3,5,3 - Triiodothyronine fetal

OH-PCBs can also influence thyroxine metabolism. Some of the OH-PCBs that are retained in blood were shown to strongly inhibit sulfation of thyroxine in vitro [204-206]. As sulfation is a major regulation pathway of thyroxine in the fetus, the OH-PCBs may negatively influence the development of the fetus, and in particular fetal brain development [44]. Diodinase mediation is another pathway for thyroxine metabolism e.g., to the active hormone triiodothyronine. Hydroxylated metabolites of CB-77 were shown to inhibit triiodothyronine formation in an in vitro assay using rat hepatic microsomes [207],... 

United Nations to alleviate iodine deficiency. Iodine is required for the thyroid hormones, thyroxine and triiodothyronine, that regulate the metabohc rate and O2 consumption of cells. Iodine is also intimately involved in the control of growth and development, particularly during fetal and infant life. 

Amiodarone may cause asymptomatic corneal microdeposits and inhibit the conversion of thyroxine (T4) to triiodothyronine (T3). Amiodarone has caused pulmonary toxicity (hypersensitivity pneumonitis or intershtial/alveo-lar pneumonihs). It is embryotoxic in that it increases fetal resorphon and causes growth retardation. Amiodarone is excreted in breast milk. 

The thyroid gland synthesizes and releases T3 (3, 3 -triiodothyronine) and (thyroxine) which regulate protein synthesis, regulate membrane-bound enzymes and stimulate mitochondrial oxidation. T3 and also regulate fetal and infant brain development and childhood growth. T3 is more potent than T. ... 

Although fetal thyroid function does not commence until the equivalent of 12 weeks gestation in man, the presence of functional fetal nuclear receptors for T3 is noted in early pregnancy, indicating that triiodothyronine is exerting an action at this time (De Nayer and Dozin, 1989). 

TH plays an important role in fetal and early postnatal brain development. The pro-hormone T4 (3,3 ,5,5 -triiodothyronine) is converted in the brain to its active form, T3, or its inactive metabofite, reverse T3, mainly by the action of DI02. 

Figure 88.2 The possible pathway of maternal-fetal TH metabolism influenoed by excess iodine. Abbreviations T4, thyroxine T3, triiodothyronine T2, 3,3 -L-diiodothyronine rl3, reverse triiodothyronine D1, type 1 iodothyronine deiodinase D2, type 2 iodothyronine deiodinase D3, type 3 iodothyronine deiodinase.

Some research indicates (Calvo et ai, 2002 Morreale de Escobar et ai, 1991, 2004) that human fetuses acquire the ability to synthesize THs at 10—12 weeks of gestation. In the second and third trimester, the fetus can potentially derive TH both from its own thyroid and the thyroid of the mother. Prior to 12 weeks gestation, the mother is the sole source of TH for the developing fetus. Current evidence indicates that there is substantial transfer of maternal TH across the placenta, and fetal TH exists in first trimester embryonic units (Contempre et ai, 1993). The mother provides small amounts ofT4 throughout the pregnancy. The main active TH, triiodothyronine (T3), is converted from T4 and the concentration is strictly regulated by a complex system. After birth, the neonate produces TH independendy. 

J. Bernal and F. Pekonen. Ontpgenesis of the nuclear 3,5 3 -triiodothyronine receptor in the human fetal brain. Endocrinology 114 677-679-679 (1984). 

L.W. Gonzales and P.L. Ballard. Identification and characterization of nuclear 3,5,3 -triiodothyronine-binding sites in fetal human lung. J. Clin. Endocrinol. Metab. 53 21-28 (1981). 

Preferential saturation of brain 3,5,3 -triiodothyronine receptor during development in fetal lambs, ENDOCRINOLOGY 122 ... 

Harris, A.R.C., Fang, S.L., Prosky, J., Braverman, L.E. and Vagenakis, A.G. (1978) Decreased outer ring monodeiodination of thyroxine and reverse triiodothyronine In the fetal and neonatal rat. Endocrinology 103 2216. 

Obregdn MJ, Mallol J, Pastor R, Morreale de Escobar G, Escobar del Rey F, Thyroxine and triiodothyronine in rat embryos before onset of fetal thyroid function. Endocrinology 114 305 (1984)... 

INFLUENCE OF TRIIODOTHYRONINE (L-T3) ON THE DEVELOPMENT OF FETAL BRAIN CHOLINERGIC NEURONS CULTURED IN A CHEMICALLY DEFINED MEDIUM. 

Iodine deficiency remains a major cause of mental retardation and infant mortality and morbidity worldwide—even though iodine was shown to be essential for human health nearly 100 years ago. More than 1 billion people are believed to be at risk for iodine deficiency. In 1986, the International Council for the Control of Iodine Deficiency Disorders was established in an effort to improve iodine nutrition and alleviate human suffering. This council works closely with the World Health Organization, the United Nations International Children s Fund, and the United Nations to alleviate iodine deficiency. Iodine is required for the thyroid hormones, thyroxine and triiodothyronine, that regulate the metabolic rate and O2 consumption of cells. Iodine is also intimately involved in the control of growth and development, particularly during fetal and infant life. 

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