Specificity of thyroid hormone synthesis The role of thyroid peroxidase

1978 ◽  
Vol 540 (1) ◽  
pp. 73-82 ◽  
Author(s):  
D. Deme ◽  
J. Pommier ◽  
J. Nunez
2020 ◽  
Vol 3 (2) ◽  
pp. 24
Author(s):  
Shiela Stefani ◽  
Lukman Halim ◽  
Diyah Eka Andayani ◽  
Fiastuti Witjaksono

Introduction: Thyroid gland has the highest selenium content compare with other endocrine organs. Enzyme that catalyzing thyroid hormone activation, iodothyronine deiodinases, were identified as selenocysteine-containing proteins. Selenium levels in soil and rice consumed in Indonesia were lower than in several other countries, which can increase the risk of selenium deficiency.Methods: This is an article review of the current literatures published up to November 2018 about the role of selenium in hyperthyroid.Result: Several studies have shown that selenium supplementation can be beneficial in patients with Graves disease and autoimmune thyroiditis. Selenium has an important immunomodulatory effect, but the effects of selenium supplementation in hyperthyroid has not been conclude. Data regarding selenium intake, prevalence of deficiency, and the relationship between selenium and thyroid disease in Indonesia are limited. Various studies of selenium supplementation in thyroid disease provide controversial results, so there are no guidelines that include selenium as standard therapy hyperthyroid. Selenium supplementation can enhance the restoration of biochemical euthyroidism in Graves disease and was associated with a significant decrease in the levels of thyroid peroxidase antibodies in autoimmune thyroiditis.Conclusions: Micronutrients that play a role in thyroid hormone synthesis and maintain thyroid function in addition to selenium are iodine, iron, zinc, and vitamin A. By correcting the deficit of selenium, and meeting other micronutrient requirements may provide health benefits in patient with hyperthyroid.


2005 ◽  
Vol 118 (2) ◽  
pp. 239-245 ◽  
Author(s):  
Alain VIRION ◽  
Danièale DEME ◽  
Jacques POMMIER ◽  
Jacques NUNEZ

1972 ◽  
Vol 69 (2) ◽  
pp. 321-328
Author(s):  
K. Liewendahl ◽  
E. Niskanen ◽  
A. Gordin

ABSTRACT The effects of excess iodide on the histology and function of the thyroid were studied in rats. A slight increase in thyroid weight and minimal histological alterations were observed. The thyroid function of rats was studied by measuring the serum total and free thyroxine. Excess iodide did not significantly change the concentration of thyroid hormone in the serum and signs of hypothyroidism were not seen. Thus, rats were capable of adaptation to chronic administration of large amounts of iodide. A slight increase in the serum thyrotrophin after prolonged ingestion of excess iodide was measured with both bioassay and radioimmunoassay techniques. The possible role of thyrotrophin in the mechanism of escape from the transient inhibition of iodide on thyroid hormone synthesis is discussed.


1988 ◽  
Vol 118 (4) ◽  
pp. 495-502 ◽  
Author(s):  
J. Golstein ◽  
B. Corvilain ◽  
F. Lamy ◽  
D. Paquer ◽  
J. E. Dumont

Abstract. Pregnant rats were submitted to a selenium-deficient diet immediately after mating; it was continued for 4 weeks after delivery. The pups were sacrificed at 3 and 4 weeks of age. Perchlorate, an antithyroid agent inhibiting iodide trapping in the thyroid, was administered via the drinking water to half of the rats. Rats submitted to a normal laboratory diet and to the experimental diet supplemented with selenium were used as controls. The effects of selenium deficiency were an increase in the number of growth abnormalities, growth retardation, and decreased seleno-dependent glutathione peroxidase (GSH-Px) activity in plasma and in various organs. These effects were relieved by selenium supplementation in the diet. Perchlorate treatment induced the classic picture of primary hypothyroidism. Selenium deficiency increased thyroid hormone levels in perchlorate-treated rats and in controls drinking tap water. In the latter group, it also decreased TSH plasma concentration and thyroid weight. These effects were partially reversed by Se supplementation. In vitro experiments, performed on adult rats, revealed increased radioiodide uptake and organification in glands from the rats submitted to the selenium-free diet. Plasma T3 half-life was similar in control and Se-deficient rats. These data suggest a higher efficiency of thyroid hormone synthesis in the thyroids of selenium-deficient rats, despite a lower thyroid stimulation as evaluated by serum TSH. They are compatible with the hypothesis that decreased selenium supply, leading to a decreased GSH-Px in the thyroid, increases hydrogen peroxide steady state level and thus thyroid peroxidase activity and thyroid hormone synthesis.


1975 ◽  
Vol 51 (2) ◽  
pp. 329-336 ◽  
Author(s):  
Daniele DEME ◽  
Enzo FIMIANI ◽  
Jacques POMMIER ◽  
Jacques NUNEZ

2021 ◽  
Vol 22 (9) ◽  
pp. 4373
Author(s):  
Gaiping Wen ◽  
Klaus Eder ◽  
Robert Ringseis

Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. The present study tested the hypothesis that resveratrol (RSV) alleviates this effect of TM in FRTL-5 cells. While treatment of FRTL-5 cells with TM alone (0.1 µg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 µg/mL) and RSV (10 µM) for 48 h attenuated this effect of TM. In conclusion, RSV alleviates TM-induced ER stress and attenuates the strong impairment of expression of genes involved in thyroid hormone synthesis and their regulators in FRTL-5 thyrocytes exposed to TM-induced ER stress. Thus, RSV may be useful for the treatment of specific thyroid disorders, provided that strategies with improved oral bioavailability of RSV are applied.


FEBS Letters ◽  
1979 ◽  
Vol 102 (1) ◽  
pp. 82-86 ◽  
Author(s):  
Jean-Claude Maurizis ◽  
Claudine Marriq ◽  
Josette Michelot ◽  
Marcel Rolland ◽  
Serge Lissitzky

2007 ◽  
Vol 21 (7) ◽  
pp. 1593-1602 ◽  
Author(s):  
Kenneth R. Johnson ◽  
Coleen C. Marden ◽  
Patricia Ward-Bailey ◽  
Leona H. Gagnon ◽  
Roderick T. Bronson ◽  
...  

Abstract Dual oxidases generate the hydrogen peroxide needed by thyroid peroxidase for the incorporation of iodine into thyroglobulin, an essential step in thyroid hormone synthesis. Mutations in the human dual oxidase 2 gene, DUOX2, have been shown to underlie several cases of congenital hypothyroidism. We report here the first mouse Duox2 mutation, which provides a new genetic model for studying the specific function of DUOX2 in the thyroid gland and in other organ systems where it is hypothesized to play a role. We mapped the new spontaneous mouse mutation to chromosome 2 and identified it as a T>G base pair change in exon 16 of Duox2. The mutation changes a highly conserved valine to glycine at amino acid position 674 (V674G) and was named “thyroid dyshormonogenesis” (symbol thyd) to signify a defect in thyroid hormone synthesis. Thyroid glands of mutant mice are goitrous and contain few normal follicles, and anterior pituitaries are dysplastic. Serum T4 in homozygotes is about one-tenth the level of controls and is accompanied by a more than 100-fold increase in TSH. The weight of adult mutant mice is approximately half that of littermate controls, and serum IGF-I is reduced. The cochleae of mutant mice exhibit abnormalities characteristic of hypothyroidism, including a delayed formation of the inner sulcus and tunnel of Corti and an abnormally thickened tectorial membrane. Hearing thresholds of adult mutant mice are on average 50–60 decibels (dB) above those of controls.


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