Selenium occurs in all cells as amino acids selenomethionine and selenocysteine
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Selenium forms a part of glutathione peroxidase, an antioxidant enzyme. Selenium is also a part of type I iodothyronine 5-deiodinase which participates in the hepatic deiodination of thyroxine; in animals it is a component of muscle proteins selenoprotein P and selenoprotein W. Selenium is absorbed from the small intestine. It is protein bound in circulation, and is excreted in urine.
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Selenium is present in diet as selenomethionine and selenocysteine. Its content in plant food depends on the content in the the soil. Its dietary sources include organ meats, fish (tuna) and shellfish, and cereals.
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Increased intake of selenium might be required during lactation. There is a rare selenium-responsive cardiomyopathy (Keshan disease), which is endemic in China in areas of very low selenium intake. Deficiency of selenium can also develop during total parenteral nutrition and may result in chronic muscle pain, abnormal nail beds, and cardiomyopathy. The excess of selenium leads to liver cirrhosis, splenomegaly, gastrointestinal bleeding and depression.
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Numerous other trace metals are required for normal biologic function, for example manganese, molybdenum, vanadium, nickel, and even cadmium. The latter is probably better known for its renal toxic effects and has been seen especially in shipyard workers exposed to this metal over long periods of time. No doubt, as techniques for separation and analysis develop, other metals and other functions of known essential minerals will become known. This will lead to a better understanding of the epidemiology of certain diseases which may have, at least in part, an environmental aetiology.
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