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OCR for page 133
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
OCR for page 134
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
OCR for page 135
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.
Representative terms from entire chapter:
toxicity results
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