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Synthesis and Regulation of Thyroid Hormones

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...

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Exposure to perfluorinated compounds: in vitro study on thyroid cells.

Francesca Coperchini¹, Patrizia Pignatti, Serena Lacerenza

¹Unit of Internal Medicine and Endocrinology, Fondazione Salvatore Maugeri I.R.C.C.S., Laboratory for Endocrine Disruptors and Chair of Endocrinology University of Pavia, Via S. Maugeri 10, 27100, Pavia, Italy.

Environmental Science and Pollution Research International

|September 4, 2014

Summary

High concentrations of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) significantly inhibit thyroid cell proliferation and increase cell death. These perfluorinated chemicals (PFCs) enter thyroid cells via passive diffusion.

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An Ex vivo Culture System to Study Thyroid Development

An Ex vivo Culture System to Study Thyroid Development

Published on: June 6, 2014

Area of Science:

Environmental Toxicology
Cell Biology
Endocrinology

Background:

Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are prevalent perfluorinated chemicals (PFCs).
PFOA and PFOS have been detected in human thyroid tissues.
Limited research exists on the in vitro impact of PFOA and PFOS on thyroid cells.

Purpose of the Study:

To investigate the in vitro effects of PFOA and PFOS on thyroid cell proliferation and viability.
To determine the mechanism of PFOA and PFOS uptake by thyroid cells.

Main Methods:

Utilized Fisher rat thyroid line-5 (FRTL-5) cells for in vitro exposure experiments.
Assessed cell viability and proliferation rates following exposure to varying concentrations of PFOA and PFOS.
Quantified PFC levels in cell pellets to elucidate uptake mechanisms.

Main Results:

Thyroid cells (FRTL-5) showed no significant changes in viability or proliferation at PFOA/PFOS concentrations up to 10(4) nM.
A significant inhibition of cell proliferation, primarily due to increased cell death, was observed at 10(5) nM PFOA/PFOS.
PFOA and PFOS were detected within FRTL-5 cells after exposure, indicating cellular uptake.
Cellular PFC levels diminished after removal of the chemicals, suggesting passive diffusion.

Conclusions:

In vitro exposure to high concentrations of PFOA and PFOS can inhibit thyroid cell proliferation and induce cell death.
PFOA and PFOS appear to enter thyroid cells through a gradient-based passive diffusion mechanism.
Further in vivo studies are warranted to assess the long-term toxicological effects of lower PFC concentrations.