Role of Iodine in Metabolism

Abstract

The natural resources of iodine are seawater, seaweeds and saltpeter-nitrate deposits in Chile. Over 1/3 of the global population is exposed to iodine deficiency, especially in the mountains. Iodine is a component of the thyroid hormones and a strong antioxidant with electric potential of -0.54 V. Iodine as iodide is taken up by the thyroid gland, gastric mucosa, salivary glands and mammary glands in pregnant and breast-feeding women. The transport of iodine to the thyroid gland is regulated by specific enzymes: Natrium Iodine Symporter, Na+/K+ATPase, Pendrin and Apical Iodine Transporter. In the thyrocytes, the thyroid hormones biosynthesis is carried out by iodization of tyrosine to T3 and T4. Secretion of T3 and T4 is regulated by TSH. On the tissue level, the active hormones are T3 and its derivative thyroamine. The most important target is the cardiac muscle, where T3 action results in an increase in the inotropic action and thyroamines exert a negative inotropic and chronotropic effects. The consequences of iodine deficiency are endemic goiter, irreversible brain damage, cretinism, impaired thyroid function and thyroid, gastric and mammary glands cancers. In 1994, the World Health Organization proposed the main strategy for iodine prophylaxis, i.e. Universal Salt Iodization. In Poland, a new model of iodine prophylaxis was introduced in 1996; the model includes obligatory iodization of household salt and neonate formulas and recommendation to take an additional daily dose of iodine for pregnant and breast-feeding women. This model allowed for eliminating endemic goiter in schoolchildren, eradicating cretinism in mountainous areas, and markedly diminished thyroid and gastric cancer incidence. In 2002, WHO classified Poland as a country with a proper daily iodine intake on the population level. No relevant patents were reported for this WHO report.

Keywords: Iodine; iodine deficiency.; iodine prophylaxis; metabolic pathway; synthesis; thyroid hormones.