Cronicon OPEN ACCESS EC NUTRITION Opinion Selenium and Autoimmune Thyroiditis Marco Giammanco 1,3 * and Gaetano Leto 2 1 Department of Surgical, Oncological and Oral Sciences, University of Palermo, Italy 2 Department of Science for Health Promotion Sciences, School of Medicine, University of Palermo,Italy 3 Research Unit in Endocrinology, Italian Society of Experimental Biology, Italy *Corresponding Author: Marco Giammanco, Department of Surgical, Oncological and Oral Sciences, University of Palermo, Palermo, Italy. Citation: Marco Giammanco and Gaetano Leto. “Selenium and Autoimmune Thyroiditis”. EC Nutrition 14.5 (2019): 449-450. Received: March 25, 2019; Published: April 29, 2019 The essential mineral, selenium, is of fundamental importance to human health. As a constituent of selenoproteins, selenium has structural and enzymic roles, in the latter context being best-known as an antioxidant and catalyst for the production of active thyroid hormone. Selenium is needed for the proper functioning of the immune system. An elevated selenium intake may be associated with reduced cancer risk [1,2]. Selenium is an trace element that is required for the correct functioning of the immune system with a recommended daily intake for adults of 55 μg [3]. Selenium-rich sources include nuts, meat, cereals, fish and shellfish [4]. Selenomethionine and sodium selenite are the two most common oral forms of selenium supplementation that are available in variable dosages (100 and 200 μg/day) [5]. Selenium plays a key role in thyroid cell physiology, it is incorporated in the molecular structure of several enzymes in the thyroid gland [6,7]. One of these enzymes, glutathione peroxidase, is critically involved in protecting the gland against oxidative damage. Thyroid peroxidase uses hydrogen peroxide (H 2 O 2 ), a free radical capable of inflicting oxidative damage, as a substrate in catalyzing the iodination and coupling of tyrosyl residues in thyroglobulin to produce thyroid hormone. The tri-iodothyronine (T3), is produced by de-iodination of the hormone T4 by type I and type II iodothyronine de-iodinases in, a two-substrate, along with degradation of H 2 O 2 to water by glutathione peroxi- dase. Iodothyronine de-iodinases are also selenoproteins, as is glutathione peroxidase. If there is selenium deficiency, these two enzymes cannot function properly, which results in both ineffective production of T3 and inefficient protection against free radicals, the latter facilitating cell damage and autoimmune destruction of the gland [6-8]. Autoimmune thyroiditis is one of the most prevalent autoimmune diseases and affects more than 10% of females and 2% of males. Cellular destruction by CD4 cell-mediated autoimmune attacks results in permanent hypothyroidism in more patients [9]. More than one- third of the patients have other autoimmune diseases. In areas with severe selenium deficiency there is a higher incidence of thyroiditis due to a decreased activity of selenium-dependent glutathione peroxidase activity within thyroid cells. Selenium is strongly involved, via the variable selenoproteins, in antioxidant, redox, and anti-inflammatory processes. Selenium enhances CD4+/CD25 FOXP3 and T regu- latory cells activity while suppressing cytokine secretion, thus preventing apoptosis of the follicular cells and providing protection from thyroiditis. Environmental factors, such as iodine intake, immunotherapeutic agents or viral infections, can also trigger the disease. Sele- nium substitution may improve the inflammatory activity in patients with autoimmune thyroiditis, especially in those with high activity. Whether this effect is specific for autoimmune thyroiditis or may also be effective in other autoimmune diseases [9]. Low selenium status is associated with an increased risk of overall mortality, a reduced immune response and a decline of cognitive functions [10]. On the other hand, dietary selenium supplementation has shown to exert antiviral effects [11], improves male and female reproduction [12] and lower the risk of autoimmune diseases [13]. Furthermore, several clinical studies have highlighted a significant association between higher selenium status and reduced risk of prostate, lung, colorectal and bladder cancer. However, other clinical observations failed to demonstrate such correlation. In this scenario,