Historical Background

Se can be highly toxic, with signs and symptoms starting to occur in humans if the daily intake exceeds approximately 0.8-1 mg. Studies in the 1940s suggested that Se may be a potential carcinogen, but, paradoxically, it is now recognized that Se has powerful anti-cancer properties. Although initially it was the toxic properties of Se that generated scientific interest, in 1957 Schwartz and Foltz (Schwartz and Foltz, 1957) found that Se could prevent hepatic

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© CAB International 2002. Nutrition and Immune Function (eds P.C. Calder, C.J. Field and H.S. Gill)

necrosis in vitamin E-deficient rats. This observation led to the acceptance that Se was an essential trace element. The discovery in 1973 that Se was a constitutive part of cytoplasmic glutathione peroxidase (cyGPX) provided a mechanism by which the trace element could exert its biological actions. It was thus hypothesized that Se exerted its effects through modifying the expression of this important antioxidant enzyme (Vernie, 1984). However, it soon became apparent that Se must have other means for exerting some of its biological actions, since, for example, changes in the expression of drug-metabolizing enzymes observed in Se-deficient mice could be reversed using doses of Se that had no effects on GPX expression. Labelling experiments on cells and animal tissue with 75Se-selenite demonstrated that more than 35 selenoproteins, with diverse roles, are expressed by tissues. It is now widely recognized that, in addition to exerting important antioxidant activity, Se can act as a growth factor and an anti-cancer agent and is required to ensure thyroid hormone homoeostasis and optimal fertility and immune function. Although many of the biological effects of Se operate through modifying the expression of selenoenzymes, there is good evidence to suggest that some actions of Se (such as its anti-cancer properties) may operate independently of these selenoproteins (Reilly, 1993; Arthur and Beckett, 1994; Foster and Sumar, 1997; Allan et al., 1999).

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