As an essential trace element, iodine belongs to the haloalkanes (salt formers). Due to its size and lower electronegativity – 2.2 according to Allrod/Rochow – iodine occurs in nature not in free but in cationically bound form. Thus, it enters the organism as iodide, iodate or organically bound via food.
Metabolism
The trace element is almost completely absorbed in the small intestine. With the help of non-enzymatic reactions, reduction of iodate to iodide occurs beforehand. Iodide is transported through the bloodstream and accumulated in the thyroid gland and other tissues, such as salivary gland, mammary gland, and stomach. Transport to the thyroid is by means of a specific sodium-dependent iodide transporter in the basolateral membrane of thyrocytes (thyroid follicle cells), the so-called “sodium-iodide symporter” (NIS). Under energy consumption, this transports two Na+ ions together with an I- ion against a concentration gradient in the same direction. Excessive intake of nitrate through food – for example via spinach, radish, radish and chard – and drinking water – > 50 ml/L – inhibits active iodide transport in the thyroid and gastrointestinal tract. Nitrate displaces iodine from its binding at the sodium-iodide symporter for this purpose. High nitrate loads thus increase the risk of iodine deficiency or struma prevalence and should be avoided for this reason.The transport of iodide into the thyrocytes of the thyroid gland is promoted by thyroid-stimulating hormone (TSH) produced in the pituitary gland. Following the oxidation of iodide by thyroperoxidase, binding to thyroxine occurs. This produces 3-monoiodotyrosine (MJT) and 3,5-diiodotyrosine (DJT) – iodization. Thyroperoxidase is a heme enzyme. Its activity, and thus the synthesis of thyroxine, may be impaired in the presence of iron deficiency.Thyreoperoxidase further initiates the coupling reaction of two molecules of DJT to form L-thyroxine (T4), as well as the formation of triiodothyronine (T3) from DJT and MJT. More than 99% of the thyroid hormones T4 and T3 are bound in plasma to transport proteins such as thyroxine-binding globulin (TBG), transthyretin and albumin. Only a small proportion of these hormones is present in free and thus unbound form. Only the free hormones, i.e. free T3 and free T4, are metabolically active. The conversion of T4 to the biologically active T3 in the liver and kidney, among other places, is carried out by the selenium-containing thyroxine 5′-deiodases. Active T3 binds with three different specific T3 receptors in mitochondria and in the nucleus and is involved in the regulation of the expression of thyroid hormone-modulated genes.Finally, iodine as an essential component of thyroid hormones and selenium as an integral building block of deiodases are essential for the metabolism of thyroid hormones. Optimal activity of the hormones is in turn essential for maintaining normal thyroid function. The total body stock of adults with long-term adequate iodine supply is estimated to be 10-20 mg (79-158 nmol). Of this, about 70-80% is in the thyroid gland. The remainder is found in muscles, bile, pituitary gland (pituitary gland), salivary glands, and in various parts of the eye, especially in the orbicularis oculi muscle (ring muscle of the eye) and in the fatty tissue of the orbit. With the help of selenium-dependent deiodases, part of the iodide is released from the thyroid gland and other tissues into the extracellular space. Finally, some iodine is available again via the enterohepatic circulation. Excretion of the trace element is 89% in urine and to a lesser extent in the form of conjugated iodothyronines via bile and faeces (stool). With adequate intake, excretion should be between 20 and 70 µg/day.
