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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...
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...
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...
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...
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...
Goiter01:27

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...

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Related Experiment Video

Updated: Jul 16, 2026

Necropsy-based Wild Fish Health Assessment
07:57

Necropsy-based Wild Fish Health Assessment

Published on: September 11, 2018

Contaminant effects on the teleost fish thyroid.

Scott B Brown1, Bruce A Adams, Daniel G Cyr

  • 1Environment Canada, P.O. Box 5050, Burlington, Ontario L7R 4A6, Canada. scott.brown@ec.gc.ca

Environmental Toxicology and Chemistry
|July 3, 2004
PubMed
Summary

Environmental chemicals impact fish thyroid function, serving as biomarkers. However, the precise mechanisms and consequences for fish health remain unclear, necessitating further research.

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Area of Science:

  • Environmental toxicology
  • Endocrinology
  • Aquatic biology

Background:

  • Numerous environmental chemicals disrupt the thyroid cascade in teleost fish.
  • Thyroid endpoints are valuable biomarkers for detecting pollutant exposure.
  • The mechanisms and physiological consequences of chemical-induced thyroid disruption are not fully understood.

Purpose of the Study:

  • To review the effects of environmental chemicals on the fish thyroid cascade.
  • To highlight the utility of thyroid endpoints as biomarkers.
  • To identify knowledge gaps and suggest future research directions.

Main Methods:

  • Review of existing literature on chemical impacts on fish thyroid function.
  • Analysis of thyroid endpoints as biomarkers of environmental pollutants.
  • Identification of challenges in interpreting thyroid disruption data.

Main Results:

  • A wide range of chemicals affect fish thyroid function across numerous species.
  • Thyroid disruption in fish is linked to environmental pollutant exposure.
  • Causal links between thyroid changes and decreased fish fitness or survival are not yet established.

Conclusions:

  • Standardizing test conditions and thyroid endpoints is crucial for future research.
  • Investigating the causal links between thyroid disruption and fish growth, reproduction, and development is essential.
  • Early life stages of fish may be particularly susceptible to thyroid disruption, requiring specific endpoints.