Chemopreventive mechanisms of selenium.
The element selenium (Se) was recognized only 40 years ago as being essential in the nutrition of animals and humans. It is recognized as being an essential component of a number of enzymes in which it is present as the amino acid selenocysteine (SeCys). Selenium compounds have also been found to inhibit tumorigenesis in a variety of animal models and recent studies indicate that supplemental Se in human diets may reduce cancer risk. Anti-tumorigenic activities have been associated with Se intakes that are more than sufficient to correct nutritionally deficient status; that is, Se appears to be anti-tumorigenic at intakes that are substantially greater than those associated with maximal expression of the known SeCys-containing enzymes. Therefore, while some cancer protection may involve one or more Se-enzymes, it is probable that anti-tumorigenic functions of Se are discharged by certain Se-metabolites produced in significant amounts at relatively high Se intakes. Thus, Se supplementation of individuals with relatively low or frankly deficient natural intakes of the element can be expected to support enhanced anti-oxidant protection due to increased expression of the Se-dependent glutathione peroxidases and thioredoxin reductase. Higher levels of Se-supplementation can be expected to affect other functions related to tumorigenesis: carcinogen metabolism, immune function, cell cycle regulation and apoptosis. Thus, according to this 2-stage model of the roles of Se in cancer prevention, even individuals with nutritionally adequate Se intakes may benefit from Se-supplementation.
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Cornell University, Ithaca, NY, USA. gfcz@cornell.edu
D000818:Animals; D005979:Glutathione Peroxidase / Q000097:blood; D006801:Humans; D009369:Neoplasms / Q000201:enzymology / Q000517:prevention & control*; D009751:Nutritional Requirements; D012307:Risk Factors; D012643:Selenium / Q000008:administration & dosage* / Q000172:deficiency
D005979:Glutathione Peroxidase; D012643:Selenium