Selenium is an essential biological trace element in mammals and adults should be intake 100 μg per day. Selenium is inserted into selenoproteins as selenocysteine (Sec), which is encoded by the UGA “STOP” codon in open reading frame. The translational process for selenoproteins in mammals is achieved by various components, such as the selenocysteineinsertion- sequence (SECIS) in the untranslated region of mRNA, the SECIS-binding protein SBP2, the Sec-specific translation factor EF-Sec, and the Sec-specific tRNASec. Generally, most selenoproteins including glutathione peroxidase and thioredoxin reductase exhibit antioxidant function to protect cells from oxidative stress. In addition, thyroxine deiodinase plays an important role in the control of thyroid hormone metabolism. These results indicate that the adequate diet of selenium is essential for maintaining redox status and hormone. On the other hand, a deficiency intake of selenium shows Keshan’s disease (cardiomyopathy), Kashin-Beck disease (osteoarthritis), white muscle disease, and cretinism as well as an excessive intake of selenium results in toxic symptoms, including blind staggers and alkaline diseases. Therefore, an adequate intake of selenium is necessary to maintain in vivo function. The aim of this review is to discuss the role of selenium in vivo.