maternal placenta. The fetal placenta not only deiodinated more actively T4 to T3 and T4 to rT3, but degraded T3 to 3,3'-diiodothyronine (3,3'-T2) more actively than rT3 to 3,3'-T2. Such divergent deiodinating activity of T4 to T3, T3 to 3,3'-T2 and rT3 to 3,3'-T2 might favor establishing a relatively high and constant rT3 concentrations in fetal and maternal placentas, and a lower T3 in the fetal placenta. The inner ring deiodinating activity (excluding a day before parturition) was always more active in the fetal placenta, while the outer ring deiodinations varied in this respect, depending on the gestation stage. These results support the hypothesis that in the fetal pig, enzymatic deiodination of thyroid hormones forms a barrier which reduces transplacental passage of the hormones and that the fetal part of the placenta is the primary factor in the mechanism regulating the hormonal transfer. In spite of the presence of the barrier, there is an adequate maternal supply of thyroid hormones to the fetus in early gestation, which suggests that the enzymatic mechanism is influenced in some way by the thyroid status of the fetus.
authors.affiliation: Department of Developmental and Experimental Endocrinology, Polish Academy of Sciences, Poznań, Poland.
authors.forename: E
authors.initials: E
authors.lastname: Krysin
authors.forename: E
authors.initials: E
authors.lastname: Brzezińska-Slebodzińska
authors.forename: A B
authors.initials: AB
authors.lastname: Slebodziński
mesh_terms: D000818:Animals; D004104:Diiodothyronines / Q000032:analysis / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000378:metabolism; D007453:Iodide Peroxidase / Q000032:analysis / Q000378:metabolism*; D010920:Placenta / Q000201:enzymology / Q000378:metabolism*; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000378:metabolism*; D011863:Radioimmunoassay; D013552:Swine / Q000378:metabolism*; D013963:Thyroid Hormones / Q000032:analysis / Q000378:metabolism*; D013974:Thyroxine / Q000032:analysis / Q000378:metabolism; D014284:Triiodothyronine / Q000032:analysis / Q000378:metabolism; D014285:Triiodothyronine, Reverse / Q000032:analysis / Q000378:metabolism
chemical_list: D004104:Diiodothyronines; D013963:Thyroid Hormones; D014284:Triiodothyronine; D014285:Triiodothyronine, Reverse; D007453:Iodide Peroxidase; D013974:Thyroxine