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Titlebook: Selenium in Biology and Medicine; Proceedings of the 4 Albrecht Wendel Conference proceedings 1989 Springer-Verlag Berlin Heidelberg 1989 b

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heir favourite trace element, selenium. This meeting continued the good tradition of three previous meetings held in Corvallis/Oregon, 1976, in Lubbock/Texas, 1980, and in Beijing/China, in 1984. Incidentally, the University of Tiibingen provided a unique historical background for a Symposium devote
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Regulation of Expression of Glutathione Peroxidase by Seleniumin in 1971 to identify GSH-Px as a Se-dependent enzyme (Rotruck et al. 1972, 1973). The background to this discovery was described succinctly at the Second Selenium in Biology and Medicine Symposium (Rotruck 1981).
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Studies on New Selenoproteins and Specific Selenium Target Tissuese. Through our studies on Se metabolism we became interested in the following two questions: First, is Se of importance also in other parts of the organism? Second, are there other biologically important Se compounds besides glutathione peroxidase? The studies which are presented here deal with these two aspects of Se research.
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Role of Glutathione Peroxidase and ,-Tocopherol in Protecting Rat Erythrocytes Against ,-Butyl Hydroyet unclear, however, regarding the protection afforded by glutathione peroxidase (GSH-Px) compared with that afforded by vitamin E (Tappel 1980; Levander 1986). This chapter presents three lines of experimental evidence pointing to the predominant function of GSH-Px in antioxidant defense mechanisms.
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Studies on Selenite-Induced DNA Fragmentation and the Role of Poly(ADP Ribose)Polymerase in SelenitePARP) (Berger 1985). This enzyme utilizes NAD as a substrate, and it has been proposed that an extensive DNA fragmentation may lead to cell death via NAD depletion. It is thus possible that selenite can interact with other DNA-damaging compounds so that it selectively kills DNA-damaged cells.
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