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Related Concept Videos

Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Published on: March 17, 2023

Methimazole increases H2O2 toxicity in human thyroid epithelial cells.

N L Landex1, J Thomsen, L Kayser

  • 1Department of Medical Anatomy, The Panum Institute, University of Copenhagen, Blegdamsvej 3b, 2200 Copenhagen N, Denmark. N.L.Landex@mai.ku.dk

Acta Histochemica
|October 19, 2006
PubMed
Summary

Hydrogen peroxide (H2O2) impacts thyroid cells, with harmful effects at higher concentrations. The antithyroid drug methimazole may worsen H2O2 damage by inhibiting glucose-6-phosphate dehydrogenase (G6PD).

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Determining the Toxicity of UV Radiation and Chemicals on Primary and Immortalized Human Corneal Epithelial Cells
09:31

Determining the Toxicity of UV Radiation and Chemicals on Primary and Immortalized Human Corneal Epithelial Cells

Published on: July 22, 2021

Area of Science:

  • Endocrinology
  • Cell Biology
  • Oxidative Stress Research

Background:

  • Hydrogen peroxide (H2O2) plays a crucial role in thyroid hormone synthesis and intracellular signaling.
  • Oxidative stress, including H2O2 dysregulation, is linked to thyroid cancer development.
  • Understanding the cellular impact of H2O2 is vital for thyroid health and disease research.

Purpose of the Study:

  • To investigate the effects of H2O2 on human thyroid epithelial cells.
  • To assess H2O2's impact on cell morphology, differentiated function, NADPH generation, and apoptosis.
  • To determine if methimazole can mitigate H2O2-induced cellular damage.

Main Methods:

  • Exposure of human thyroid epithelial cells to varying concentrations of H2O2.
  • Morphological assessment and histochemical analysis of intracellular thyroglobulin.
  • Assay of glucose-6-phosphate dehydrogenase (G6PD) activity to measure NADPH generation.
  • Apoptosis assays to evaluate cell vitality.
  • Treatment with methimazole to assess its protective or sensitizing effects.

Main Results:

  • Human thyroid epithelial cells exhibit tolerance to H2O2 below 0.3mM.
  • Higher H2O2 concentrations induce harmful effects on cell morphology and vitality.
  • Methimazole (10mM) sensitizes cells to H2O2 toxicity.
  • Methimazole appears to inhibit G6PD activity in a dose-dependent manner, potentially explaining the sensitization.

Conclusions:

  • The study highlights the critical role of the cellular antioxidative system in thyroid cells.
  • H2O2 concentration is a key factor determining its cellular impact.
  • Methimazole's interaction with H2O2, possibly via G6PD inhibition, warrants further investigation in thyroid pathophysiology.