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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids
of selenium, selenite (SeO32−), has a more variable absorption, probably related to interactions with substances in the gut lumen, but it is better retained, once absorbed, than is selenate (Thomson and Robinson, 1986). Absorption of selenite is generally greater than 50 percent (Thomson and Robinson, 1986). Although selenate and selenite are not major dietary constituents, they are commonly used to fortify foods and as selenium supplements.
Two pools of reserve selenium are present in humans and animals. One of them, the selenium present as selenomethionine, depends on dietary intake of selenium as selenomethionine (Waschulewski and Sunde, 1988). The amount of selenium made available to the organism from this pool is a function of turnover of the methionine pool and not the organism's need for selenium.
The second reserve pool of selenium is the selenium present in liver glutathione peroxidase (GSHPx-1). In rats, 25 percent of total body selenium is present in this pool (Behne and Wolters, 1983). As dietary selenium becomes limiting for selenoprotein synthesis, this pool is downregulated by a reduction of GSHPx-1 messenger ribonucleic acid (RNA) concentration (Sunde, 1994). This makes selenium available for synthesis of other selenoproteins.
Selenomethionine, derived mainly from plants, enters the methionine pool in the body and shares the fate of methionine until catabolized by the transsulfuration pathway. The resulting free selenocysteine is further broken down with liberation of a reduced form of the element, which is designated selenide (Esaki et al., 1982). Ingested selenite, selenate, and selenocysteine are all apparently metabolized directly to selenide. This selenide may be associated with a protein that serves as a chaperone (Lacourciere and Stadtman, 1998). The selenide can be metabolized to selenophosphate, the precursor of selenocysteine in selenoproteins (Ehrenreich et al., 1992) and of selenium in transfer RNA (Veres et al., 1992), or it can be converted to excretory metabolites (Mozier et al., 1988), some of which have been characterized as methylated forms.
The mechanism that regulates production of excretory metabolites has not been elucidated, but excretion has been shown to be responsible for maintaining selenium homeostasis in the animal