Selenium is effective in reducing
cancer incidence in animal models, and epidemiologic data, as well as supplementation trials, have indicated that
selenium is likely to be effective in humans. The mechanism by which
selenium prevents
cancer remains unknown. The mammalian genome encodes 25
selenoprotein genes, each containing one or more molecules of
selenium in the form of the
amino acid selenocysteine, translationally inserted into the growing
peptide in response to the
UGA codon. There is evidence that several of these
proteins may be involved with the mechanism by which
selenium provides its anticancer effects. Data are reviewed indicating that genetic variants of the
cytosolic glutathione peroxidase are associated with increased
cancer risk, and that loss of one of the copies of this same gene may be involved with malignant progression. Similarly, allelic differences in the gene for a second
selenoprotein, Sep15, may be relevant to the protection provided by
selenium, and allelic loss at this locus have been reported as well. These data, along with the differential expression patterns reported for other
selenoproteins in
tumor vs. normal tissues, support the role of
selenoproteins in the chemoprotection by
selenium.