Differences in iodinated peptides and thyroid hormone formation after chemical and thyroid peroxidase-catalyzed iodination of human thyroglobulin

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.

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Manipulating plasma thyroid hormone levels at hatching alters development of endothermy and ventilation in Pekin duck (Anas platyrhynchos domestica)

Journal of Experimental Biology ◽

10.1242/jeb.237701 ◽

2020 ◽

Vol 223 (22) ◽

pp. jeb237701

Author(s):

Tushar S. Sirsat ◽

Edward M. Dzialowski

Keyword(s):

Thyroid Hormone ◽

Tidal Volume ◽

Developmental Trajectory ◽

Pekin Duck ◽

Thyroid Peroxidase ◽

Hormone Levels ◽

Ventilation Frequency ◽

Thyroid Hormone Levels ◽

And Control

ABSTRACTAt hatching in precocial birds, there are rapid physiological and metabolic phenotypic changes associated with attaining endothermy. During the transition to ex ovo life, thyroid hormone levels naturally increase, peaking at hatching, and then decline. To better understand the role of the natural increase in thyroid hormone at hatching in regulating the developmental trajectory of the Pekin duck's endothermic phenotype, we examined development of O2 consumption (V̇O2) and ventilation (frequency, tidal volume and minute ventilation) while inhibiting the developmental increase in thyroid hormones that occurs at hatching via administration of the thyroid-peroxidase inhibitor methimazole (MMI) or accelerating the developmental increase via triiodothyronine (T3) supplementation. Animals were dosed only on day 24 of a 28-day incubation period and studied on incubation day 25, during external pipping (EP) and 1 day post-hatching (dph). On day 25, there was an increase in V̇O2 in the hyperthyroid treatment compared with the other two treatments. During the EP stage, there was a significant effect of thyroid status on V̇O2, with hyperthyroid V̇O2 being highest and hypothyroid V̇O2 the lowest. By 1 dph, the supplemented T3 and control animals had similar V̇O2 responses to cooling with comparable thermal neutral zones followed by increased V̇O2. Hypothyroid 1 dph hatchlings had a lower resting V̇O2 that did not increase to the same extent as the supplemented T3 and control animals during cooling. During EP, inhibiting the rise in T3 resulted in embryos with lower ventilation frequency and tidal volume than control and supplemented T3 embryos. At 1 dph, ventilation frequency of all animals increased during cooling, but tidal volume only increased in supplemented T3 and control hatchlings. Our data support the role of the late incubation increase in T3 in regulating the systemic development of endothermic metabolic capacity and associated control of ventilation occurring at hatching of the Pekin duck.

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Thyroid Peroxidase Revisited – Whatʼs New?

Hormone and Metabolic Research ◽

10.1055/a-1057-9469 ◽

2019 ◽

Vol 51 (12) ◽

pp. 765-769 ◽

Cited By ~ 2

Author(s):

Marlena Godlewska ◽

Damian Gawel ◽

Ashley M. Buckle ◽

J. Paul Banga

Keyword(s):

Thyroid Hormone ◽

Environmental Factors ◽

Recent Progress ◽

Thyroid Peroxidase ◽

Autoimmune Thyroid Diseases ◽

Autoimmune Thyroid ◽

Thyroid Hormone Biosynthesis ◽

Hormone Biosynthesis ◽

Genetic And Environmental Factors ◽

Thyroid Dysfunctions

AbstractThyroid peroxidase (TPO) is an enzyme that participates in thyroid hormone biosynthesis. TPO is also a major autoantigen in autoimmune thyroid diseases (AITD). In this review, we summarize the latest developments in the field of TPO research. We present the current understanding of immunodominant serologic determinants, frequency of TPO-specific autoantibodies in the population, as well as genetic and environmental factors contributing to their development. Moreover, we report recent progress in the clinical utilities of TPO autoantibody testing, including thyroid dysfunctions and extra-thyroidal disorders.

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Exogenous free iodotyrosine inhibits iodide transport through the sequential intracellular events

Acta Endocrinologica ◽

10.1530/eje.0.1300601 ◽

1994 ◽

Vol 130 (6) ◽

pp. 601-607 ◽

Cited By ~ 1

Author(s):

Michiyo Nasu ◽

Masahiro Sugawara

Keyword(s):

Los Angeles ◽

Thyroid Peroxidase ◽

Thyroid Cell ◽

Camp Production ◽

Thyroid Follicle ◽

Iodide Uptake ◽

Iodide Transport ◽

Camp Generation ◽

Iodotyrosine Deiodinase ◽

Hormone Formation

Nasu M, Sugawara M. Exogenous free iodotyrosine inhibits iodide transport through the sequential intracellular events. Eur J Endocrinol 1944;130:601–7. ISSN 0804–4643 We describe a new function of exogenous iodotyrosine as a regulator of iodide transport. Porcine thyroid follicles in culture were preincubated with 0–20 μmol/l monoiodotyrosine or diiodotyrosine (DIT) in the presence of bovine thyrotropin (TSH) for 24 h; these iodotyrosines inhibited iodide uptake in a dose–response manner. Extracellular [125I]DIT was actively transported to the thyroid follicle in the presence of TSH or (Bu)2cAMP. Inhibition of iodide uptake by iodotyrosine required preincubation with iodotyrosine in the presence of TSH; without TSH, iodotyrosine was ineffective. Follicles preincubated with DIT for 24 h inhibited TSH-mediated cAMP production, which is an important signal for iodide transport. Inhibition of iodide uptake and cAMP generation by iodotyrosine was negated characteristically by 3-nitro-l-tyrosine, an inhibitor of iodotyrosine deiodinase, or by methimazole, an inhibitor of thyroid peroxidase. Our findings suggest that iodotyrosine regulates iodide transport through the following sequential intracellular events: TSH-dependent iodotyrosine transport into the thyroid cell; deiodination of iodotyrosine and release in iodide; iodine organification by the peroxidase system; inhibition of cAMP generation by organified iodine; and inhibition of iodide transport. Thus, exogenous iodotyrosine can serve as an inhibitor of thyroid hormone formation only when TSH is present M Sugawara, Wadsworth VA Hospital (11 IM), Wilshire and Sawtelle Blvds, Los Angeles, CA 90073, USA

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Effect of exogenous hydrogen peroxide on iodide transport and iodine organification in FRTL-5 rat thyroid cells

Acta Endocrinologica ◽

10.1530/acta.0.1290089 ◽

1993 ◽

Vol 129 (1) ◽

pp. 89-96 ◽

Cited By ~ 7

Author(s):

Ge Chen ◽

A Eugene Pekary ◽

Masahiro Sugawara ◽

Jerome M Hershman

Keyword(s):

Hydrogen Peroxide ◽

Cyclic Adenosine Monophosphate ◽

Adenosine Monophosphate ◽

Thyroid Peroxidase ◽

Thyroid Cells ◽

Iodide Transport ◽

Biphasic Effect ◽

Rat Thyroid ◽

Camp Levels ◽

Hormone Formation

Hydrogen peroxide plays an important role in the regulation of iodination and thyroid hormone formation. In the present study, the effect of exogenous H2O2 on 125I transport and organification was investigated in FRTL-5 rat thyroid cells. Less than 20 passages after subcloning, cells in 24-well plates (6 × 104 cells/well) were maintained in a thyrotropin (TSH)-containing medium (6H) for 3 days. A TSH-free medium (5H) was then used for the next 7 days. A 1-h exposure to H2O2 stimulated 125I transport and 125I organification at 0.1–0.5 mmol/l H2O2 and had a toxic effect on FRTL-5 cells at 5 mmol/l. Hydrogen peroxide (0.5 mmol/l) augmented the iodide transport and iodine organification induced by TSH (333U/l) by two- and threefold, respectively. The biphasic effect of H2O2 was blocked totally by 5–200 μg/l of catalase. Catalase by itself did not influence TSH-mediated 125I transport and 125I organification. Hydrogen peroxide (0.5 mmol/l) added to cells in 5H medium increased Na+K+-ATPase activity twofold. Ouabain (1 mmol/l), an inhibitor of Na+K +-ATPase, completely inhibited the twofold increase in 125I transport induced by 0.5 mmol/l H2O2 but only inhibited H2O2-induced 125I organification by 28%. Methimazole (1 mmol/l), an inhibitor of thyroid peroxidase, had no effect on H2O2-mediated 125I transport but totally blocked the fivefold rise in 125I organification induced by 0.5 mmol/1 H2O2. The effect of H2O2 on intracellular cyclic adenosine monophosphate (cAMP) levels also was studied. Hydrogen peroxide (0.5 mmol/l) decreased baseline and 160 mU/l TSH-induced cAMP levels by 35 and 87%, respectively, while a 3-h incubation with 0.5 mmol/l H2O2 increased Na + K +-ATPase in 5H and 6H media. We conclude that H2O2 plays an important role in the regulation of iodide transport and organification and also may affect signal transduction and the electrochemical gradient in thyroid cells. Our results also provide evidence that functional thyroid peroxidase activity is present in FRTL-5 cells.

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THE EARLY STAGE OF THYROID HORMONE FORMATION: STUDIES ON RAT THYROIDSIN VIVO1

Endocrinology ◽

10.1210/endo-69-4-695 ◽

1961 ◽

Vol 69 (4) ◽

pp. 695-705 ◽

Cited By ~ 9

Author(s):

LESLIE J. DEGROOT ◽

ANN M. DAVIS

Keyword(s):

Thyroid Hormone ◽

Early Stage ◽

Hormone Formation

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Thyroid Status in Patients with Low Serum Ferritin Level

Bangladesh Journal of Medical Biochemistry ◽

10.3329/bjmb.v5i1.13424 ◽

2013 ◽

Vol 5 (1) ◽

pp. 5-11

Author(s):

S Akhter ◽

ZU Nahar ◽

S Parvin ◽

A Alam ◽

S Sharmin ◽

...

Keyword(s):

Thyroid Hormone ◽

Iron Deficiency ◽

Serum Ferritin ◽

Serum Ferritin Level ◽

Ferritin Level ◽

Thyroid Peroxidase ◽

Hormone Synthesis ◽

Tissue Iron ◽

Iron Deficient ◽

Significant Difference

Iron deficiency is the most important but preventable nutritional problem in Bangladesh. Thyroid peroxidase, an iron containing enzyme, is essential for initial two steps of thyroid hormone synthesis which is a component of tissue iron. Tissue iron diminishes early in the course of iron deficiency. So thyroid hormone level may be altered in iron deficient patients. This case-control study was carried out in the Department of Biochemistry, Bangabandhu Sheikh Mujib Medical University (BSMMU) from July 2006 to June 2007. This study was done to find out the changes of thyroid hormonal activity in iron deficiency.In this study 72 subjects were selected from the out-patient department of the hospital. Patients with low serum ferritin level <12 mgm/L were selected as cases (n=36) and healthy persons with normal serum ferritin level were taken as controls. Serum ferritin, thyroid stimulating hormone (TSH), free thyroxine (FT4) and free triiodothyronine (FT3) were measured in all study subjects. Values were expressed as mean ± SD. Unpaired 't' test and Pearson's correlation test were performed to see the level of significance and p value <0.05 was taken as significant. Serum ferritin level in cases and controls were 6.78±4.05 mgm/L and 79.04±28.08 mgm/L respectively which showed significant difference (P<0.0001).Serum TSH concentration in cases and controls were 3.32±1.54 mIU/L and 1.89±0.86 mIU/L respectively. Serum FT4 concentration in cases and controls were 11.66±1.77 pmol/L and 13/10±1.36 pmol/L respectively and that of FT3 were 3.00±0.68 and 3.31±0.61 pmol/L respectively. All showed significant difference between groups.Serum ferritin and Serum TSH showed significant negative correlation in controls whereas in cases they showed negative correlation which was not statistically significant.Both serum FT4 and FT3 revealed positive correlation with serum ferritin but that too was not significant statistically.Though the study failed to show any significant positive correlation between serum ferritin and thyroid hormones, lower level of thyroid status in iron deficient patients suggest that it could be a reflection of disturbed activities of iron dependent enzymes such as thyroid peroxidase that impairs thyroid hormone synthesis. However, a large scale study is recommeded to establish the fact.This study showed that there was significant difference in thyroid hormonal status between iron deficient patients and normal healthy persons. Therefore it can be concluded that iron deficiency may impair normal thyroid hormone status. DOI: http://dx.doi.org/10.3329/bjmb.v5i1.13424 Bangladesh J Med Biochem 2012; 5(1): 5-11

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Effects of a selenium deficient diet on thyroid function of normal and perchlorate treated rats

Acta Endocrinologica ◽

10.1530/acta.0.1180495 ◽

1988 ◽

Vol 118 (4) ◽

pp. 495-502 ◽

Cited By ~ 32

Author(s):

J. Golstein ◽

B. Corvilain ◽

F. Lamy ◽

D. Paquer ◽

J. E. Dumont

Keyword(s):

Thyroid Hormone ◽

Tap Water ◽

Selenium Deficiency ◽

Thyroid Peroxidase ◽

Deficient Diet ◽

Adult Rats ◽

Pregnant Rats ◽

Hormone Synthesis ◽

Thyroid Hormone Synthesis

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.

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