Selenium in Human and Animal Nutrition

After its discovery, selenium was most noted for its harmful effects. Selenium was the first element identified to occur in native vegetation at levels toxic to animals. Poisoning of animals can occur through consumption of plants containing toxic levels of selenium (79). Livestock consuming excessive amounts of selenized forages are afflicted with ‘alkali disease’ and ‘blind staggers.’ Typical symptoms of these diseases include loss of hair, deformed hooves, blindness, colic, diarrhea, lethargy, increased heart and respiration rates, and eventually death. On the other hand, selenium deficiency in animal feeds can cause ‘white muscle disease,’ a degenerative disease of the cardiac and skeletal muscles (9). Perceptions of selenium changed when Schwarz and Foltz (80) reported that additions of selenium prevented liver necrosis in rats (Rattus spp.) deficient in vitamin E. Its role in human health was established in 1973 when selenium, the last of 40 nutrients proven to be essential, was shown to be a component of glutathione peroxidase (GSHx), an enzyme that protects against oxidative cell damage (81). The United States’ recommended daily allowance for selenium is 50 to 70 µg in human diets (5). Currently, all of the known functions of selenium as an essential nutrient in humans and other animals have been associated with selenoproteins (82).

Dietary Forms

Organic forms of selenium appear to be more bioavailable than the inorganic ones because the organic forms are more easily absorbed, have the ability to be stored in seleno- and other nonspecific proteins, and have lower renal clearance (83). The organic-selenium compounds identified in plants include Se-Cys, Se-methylselenocysteine, selenohomocystine, Se-Met, Semethyl- selenomethionine, selenomethionine selenoxide, selenocystathionine, and di-methyl diselenide, selenoethionine, and Se-allyl selenocysteine (41,84,85). The majority of selenium in seleniferous wheat was shown to be Se-Met (86). The effect of consumption of seleniferous wheat on urinary excretion and retention in the body was similar to that of Se-Met supplementation (87). The form of selenium in nuts is selenocystathionine (88). The high-selenium-accumulating species of milkvetch (Astragalus spp. L.) contain Se-methylselenocysteine and selenocystathionine (89). Most fruits and vegetables contain <0.1 mg Se kg^-1, (13) but some have the potential to be enriched. Marine fish such as tuna are high in selenium, but bioactivity is much lower than selenium from other foods (90). Inorganic SeO₃^2-, SeO₄^2-, and Se^2- have been identified in plants at low levels (91). Selenate and SeO₃^2- are not regarded as naturally occurring forms of selenium in foods, but they have high biological activity, and animals can metabolize them into more active forms such as Se-Cys (90). Selenocysteine is a component of glutathione peroxidase and constitutes the majority of selenium in animal proteins.

Metabolism and form of Selenium

The bioavailability and metabolism of selenium and its distribution in an organism depend on the form of selenium ingested (83). The chemical form of selenium in foods and supplements determines absorption, speciation, and metabolism within the body, bioavailability for selenoproteins, and toxicity (87). Inorganic forms of selenium are absorbed rapidly, but are equally rapidly excreted in the urine, in contrast to Se-Met, which is retained in the body. Total recovery of inorganic forms of selenium in urine and feces of human subjects was 82 to 95% of the total dose, whereas only 26% of the total Se-Met was recovered after being ingested (87). Prolonged consumption of any one single form of selenium can produce side effects such as exaggerated accumulation in body tissues (Se-Met) and changes in cellular glutathione homeostasis (selenite) (92). When high levels of inorganic SeO₃^2- or organic Se-Met were fed to rats, higher selenium concentrations in body tissues were found for Se-Met than for SeO₃^2-. Selenium levels in erythrocytes, testes, kidney, and lungs were not significantly different between rats fed with 0.2 mg kg^-1 Se as SeO₃^2- and those fed with Se as Se-Met, but higher levels of selenium were found in liver, muscle, and brain tissues for rats fed with Se-Met (93). There was an increase of up to 26-fold in the concentration of selenium localized in muscle tissues for rats fed with high levels of selenium as Se-Met when compared with those fed with SeO₃^2-. Selenium from Se-Met and seleno yeast showed higher accumulation in liver and muscle tissues than that from SeO₃^2- for channel catfish (94).