Selenium (Se) was discovered 180 years ago. The toxicological properties of Se in livestock were recognized first; its essential nutritional role for animals was discovered in the 1950s and for humans in 1973. Only one reductive metabolic pathway of Se is well characterized in biological systems, although several naturally occurring inorganic and organic forms of the element exist. The amount of Se available for assimilation by the tissues is dependent on the form and concentration of the element. Se is incorporated into a number of functionally active selenoproteins, including the enzyme glutathione peroxidase, which acts as a cellular protector against free radical oxidative damage and type 1 iodothyronine 5'-deiodinase which interacts with iodine to prevent abnormal hormone metabolism. Se deficiency has been linked with numerous diseases, including endemic cardiomyopathy in Se-deficient regions of China; cancer, muscular dystrophy, malaria, and cardiovascular disease have also been implicated, but evidence for the association is often tenuous. Information on Se levels in foods and dietary intake is limited, and an average requirement for Se in the U.K. has not been established. Available data suggest that intake in the U.K. is adequate for all, except for a few risk groups such as patients on total parenteral nutrition or restrictive diets.
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