Histologic effects of chronic selenium deficiency in selected tissues of laboratory rats Public Deposited

http://ir.library.oregonstate.edu/concern/graduate_thesis_or_dissertations/6395wb601

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  • The selenium-responsive syndromes and the discovery of Factor 3-selenium focused attention on selenium in metabolism. Two hypotheses have been advanced to explain the metabolic effect of selenium: 1) substitution or sparing of alpha tocopherol, and 2) a primary role in metabolism. The first hypothesis is supported by Scott and Desai, who found that selenium and alpha tocopherol produced similar responses in certain deficiency diseases. The earlier inability to produce lesions of a selenium deficiency in the rat in the presence of ample vitamin E has caused the validity of the second hypothesis to be questioned. This obstacle to identifying the metabolic role of selenium was overcome when Weswig and Whanger succeeded in developing a selenium-deficient rat. Selenium-deficient rats were obtained from the colony of Weswig and Whanger and observed until deficiency lesions appeared. At this time they were divided randomly into selenium deficient and supplemented groups. The deficient group was maintained on the low selenium rations and the supplemented group was fed this diet with 100 ppb selenium added as sodium selenite. The rats were necropsied at 80, 147 and 221 days of age. Body, heart, liver and genital weights were recorded and tissues were selected for histological and histochemical studies. Signs in the selenium deficient rats were poor growth, alopecia and sterility. The histopathologic lesions of the skin, liver, genitalia, and musculoskeletal system are described. The pathologic changes resembled those found in exudative diathesis of chicks, un-thriftiness in lambs and calves, and infertility in ewes. Liver necrosis and myopathy were not observed, Histochemical changes included a reduction in the number of sulfhydryl reactive sites in the liver, testicle, muscle and back skin. Morphological changes were directly related to endothelial degeneration and hypoplasia. Correlation of clinical lesions and cellular changes indicated that selenium deficiency in the rat altered protein production and physiology of the vasculature.
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