## 1 Introduction  
Selenium is one of the most intriguing trace elements of the periodic table. After its discovery in 1818 by the Swedish [PERSON] in a sulfuric acid plant, it was used for its electric and photoelectric properties [1]. Its first medical application dates back to 1911, when an unidentified Se compound had caused necrosis and the disappearance of [PERSON]'s carcinoma and sarcoma in mice [1]. A year later, a publication by Delbet in 1912 reported the death of patients who received high doses of sodium selenite [2]. However, all therapeutic applications of Se ceased when, in 1943, [PERSON] et al. had declared the element itself carcinogenic [3]. It was not until 1957 that scientists collected evidence for the other face of the moon (_Selen_ in Greek), that is, for the essentiality of the trace element Se for humans and animals [1, 4].  
Despite the importance of selenium in human health, the major impact of supply, speciation and restricted uptake of this micronutrient, is currently not well understood [5]. Much research is still needed to improve our understanding of optimized requirements, taking into account the very narrow range between the beneficial and toxic effects of the mineral [5].  
Selenium is essential for many cellular functions including redox homeostasis and antioxidant defense [6]. In the body, Se is ingested from food, absorbed in the gastrointestinal tract (GIT), transported to the liver and kidney for metabolism and distribution to the body tissues [7].  
In humans, Se is integrated into 25 selenoproteins in the form of the amino acid Se-Cys. Some of them such as glutathione peroxididases (GPx), iodothyronine deididinases (DIO) and thioredoxinine reductases (TRx) play an important role in the metabolism of the thyroid gland [8]. Se is present at higher concentrations in the thyroid than in other organs and is an essential element for the biosynthesis of thyroid hormones [9]. Another important role of selenoproteins in the thyroid is the detoxification by GPx of hydrogen peroxide (H\({}_{2}\)O\({}_{2}\)) massively synthetized in order to oxidize iodide (I\({}^{-}\)) and introduce it into thyroglobulin, a precursor of L-3,5,3',5'-tetraiodothyonine (thyroxine; T4) and L-3,5,3'-triiodothyronine (T3) [10]. Therefore, Se is considered to be the second most important element in thyroid metabolism after iodine [11].  
The results of initial epidemiological studies have suggested a significant association between low Se status and cancer, suggesting that Se may have anticarcinogenic effect [12]. Surprisingly, recent studies have shown an increased risk of some cancers such as prostate cancer with high Se levels [13] and the chemotherapeutic effect of Se have not been proven at safe and tolerated doses (<90 \(\upmu\)g/day) [14].  
However, in the case of thyroid cancer, serum Se deficiency may be considered a risk factor but the results are inconclusive [15,16].  
This review synthesizes the speciation-controlled transport of Se from soil to humans via food and its absorption in human gastrointestinal tract. We then focus on the use of Se by thyroid gland and on the relationship between Se and thyroid cancer, according to the latest knowledge produced on this pathology.