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Related Concept Videos

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...
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...
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...
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...
The Thyroid Gland01:23

The Thyroid Gland

The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
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...

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Related Experiment Video

Updated: Jun 26, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Minimal oxidative load: a prerequisite for thyroid cell function.

Sylvie Poncin1, Ides M Colin, Anne-Catherine Gérard

  • 1Unité de Morphologie Expérimentale, Université Catholique de Louvain, UCL-5251, Bruxelles, Belgium.

The Journal of Endocrinology
|January 27, 2009
PubMed
Summary
This summary is machine-generated.

Thyroid cells require a basal level of reactive oxygen species (ROS) for normal function. Reducing ROS with N-acetylcysteine (NAC) hampers key thyroid protein expression, impacting hormone production.

Related Experiment Videos

Last Updated: Jun 26, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Area of Science:

  • Biochemistry
  • Cell Biology
  • Endocrinology

Background:

  • Thyrocytes produce hydrogen peroxide (H2O2) for hormone synthesis.
  • The role of basal reactive oxygen species (ROS) in non-stimulated thyrocytes is unknown.

Purpose of the Study:

  • To investigate the involvement of ROS in normal thyrocyte function.
  • To determine the effects of the antioxidant N-acetylcysteine (NAC) on thyrocyte gene and protein expression.

Main Methods:

  • Thyrocytes were incubated with N-acetylcysteine (NAC).
  • Gene and protein expression of key thyroid proteins (dual oxidases, thyroperoxidase, pendrin, thyroglobulin, Na+/I- symporter) and antioxidant systems (peroxiredoxins, catalase) were analyzed.
  • In vivo studies were conducted using NAC treatment.

Main Results:

  • NAC blocked intracellular ROS production.
  • NAC decreased the expression of dual oxidases, thyroperoxidase, pendrin, and thyroglobulin.
  • Na+/I- symporter mRNA expression remained unaffected.
  • Peroxiredoxin 5 (PRDX5) expression decreased, while PRDX3 increased; catalase was unchanged.
  • In vivo, NAC reduced dual oxidases and PRDX5 protein expression.

Conclusions:

  • Basal ROS levels are essential for maintaining the expression of proteins involved in thyroid cell function.
  • A minimal level of ROS is required to safeguard thyrocyte function and hormone production.