Characteristics of thyroxine 5'-deiodination in cultured human placental cells. Regulation by iodothyronines.

Hidal, Jairo Tabacow; Kaplan, M M

doi:10.1172/jci112094

Cited by 41 publications

(22 citation statements)

References 39 publications

(25 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1. More than 97% of 125I-activity was found in fractions [1][2][3][4] Time dependence of3,3-T2 and rT3 metabolism. was the main metabolite, the amount of which was inversely correlated with that of remaining 3,3'-T2.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Metabolism of reverse triiodothyronine by isolated rat hepatocytes.

Rooda¹,

Loon²,

Tj³

1987

J. Clin. Invest.

View full text Add to dashboard Cite

Reverse triiodothyronine (rT3) is metabolized predominantly by outer ring deiodination to 3,3'-diiodothyronine (3,3'-T2) in the liver. Metabolism of rT3 and 3,3'-T2 by isolated rat hepatocytes was analyzed by Sephadex LH-20 chromatography, high performance liquid chromatography, and radioimmunoassay, with closely agreeing results. Deiodinase activity was inhibited with propylthiouracil (PTU) and sulfotransferase activity by sulfate depletion or addition of salicylamide or dichloronitrophenol. Normally, little 3,3'-T2 production from rT3 was observed, and 1251 was the main product of both 3,13'-'25iT2 and 13',5'-25IlrT3. PTU inhibited rT3 metabolism but did not affect 3,3'-T2 clearance as explained by accumulation of 3,3'-T2 sulfate. Inhibition of sulfation did not affect rT3 clearance but 3,3'-T2 metabolism was greatly diminished. The decrease in I formation from rT3 was compensated by an increased recovery of 3,3'-T2 up to 70% of rT3 metabolized. In conclusion, significant production of 3,3'-T2 from rT3 by rat hepatocytes is only observed if further sulfation is inhibited.

show abstract

Section: Resultsmentioning

confidence: 99%

“…It deiodinates only the outer ring of substrates such as T4 and rT3 (2)(3)(4). Type III enzyme is found in brain, placenta, and skin, and it is a specific inner ring deiodinase (2,5).…”

Section: Introductionmentioning

confidence: 99%

Metabolism of reverse triiodothyronine by isolated rat hepatocytes.

Rooda¹,

Loon²,

Tj³

1987

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Whereas placental D2 and D3 activities can be measured in cell dispersions or tissue sonicates (179)(180)(181)(182), in situ preparations can be used to study the placental D3 pathway (183,184). In an anesthetized pregnant guinea pig, the placenta is surgically exposed and a single umbilical artery and the umbilical vein cannulated, while the fetus is removed.…”

Section: Bianco Et Almentioning

confidence: 99%

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

Bianco

Anderson

Forrest

et al. 2014

Thyroid

173

106

View full text Add to dashboard Cite

“…Since the human thyroid does not fully develop until 10-12 week of gestation and the feedback regulatory process does not mature until 18-20 weeks, most of the fetal thyroid hormones in the first half of human gestation derive from the maternal circulation. These are modified by deiodinases expressed in the fetus as well as in surrounding tissues: D3 is expressed in the placenta, uterus, and in all of the epithelial surfaces of the human fetus (skin, respiratory epithelium, gastrointestinal tract and urinary epithelium) (94)(95)(96). This barrier controls the rate of transfer of maternal thyroid hormone to the fetus, allowing the fetal hypothalamic-pituitary-thyroid axis to be autonomous with respect to the mother (97).…”

Section: Deiodinases and Maternal-fetal Physiologymentioning

confidence: 99%

Physiological role and regulation of iodothyronine deiodinases: A 2011 update

Marsili

Zavacki

Harney

et al. 2011

J Endocrinol Invest

View full text Add to dashboard Cite

Thyroxine (T4) is a prohormone secreted by the thyroid. T4 has a long half life in circulation and it is tightly regulated to remain constant in a variety of circumstances. However, the availability of iodothyronine selenodeiodinases allow both the initiation or the cessation of thyroid hormone action and can result in surprisingly acute changes in the intracellular concentration of the active hormone T3, in a tissue-specific and chronologically-determined fashion, in spite of the constant circulating levels of the prohormone. This fine-tuning of thyroid hormone signaling is becoming widely appreciated in the context of situations where the rapid modifications in intracellular T3 concentrations are necessary for developmental changes or tissue repair. Given the increasing availability of genetic models of deiodinase deficiency, new insights into the role of these important enzymes are being recognized. In this review, we have incorporated new information regarding the special role played by these enzymes into our current knowledge of thyroid physiology, emphasizing the clinical significance of these new insights.

show abstract

Characteristics of thyroxine 5'-deiodination in cultured human placental cells. Regulation by iodothyronines.

Abstract: Human and rat placental homogenates convert L-thyroxine (T4) to 3,5,3'-L-triiodothyronine (T3)

Cited by 41 publications

References 39 publications

Metabolism of reverse triiodothyronine by isolated rat hepatocytes.

Metabolism of reverse triiodothyronine by isolated rat hepatocytes.

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

Physiological role and regulation of iodothyronine deiodinases: A 2011 update

Contact Info

Product

Resources

About