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1 Introduction In 1818, Berzelius in Gripsholm, Sweden, identified selenium as a new chemical element. From humble beginnings as a residue in a sulfuric acid vat, selenium has found exciting uses in commerce. Many of these depend on the remarkable susceptibility of selenium electrons to excitation by light, resulting in generation of an electric current. This has led to use of selenium in photoelectric cells, light meters, rectifiers, and xerographic copying machines. It is also used to decolorize the greenish tint of glass due to iron impurities or, in excess, to create the ruby-red color seen in warning signals and automobile tail lights. These and other uses are met by produc- tion of approximately 266 metric tons of selenium annually in the United States and worldwide production of 1,559 metric tons (Anonymous, 1979a, 1979b). The biological significance of selenium was not recognized until it was identified as the toxic principle causing lameness and death in livestock grazing certain range plants in the Dakotas and Wyoming (Franke, 1934~. Dr. Madison (1860) had earlier observed a number of toxicity signs, in- cluding hair loss, in cavalry horses at Fort Randall in the old Nebraska Territory. Lameness resulted from inflammation of the feet, followed by suppuration at the point where the hoof joins the skin and ultimate loss of the hoof. The consequent tenderness inhibited the search for food and water, and since no stored forage was available, death was at least partly attributable to starvation. Similar signs were described by Marco Polo (Komroff, 1926) in his travels in western China near the borders of Turkes- tan and Tibet about the year 1295. Loss of hair and nails in humans pre 1
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2 SELENIUM IN NUTRITION sumably suffering from chronic selenosis was first described in Colombia by Father Pedro Simon in 1560. The discovery in 1957 (Schwarz and Foltz, 1957) that selenium was an essential nutrient led to an entirely new era of research that continues to- day. Instead of a primary concern with the toxicity of selenium, nutrition- ists turned their attention to the metabolic function of this element and the consequences of its deficiency. Hepatic necrosis in rats, probably associ- ated with inadequate selenium and vitamin E, was seen by Klaus Schwarz in 1939 as he used purified diets to study vitamins in Richard Kuhn's labo- ratory at the Kaiser Wilhelm Institute (now the Max Planck Institute) in Heidelberg (Schwarz, 1976~. Interestingly, Alvin Moxon, as a graduate student at South Dakota State University in the early 1930s, documented a growth response in chicks fed low levels of selenium in a series of studies designed to explore the toxicity of selenium at graded levels (Oldfield, 1981~. When workers in William Hoekstra's laboratory at the University of Wisconsin (Rotruck et al., 1973) and Dr. Flohe and his associates (1973) at Tubingen established the unequivocal relationship between selenium and glutathione peroxidase, a fundamental connection between this element and metabolic processes was made. Despite the significance of this find- ing, it is probable that this is not the only metabolic role that selenium fulfills. A number of research groups are actively investigating evidence that other functions exist. These studies and others suggesting a relation- ship between selenium deficiency and human disease are documented in the following pages. The reader is invited to peruse them critically, but the authors would caution that the final chapter for selenium in nutrition has not yet been written.