National Academies Press: OpenBook

Selenium in Nutrition,: Revised Edition (1983)

Chapter: 9 SUMMARY

Suggested Citation:"9 SUMMARY." National Research Council. 1983. Selenium in Nutrition,: Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/40.
Page 133
Suggested Citation:"9 SUMMARY." National Research Council. 1983. Selenium in Nutrition,: Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/40.
Page 134
Suggested Citation:"9 SUMMARY." National Research Council. 1983. Selenium in Nutrition,: Revised Edition. Washington, DC: The National Academies Press. doi: 10.17226/40.
Page 135

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9 Summary Selenium was identified in 1818 by Berzelius. It has both metallic and non- metallic properties and occurs in four oxidation states of biological signifi- cance: as selenide (Se-2), elemental selenium (See), selenite (Se+4), and selenate (Se+6~. Although the chemistry of selenium is similar to that of sulfur, biological systems tend to reduce selenium compounds and to oxi- dize sulfur compounds. Selenium is most commonly analyzed in biological samples by digestion with nitric and perchloric acids, reaction with diami- nonaphthalene to form a piazselenol, extraction with cyclohexane, and quantitation by fluorometry. Selenium is widely but variably distributed in the earth's crust, with an average abundance of about 0.09 ppm. That entering commerce is derived primarily from the electrolytic refining of copper. The selenium concentra- tion of most surface soils lies between 0.1 and 2.0 ppm, even in some that support growth of toxic plants. Toxic seleniferous soils are usually alkaline and occur in regions of low rainfall in extensive areas of Alberta, Saskatch- ewan, Manitoba, South Dakota, Wyoming, Montana, North Dakota, Ne- braska, Kansas, Colorado, Utah, Arizona, and New Mexico. Nontoxic sel- eniferous soils are found in Hawaii and Puerto Rico, are acid (pH 4.5 to 6.5), have a zone of iron and aluminum compounds that bind selenium, and developed under humid conditions. Low-selenium soils are found in the Pacific Northwest, northern and eastern Canada, the northeastern United States, the South Atlantic seaboard, and in a border region of Ar- izona and New Mexico. In alkaline, well-aerated soils, selenium tends to form selenates that are quite available to plants and may lead to toxic con 133

134 SELENIUM IN NUTRITION centrations, particularly in accumulator plants such as species of Astraga- lus, Machaeranthera, Haplopappus, and Stanleya. In acid soils, a ferric hydroxide-selenite complex is formed that is only slightly available to plants. Plants growing on such soils frequently contain inadequate concen- trations of selenium (< 0.1 ppm dry basis) for animals that consume them. Selenium concentrations in surface or well water in the United States are generally less than 10 ,ug/liter. Daily selenium intakes of hu- mans in the United States and Canada are probably in the range of 50 to 250 ,ug. The essentiality of selenium for animals was discovered in 1957. The biochemical functions of selenium that are currently recognized include its role as a component of glutathione peroxidase (GSH-Px) in animals and of several bacterial enzymes. Other functions are under active investigation. GSH-Px is a protein with a molecular weight of about 80,000 daltons and with 4 subunits and 4 g-atoms of selenium per mole. Tissue concentrations of this enzyme differ from species to species, with localization demon- strated in the cytosol and mitochondrial matrix space of the liver. This enzyme appears to protect tissues against peroxidation by destroying H2O2 or organic hydroperoxides. The metabolic interrelationship of GSH-Px with vitamin E is particularly evident in deficiency diseases that can be prevented either by vitamin E or selenium. Liver cells seemingly have vita- min E and GSH-Px organized in a serial fashion, with vitamin E found in the lipophilic cell membrane. Prooxidants presumably originate in the hy- drophilic portions of the cell, and their molecular target is the membrane. If GSH-Px does not destroy the peroxides, then vitamin E can still protect the membrane by serving as a free-radical trapper. The major selenium compounds in seeds or forages consumed by live- stock appear to be selenocystine, selenocysteine, selenomethionine, and selenium-methylselenomethionine. Supplements to deficient animal diets are most commonly sodium selenite. Ruminants absorb less selenium than monogastric animals, with the primary absorption sites in both groups be- ing the small intestine, cecum, and colon. Vascular transport varies with species, with evidence of binding via sulthydryl groups to erythrocytes and to plasma proteins. Tissue concentrations tend to be highest in kidney, followed by liver, pancreas, and spleen. Cardiac muscle has higher concen- trations than skeletal muscle. Wool and hair may be relatively high, but nervous and adipose tissue are low. In general, selenium is deposited in tissues at higher concentrations when present in the diet in organic rather than inorganic form. Various organic selenium compounds are not neces- sarily metabolized to common intermediates; e.g., selenomethionine is more effective than selenocystine in prevention of pancreatic degeneration in chicks but is less effective in preventing exudative diathesis. Animal tis

Summary 135 sues convert inorganic selenium to organic forms, and the pathways for conversion of selenite to selenide have been fairly well established. How- ever, the means by which selenide is incorporated into selenocysteine have not been fully delineated. Within limits, absorbed selenium in excess of need is excreted, primarily via the urine. Signs of selenium deficiency are frequently indistinguishable from those of vitamin E deficiency and include hepatic necrosis, icterus, edema, hya- linization of the walls of arterioles, abnormal sperm morphology, and skel- etal and cardiac muscular degeneration. Pancreatic dystrophy in chicks can result from an uncomplicated selenium deficiency. Plasma activity of certain enzymes, such as aspartate aminotransferase, ornithine carbamyl transferase, alanine aminotransferase, isocitrate dehydrogenase, lactate dehydrogenase, and verb ate dehydrogenase may increase in response to different types of tissue damage. A variety of stresses in animals tends to increase the incidence of lesions that are morphologically similar to lesions caused by a deficiency of selenium or vitamin E. Such stresses include forced exercise, infectious disease, high levels of dietary fat, and exposure to unusual amounts of prooxidants. Levels of selenium above minimum requirements do not appear to be protective against these stresses. An en- demic cardiomyopathy (Keshan disease), which is responsive to selenium supplementation, has been observed in humans in the People's Republic of China. Dietary requirements of most animals for selenium appear to fall in the range of 0.05 to 0.3 mg/kg dry matter. The safe and adequate range of daily intakes recommended by the Food and Nutrition Board (NRC, 1980a) for adult humans is 50 to 200 ,ug. Acute selenium toxicity results in garlic breath, vomiting, dyspnea, te- tanic spasms, and death from respiratory failure. Chronic toxicity results in growth failure. Depending on the species, liver damage, splenomegaly, pancreatic enlargement, anemia, elevated serum bilirubin levels, dermati- tis, hair loss, and abnormal hooves and nails may also be seen. Maximum tolerable dietary concentrations proposed for animals are 2 mg/kg dry matter.

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