Abstract
Since the discovery of the essentiality of selenium (Se) for rats by Schwarz and Foltz (1957) and for chicks by Patterson et al. (1957), several naturally occurring animal diseases related to Se and vitamin E (VE) deficiency have been reported (Muth et al., 1958; Hartley and Grant, 1961). Since the recognition of Se as an essential nutrient for animals, suggestions that Se may also be essential in human nutrition have been based upon three kinds of findings. One was the demonstration of certain uncomplicated Se-deficiency diseases produced in the laboratory chick (Thompson and Scott, 1970) and rat (McCoy and Weswig, 1969; Wu et al., 1979), with the assumption that a similar specific requirement should occur in humans. Second was the isolation of glutathione peroxidase (GSHpx) from human erythrocytes (Awasthi et al., 1975) and human placenta (Awasthi and Dao, 1978). There was also the finding that Se is required for the growth of human fibroblasts in culture (McKeehan et al., 1976). It was, therefore, reasonable to assume that some human disorders may be related to nutritional Se deficiency. The association of Se with protein-rich foods prompted the early investigation of its possible relation to the pathogenesis of protein-calorie malnutrition (Schwarz, 1965a; Burk et al., 1967). Moreover, the detrimental effects of Se deficiency on heart function observed in animals (Godwin, 1965;) Godwin and Frash, 1966) led some relationship between Se deficiency and human cardiovascular disease.
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Yang, G. et al. (1984). The Role of Selenium in Keshan Disease. In: Draper, H.H. (eds) Advances in Nutritional Research. Advances in Nutritional Research, vol 110. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2801-8_8
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DOI: https://doi.org/10.1007/978-1-4613-2801-8_8
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