Abstract
Clinical evidence has implicated cobalt (Co) in the etiology of a primary myocardial disease occurring among certain heavy beer drinkers when Co was added to the beer (McDermott et al. 1966; Bonenfant et al. 1967; Morin et al. 1967; Kesteloot et al. 1968; Alexander 1972). Investigators have reported in experimental animals Co-induced myocardial damage similar to the pathologic manifestations of the beer drinker’s heart disease (Sandusky et al. 1981). It has been reported that Co acts to accelerate the in vivo formation of lipid peroxides (LPO) in the blood of rabbits and causes a decrease in superoxide dismutase (SOD) activity, but fails to alter glutathione peroxidase (GSH-Px) in erythrocytes (Kuno et al. 1980; Morita et al. 1982). Selenium (Se)-vitamin E protection against acute Co cardiotoxicity has been observed in swine (Van Vleet et al. 1977).
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References
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© 1989 Springer-Verlag Berlin Heidelberg
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Cui, JQ., Xu, GL. (1989). Protection of Experimental Cobalt Cardiomyopathy in the Rat by Selenium Pretreatment. In: Wendel, A. (eds) Selenium in Biology and Medicine. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-74421-1_37
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DOI: https://doi.org/10.1007/978-3-642-74421-1_37
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