Abstract

The global effort to prevent iodine deficiency disorders through iodine supplementation, such as universal salt iodization, has achieved impressive progress during the last few decades. However, iodine excess, due to extensive environmental iodine exposure in addition to poor monitoring, is currently a more frequent occurrence than iodine deficiency. Iodine excess is a precipitating environmental factor in the development of autoimmune thyroid disease. Excessive amounts of iodide have been linked to the development of autoimmune thyroiditis in humans and animals, while intrathyroidal depletion of iodine prevents disease in animal strains susceptible to severe thyroiditis. Although the mechanisms by which iodide induces thyroiditis are still unclear, several mechanisms have been proposed: (1) excess iodine induces the production of cytokines and chemokines that can recruit immunocompetent cells to the thyroid; (2) processing excess iodine in thyroid epithelial cells may result in elevated levels of oxidative stress, leading to harmful lipid oxidation and thyroid tissue injuries; and (3) iodine incorporation in the protein chain of thyroglobulin may augment the antigenicity of this molecule. This review will summarize the current knowledge regarding excess iodide as an environmental toxicant and relate it to the development of autoimmune thyroid disease.

Highlights

  • This study suggests that excess iodine can induce oxidative stress-related thyrocyte injury in individuals, whether this cell injury leads to lymphocytic infiltration will depend on the additional effects of genetic factors

  • This study suggests that high iodine diets can lead to the production of thyroglobulin with high iodine content and that the anti-thyroglobulin autoantibody has a higher affinity to high iodine thyroglobulin (HI-Tg) than to low iodine thyroglobulin (LI-Tg)

  • Iodine excess is recognized as an environmental risk factor for the development of autoimmune thyroid disease (ATD) in humans and animals

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Summary

Iodine as an Essential Element for Thyroid Hormone

Iodine (symbol: I; atomic number: 53; average atomic weight: 126.9) is a trace chemical element primarily found in oceans as the highly water-soluble iodide ion (I−). Iodine is an essential element required for the production of thyroid hormone (TH). The synthesis of mammalian thyroid hormone requires the transport of I− into thyroid cells. Thyroglobulin, a large glycoprotein precursor of thyroid hormone, is found in the colloid, following synthesis in the endoplasmic reticulum. The enzyme thyroid peroxidase catalyzes the oxidation of I− to I2 and iodination of the tyrosyl residues of thyroglobulin molecules to generate monoiodotyrosine (MIT) and diiodotyrosine (DIT). Iodinated thyroglobulin is re-absorbed by the action of thyroid stimulating hormone (TSH) into thyroid cells, where it is digested by proteases to release thyroid hormone (T4 and T3) from the backbone of its protein chain into circulation [8]

Global Prevention and Elimination of Iodine Deficiency
Iodine Excess as Another Concern
Excessive Iodine Exposure in the Environment
Excess Iodine Is a Recognized Environmental Factor for Autoimmune Thyroiditis
Stimulation of Lymphocytic Response in Thyroid by Excess Iodine
Induction of Oxidative Thyroid Tissue Injury by Excess Iodine
Influence of Iodine on Thyroglobulin Auto-Antigenicity
Findings
Conclusions

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