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Endocrinology, Vol 122, 1521-1531, Copyright © 1988 by Endocrine Society
ARTICLES |
G Morreale de Escobar, MJ Obregon, C Ruiz de Ona and F Escobar del Rey
Instituto de Investigaciones Biomedicas, Consejo Superior de Investigaciones Cientificas, Madrid, Spain.
It has recently been shown that thyroid hormones are transferred from the mother to the developing rat embryo early in gestation, before the onset of fetal thyroid function. We have now studied whether there is transfer of T4 from the mother to the fetus late in gestation when the fetal thyroid is impaired. Normal and thyroidectomized females were mated, given a goitrogen [methimazole (MMI)], starting before the onset of fetal thyroid function and until term, alone or together with a constant infusion of T4 (1.8 micrograms/100 g BW.day). T4 and T3 were determined by RIA in several maternal samples and in tissues from 21- day-old fetuses. The administration of MMI blocked the fetal thyroid, as assessed from the decreased thyroid concentrations of T4 and T3. The concentrations of both iodothyronines also decreased in placenta, thyroid, plasma, brain, liver, lung, and carcass of fetuses from MMI- treated dams. Infusion of T4 into such MMI-treated mothers partly avoided this decrease, and T4 levels increased in all fetal tissues to 41-57% of those in normal fetuses. In contrast to this, T4 infusion affected the concentration of T3 to varying degrees in different tissues. The T3 concentration in plasma and lung increased very little when the MMI-treated mother was infused with T4, but in the brain T3 reached concentrations comparable to those in normal fetuses. Results not only show transfer of T4 from the mother to the fetus near term, at least when the fetal thyroid is impaired, but also suggest that it might mitigate, or avoid, the adverse effects of such failure on the developing brain.
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