Most epidemiological studies have shown inverse associations of selenium (Se) status and cancer risk; almost all experimental animal studies have shown that supranutritional exposures of Se can reduce tumor yield; and each of the limited number of clinical intervention trials conducted to date has found Se treatment to be associated with reductions in cancer risks. The known metabolic functions of Se, which appear to be discharged by a fairly small number of selenoproteins may not fully explain these effects, particularly those observed in response to Se-supplementation of non-deficient subjects. Emerging evidence indicates anticarcinogenic roles of at least some selenoproteins, namely, those involved in antioxidant protection (the glutathione peroxidases), redox regulation (the thioredoxin reductases) and hormonal regulation of metabolism (iodothyronine 5'-deiodinases). The fact that abundant empirical evidence has shown anti-carcinogenic effects of Se in individuals with apparently full selenoenzyme expression suggests other mechanisms with relevance to non-deficient populations. Certain Se-metabolites (hydrogen selenide, methylselenol, seleno-diglutathione) can be anti-carcinogenic by inhibiting cell proliferation, stimulating cell death by apoptosis, and inhibiting neoangiogenesis. Therefore, while the hypothesis remains plausible that Se-deprivation may increase cancer risk by compromising selenoprotein expression, there is strong support for the hypothesis that supranutritional exposures to Se can reduce cancer risk. These hypotheses are not mutually exclusive, and it is likely that Se can function as a cancer preventive agent through both nutritional and supranutritional mechanisms.
|Original language||English (US)|
|Title of host publication||Selenium|
|Subtitle of host publication||Its Molecular Biology and Role in Human Health, Second Edition|
|Number of pages||16|
|ISBN (Print)||0387338268, 9780387338262|
|State||Published - 2006|
All Science Journal Classification (ASJC) codes