CHARACTERIZATION OF T3 IMMUNOREACTIVITY RELEASE FROM THYROID GLAND IN VITRO: A REFLECTION OF COLLOID DROPLET FORMATION

1977 ◽  
Vol 86 (1) ◽  
pp. 119-127 ◽  
Author(s):  
Sadhana Chatterjee ◽  
Masaru Takaishi ◽  
Taeko Shimizu ◽  
Yoshimasa Shishiba
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Hormone Secretion ◽  
Droplet Formation ◽  
Considerable Extent ◽  
Sephadex Column ◽  
Hormone Synthesis ◽  
Thyroid Glands

ABSTRACT T3 immunoreactivity release from the thyroid gland in vitro was shown to be increased by TSH. In the present study, we sought to determine whether the T3 immunoreactivity release is an indicator of thyroid hormone secretion or due to hormone synthesis. When thyroid glands from mice were incubated with TSH, T3 immunoreactivity release was increased in parallel with intracellular colloid droplet formation in a dose related manner. When colchicine, a known inhibitor of colloid droplet formation, was added, both T3 immunoreactivity release and colloid droplet formation were inhibited, whereas MMI, an inhibitor of hormone synthesis, failed to influence both aspects. Thus, T3 immunoreactivity release as a reflection of colloid droplet formation was demonstrated. The analysis of the released immunoreactivity by Sephadex column and subsequent radioimmunoassay suggested that the T3 immunoreactivity was, to a considerable extent, due to macromolecule instead of T3 itself. The effect of I− or Li+ to inhibit thyroid hormone secretion was shown to be on the step prior to, but not subsequent to, colloid droplet formation.

Selenoenzyme expression in thyroid and liver of second generation selenium- and iodine-deficient rats

1996 ◽  
Vol 16 (3) ◽  
pp. 259-267 ◽  
Author(s):  
J H Mitchell ◽  
F Nicol ◽  
G J Beckett ◽  
J R Arthur
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Glutathione Peroxidase ◽  
Iodine Deficiency ◽  
Enzyme Activities ◽  
Second Generation ◽  
Mrna Abundance ◽  
Mrna Levels ◽  
Hormone Synthesis ◽  
Thyroid Glands

ABSTRACT The stimulation of thyroid hormone synthesis in iodine deficiency may increase the requirement for the selenoproteins which are involved in thyroid hormone synthesis in the thyroid gland. Selenoenzyme activity and expression were investigated in the thyroid and liver of second generation selenium-and/or iodine-deficient rats. Selenium deficiency caused substantial decreases in hepatic seleniumcontaining type I iodothyronine deiodinase (ID-I) and cytosolic glutathione peroxidase (cGSHPx) activities and mRNA abundances, but phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activity was only 55% of selenium-supplemented control levels, despite the absence of change in its mRNA abundance. Selenoenzyme mRNA concentrations were maintained at control levels in thyroid glands from the selenium-deficient rat pups. Despite this, a differential effect was observed in selenoenzyme activities: ID-I activity was decreased to 61%, cGSHPx activity to 45% and phGSHPx to 29% of that in selenium-adequate controls. In iodine-deficient thyroid glands, mRNA levels were increased 2·2, 50 and 2·8 times for ID-I, cGSHPx and phGSHPx respectively. ID-I and cGSHPx enzyme activities were also increased but the activity of phGSHPx was decreased despite the high mRNA abundance. Thyroid selenoprotein mRNA levels were also increased in combined selenium and iodine deficiency but again there were differential effects on enzyme activities, with ID-I activity increased, cGSHPx unchanged and phGSHPx decreased. Thus, iodine deficiency may produce an oxidant stress on the thyroid gland, increasing the requirement for selenium to maintain selenoenzyme activity. When dietary supplies of selenium are limiting, thyroid selenoprotein mRNA levels are increased to compensate for overall lack of the micronutrient. Furthermore, there is a preferential supply of available selenium to ID-I and cGSHPx to allow maintenance of thyroid function.

H9c2 cardiomyoblasts produce thyroid hormone

2008 ◽  
Vol 294 (5) ◽  
pp. C1227-C1233 ◽  
Author(s):  
Christof Meischl ◽  
Henk P. Buermans ◽  
Thierry Hazes ◽  
Marian J. Zuidwijk ◽  
René J. P. Musters ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Peroxidase ◽  
Sodium Iodide Symporter ◽  
Hormone Synthesis ◽  
Cardiovascular Hemodynamics ◽  
Wide Range ◽  
Vitro Model

Thyroid hormone acts on a wide range of tissues. In the cardiovascular system, thyroid hormone is an important regulator of cardiac function and cardiovascular hemodynamics. Although some early reports in the literature suggested an unknown extrathyroidal source of thyroid hormone, it is currently thought to be produced exclusively in the thyroid gland, a highly specialized organ with the sole function of generating, storing, and secreting thyroid hormone. Whereas most of the proteins necessary for thyroid hormone synthesis are thought to be expressed exclusively in the thyroid gland, we now have found evidence that all of these proteins, i.e., thyroglobulin, DUOX1, DUOX2, the sodium-iodide symporter, pendrin, thyroid peroxidase, and thyroid-stimulating hormone receptor, are also expressed in cardiomyocytes. Furthermore, we found thyroglobulin to be transiently upregulated in an in vitro model of ischemia. When performing these experiments in the presence of 125I, we found that 125I was integrated into thyroglobulin and that under ischemia-like conditions the radioactive signal in thyroglobulin was reduced. Concomitantly we observed an increase of intracellularly produced, 125I-labeled thyroid hormone. In conclusion, our findings demonstrate for the first time that cardiomyocytes produce thyroid hormone in a manner adapted to the cell's environment.

THE EFFECT OF PREDNISONE ON THE THYROID FUNCTION WITH SPECIAL REFERENCE TO THE IN VITRO UPTAKE BY ERYTHROCYTES OF L-TRIIODOTHYRONINE LABELED WITH 131I

1963 ◽  
Vol 42 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Thorkild Friis ◽  
Vagn Reinicke
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Function ◽  
Serum Proteins ◽  
Binding Capacity ◽  
Hormone Secretion ◽  
Steroid Treatment ◽  
Secretion Rate ◽  
In Vitro Uptake

ABSTRACT In order to study the effect of steroids on the function of the thyroid gland, the uptake by erythrocytes of l-triiodothyronine labeled with 131I was investigated in 29 euthyroid patients treated with prednisone. At the same time the thyroid function was studied by determinations of the serum PBI, the thyroid 131I-uptake and the thyroid hormone secretion rate. In addition some studies of the renal 131I-clearance were performed. Prednisone was found to increase the erythrocyte uptake of the thyroid hormone triiodothyronine in two-thirds of the patients investigated probably as a result of decreased binding capacity of the serum proteins. Simultaneously, the function of the thyroid gland was found to decrease, according to the thyroid 131I-uptake and the thyroid hormone secretion rate. A slightly increased renal 131I-clearance was found during the steroid treatment. This increase cannot completely explain the decreased thyroid 131I-uptake The relation between the decreased function of the thyroid gland and the increased uptake of triiodothyronine in erythrocytes during steroid treatment is discussed.

scholarly journals Effects of 99mTc on the electrochemical properties of thiamazole in vitro

2021 ◽  
Vol 40 (1) ◽  
pp. 21
Author(s):  
Safija Herenda ◽  
Anera Kazlagić ◽  
Edhem Hasković ◽  
Jelena Šćepanović ◽  
Jasmina Marušić
Keyword(s):  
Cyclic Voltammetry ◽  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Cyclic Voltammograms ◽  
Reduction Peak ◽  
Hormone Synthesis ◽  
Reduction Peak Current ◽  
Sodium Pertechnetate ◽  
99Mtc Activity

Thiamazole inhibits the thyroid hormone synthesis and does not inactivate the existing thyroxine and triiodothyronine that circulate in the blood. In this paper Thiamazole electrochemical behavior was monitored by cyclic voltammetry on glassy carbon (GC) electrode in the absence and presence of sodium pertechnetate (99mTc). The influence of different Thiamazole concentrations without and in the presence of radiopharmaceutical 99mTc, the effect of the number of scan cycles, and the effect of 99mTc activity on the appearance of cyclic voltammograms were examined. The results show that there is an observed increase in the reduction peak current with an increase of Thiamazole concentration. It was found that the concentration of the tested drug had a significant effect on its redox characteristics. The results obtained show that the application of different concentrations of sodium pertechnetate exhibits the inhibitory properties of the used radiopharmaceutical on the drug in the treatment of thyroid gland disease.

Phenotypic Variability of Patients With PAX8 Variants Presenting With Congenital Hypothyroidism and Eutopic Thyroid

2020 ◽  
Vol 106 (1) ◽  
pp. e152-e170
Author(s):  
Núria Camats ◽  
Noelia Baz-Redón ◽  
Mónica Fernández-Cancio ◽  
María Clemente ◽  
Ariadna Campos-Martorell ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Congenital Hypothyroidism ◽  
Phenotypic Variability ◽  
Hereditary Diseases ◽  
Hormone Synthesis ◽  
Functional Studies ◽  
Thyroid Hormone Synthesis ◽  
Thyroid Dyshormonogenesis

Abstract Purpose Thyroid dyshormonogenesis is a heterogeneous group of hereditary diseases produced by a total/partial blockage of the biochemical processes of thyroid-hormone synthesis and secretion. Paired box 8 (PAX8) is essential for thyroid morphogenesis and thyroid hormone synthesis. We aimed to identify PAX8 variants in patients with thyroid dyshormonogenesis and to analyze them with in vitro functional studies. Patients and Methods Nine pediatric patients with a eutopic thyroid gland were analyzed by the Catalan screening program for congenital hypothyroidism. Scintigraphies showed absent, low, or normal uptake. Only one patient had a hypoplastic gland. On reevaluation, perchlorate discharge test was negative or compatible with partial iodine-organization deficit. After evaluation, 8 patients showed permanent mild or severe hypothyroidism. Massive-sequencing techniques were used to detect variants in congenital hypothyroidism-related genes. In vitro functional studies were based on transactivating activity of mutant PAX8 on a TG-gene promoter and analyzed by a dual-luciferase assays. Results We identified 7 heterozygous PAX8 exonic variants and 1 homozygous PAX8 splicing variant in 9 patients with variable phenotypes of thyroid dyshormonogenesis. Five were novel and 5 variants showed a statistically significant impaired transcriptional activity of TG promoter: 51% to 78% vs the wild type. Conclusions Nine patients presented with PAX8 candidate variants. All presented with a eutopic thyroid gland and 7 had deleterious variants. The phenotype of affected patients varies considerably, even within the same family; but, all except the homozygous patient presented with a normal eutopic thyroid gland and thyroid dyshormonogenesis. PAX8 functional studies have shown that 6 PAX8 variants are deleterious. Our studies have proven effective in evaluating these variants.

DER EINFLUSS VON RESERPIN AUF DIE ANTITHYREOIDALE WIRKUNG VON KALIUMPERCHLORAT

1962 ◽  
Vol 39 (3) ◽  
pp. 423-430
Author(s):  
H. L. Krüskemper ◽  
F. J. Kessler ◽  
E. Steinkrüger
Keyword(s):  
Thyroid Gland ◽  
Male Rats ◽  
Normal Male ◽  
Tissue Respiration ◽  
List Type ◽  
Morphological Alterations ◽  
Hormone Synthesis ◽  
Stimulation Of

ABSTRACT 1. Reserpine does not inhibit the tissue respiration of liver in normal male rats (in vitro). 2. The decrease of tissue respiration of the liver with simultaneous morphological stimulation of the thyroid gland after long administration of reserpine is due to a minute inhibition of the hormone synthesis in the thyroid gland. 3. The morphological alterations of the thyroid in experimental hypothyroidism due to perchlorate can not be prevented with reserpine.

INHIBITION OF THYROGLOBULIN BIOSYNTHESIS AND DEGRADATION BY EXCESS IODIDE. SYNERGISM WITH LITHIUM

1976 ◽  
Vol 81 (2) ◽  
pp. 495-506 ◽  
Author(s):  
A. Radvila ◽  
R. Roost ◽  
H. Bürgi ◽  
H. Kohler ◽  
H. Studer
Keyword(s):  
Protein Synthesis ◽  
Thyroid Gland ◽  
Inhibitory Action ◽  
Inhibit Protein Synthesis ◽  
Thyrotrophic Hormone ◽  
Thyroid Glands ◽  
Pre Treatment ◽  
Excess Iodide ◽  
Kidney Liver

ABSTRACT Lithium and excess iodide inhibit the release of thyroid hormone from preformed stores. We thus tested the hypothesis that this was due to an inhibition of thyroglobulin breakdown. Rats were pre-treated with propylthiouracil (PTU) for 3 weeks in order to deplete their thyroids of thyroglobulin. While the PTU was continued, lithium chloride (0.25 mEq./100 g weight) or potassium iodide (3 mg per rat) were injected every 12 h for 3 days. Thereafter the thyroglobulin content in thyroid gland homogenates was measured. PTU pre-treatment lowered the thyroglobulin content from 4.21 to 0.22 mg/100 mg gland. Lithium caused a marked re-accumulation of thyroglobulin to 0.60 mg/100 mg within 3 days. While iodide alone had only a borderline effect, it markedly potentiated the action of lithium and a combination of the two drugs increased the thyroglobulin content to 1.04 mg/100 mg. Thyroxine was injected into similarly pre-treated animals to suppress secretion of thyrotrophic hormone. This markedly inhibited the proteolysis of thyroglobulin and 1.3 mg/100 mg gland accumulated after 3 days. Excess iodide, given in addition to thyroxine, decreased the amount of thyroglobulin accumulated to 0.75 mg/100 mg gland. To study whether this could be explained by an inhibitory action of iodide on thyroglobulin biosynthesis, thyroid glands from animals treated with excess iodide were incubated in vitro in the presence of 0.2 mm iodide for 3 h. Iodide decreased the incorporation of radioactive leucine into total thyroidal protein and into thyroglobulin by 25 and 35 % respectively. Iodide did not inhibit protein synthesis in the kidney, liver or muscle tissue. Thus, large doses of iodide selectively inhibit thyroglobulin biosynthesis.

scholarly journals AMIODARON SEBAGAI OBAT ANTI ARITMIA DAN PENGARUHNYA TERHADAP FUNGSI TIROID

2013 ◽  
Vol 3 (2) ◽  
Author(s):  
Starry H. Rampengan
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Function ◽  
Hormone Replacement ◽  
Type I ◽  
Peripheral Tissues ◽  
Hormone Synthesis ◽  
Thyroid Hormone Metabolism ◽  
Serum T4 ◽  
Life Threatening

Abstract: Amiodarone is a highly effective anti-arrhythmic agent used in certain arrhythmias from supraventricular tachycardia to life-threatening ventricular tachycardia. Its use is associated with numerous side-effects that could deteriorate a patient’s condition. Consequently, a clinician should consider the risks and benefits of amiodarone before initiating the treatment.The thyroid gland is one of the organs affected by amiodarone. Amiodarone and its metabolite desethyl amiodaron induce alterations in thyroid hormone metabolism in the thyroid gland, peripheral tissues, and probably also in the pituitary gland. These actions result in elevations of serum T4 and rT3 concentrations, transient increases in TSH concentrations, and decreases in T3 concentrations. Both hypothyroidism and hyperthyroidism are prone to occur in patients receiving amiodarone. Amiodarone-induced hypothyroidism (AIH) results from the inability of the thyroid to escape from the Wolff-Chaikoff effect and is readily managed by either discontinuation of amiodarone or thyroid hormone replacement. Amiodarone-induced thyrotoxicosis (AIT) may arise from either iodine-induced excessive thyroid hormone synthesis (type I, usually with underlying thyroid abnormality), or destructive thyroiditis with release of preformed hormones (type II, commonly with apparently normal thyroid glands). Therefore, monitoring of thyroid function should be performed in all amiodarone-treated patients to facilitate early diagnosis and treatment of amiodarone-induced thyroid dysfunction. Key words: Amiodarone, thyroid function, side effect, management, monitoring.     Abstrak: Amiodaron adalah obat antiaritmia yang cukup efektif dalam menangani beberapa keadaaan aritmia mulai dari supraventrikuler takikardia sampai takikardia ventrikuler yang mengancam kehidupan. Namun penggunaan obat ini ternyata menimbulkan efek samping pada organ lain yang dapat menimbulkan perburukan keadaan pasien. Sehingga, dalam penggunaan amiodaron, klinisi juga harus menimbang keuntungan dan kerugian yang ditimbulkan oleh obat ini. Salah satu organ yang dipengaruhi oleh amiodaron adalah kelenjar tiroid. Amiodaron dan metabolitnya desetil amiodaron memengaruhi hormon tiroid pada kelenjar tiroid, jaringan perifer, dan mungkin pada pituitari. Aksi amiodaron ini menyebabkan peningkatan T4, rT3 dan TSH, namun menurunkan kadar T3. Hipotiroidisme dan tirotoksikosis dapat terjadi pada pasien yang diberi amiodaron. Amiodarone-induced hypothyroidism (AIH) terjadi karena ketidakmampuan tiroid melepaskan diri dari efek Wolff Chaikof, dan dapat ditangani dengan pemberian  hormon substitusi T4 atau penghentian amiodaron. Amiodarone-induced thyrotoxicosis (AIT) terjadi karena sintesis hormon tiroid yang berlebihan yang diinduksi oleh iodium (tipe I, biasanya sudah mempunyai kelainan tiroid sebelumnya) atau karena tiroiditis destruktif yang disertai pelepasan hormon tiroid yang telah terbentuk (tipe II, biasanya dengan kelenjar yang normal). Pemantauan fungsi tiroid seharusnya dilakukan pada semua pasien yang diberi amiodaron untuk memfasilitasi diagnosis dan terapi yang dini terjadinya  disfungsi tiroid yang diinduksi amiodaron. Kata Kunci: Amiodaron, fungsi tiroid, efek samping, penanganan, pemantauan.

LINGUAL AND SUBLINGUAL THYROID GLANDS IN EUTHYROID CHILDREN

PEDIATRICS ◽  
1966 ◽  
Vol 38 (4) ◽  
pp. 647-651
Author(s):  
Wellington Hung ◽  
Judson G. Randolph ◽  
Domenic Sabatini ◽  
Theodore Winship
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Physical Examination ◽  
Thyroid Hormones ◽  
Hormone Therapy ◽  
Surgical Intervention ◽  
Ectopic Thyroid ◽  
Lingual Thyroid ◽  
Thyroid Glands ◽  
Careful Physical Examination

Five clinically euthyroid children with lingual or sublingual thyroid glands were seen during a 12-month period. Certain recommendations have been formulated based upon our experience with these patients. A careful physical examination should be performed to demonstrate the presence of a normally located thyroid gland in all children presenting with midline masses in the lingual or sublingual areas. When the thyroid gland cannot be palpated with certainty in these children, a scintiscan with I-131 should be carried out to determine if the mass is an ectopic thyroid gland and if a normally located thyroid gland is present. All children with lingual on sublingual thyroid glands should have a trial of full replacement thyroid hormone therapy before excision is contemplated. Thyroid therapy will prevent further hypertrophy and hyperplasia. Surgical intervention should be reserved for those children in whom there is dysphagia, dysphonia, ulceration, or hemorrhage due to a lingual thyroid gland or if the ectopic thyroid gland fails to decrease in size following a course of treatment with thyroid hormones.

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