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OCR for page 392
Selenium
Selenium (Se) is a semimetal (or metalloid), which is very similar to
sulfur in its chemical properties. Its allotropic forms include a red
powder, red crystals, a dark brown moss, and a silver gray form pro-
duced after extended heating at 200 220°C. It is present chiefly in
Cretaceous rocks, volcanic material, some seafloor deposits, and
glacial drift in central Canada and North Dakota in the form of metallic
selenides. These selenides are often associated with sulfides (as in
pyrites). Selenium exists in soil as basic femc selenite [Fe2~0H)SeO3],
calcium selenate (CaSeO4), elemental selenium, and organic com-
pounds denved from plant tissue.
Nearly all primary production of selenium results from treatment of
residue slimes generated during electrolytic refining of copper. Annual
U.S. use of selenium is approximately 500,000 kg, with substantial use
in rectifiers, xerographic copying machines, and photoelectric cells.
Selenium is also used in ~ass, ceramics, rubber, pigments, and plating
solutions.
Selenium was once used in insecticides for use on ornamental plants,
but this is no longer done. Current primary agricultural use involves the
supplementation of animal diets with selenite or selenate to prevent a
specific deficiency.
Much of the early interest in selenium among nutritionists concerned
its role as a toxic element. Indirect suggestions of its involvement in
certain animal disease syndromes have been known for years. Marco
Polo referred in his journals to " . . . a poisonous plant . . . which
392
OCR for page 393
Selenium
393
if eaten by (horses) has the effect of causing the hoofs . . . to drop
on' (Polo [Marsden's transI.l, 19261. In 1857, Dr. T. C. Madison, a
U.S. Army surgeon at Fort Randall, Nebraska Territory, described
similar signs in horses which he attributed to "alkali disease"
(Madison, 1860~. Selenium was identified as the toxic principle by
scientists from the U.S. Department of Agriculture and the South Da-
kota and Wyoming State Agricultural Experiment Stations through a
series of studies begun in 1929 (Franke, 1934~. Not until 1957 (Patterson
et al., 1957; Schwarz and Foltz, 1957; Scott et a]., 1957; Stokstad et al.,
1957) was the role of selenium as an essential nutrient established.
Kubota et al. (1967) subsequently determined that the selenium-
deficient areas of the United States are much larger than those areas
that are selenium-toxic.
ESSENTIALITY
The first evidence that selenium was an essential nutrient involved the
discovery that it would prevent liver necrosis in rats (Schwarz and
Foltz, 1957) and exudative diathesis in chicks (Patterson et al., 1957~.
Eggert e! al. (1957) found selenium would prevent hepatosis dietetica in
swine, and DeWitt and Schwarz (1958) found it prevented a number of
lesions in mice. Selenium was used successfully by Muth e' al. (1958)
and Hogue (1958) to prevent white muscle disease in young ruminants.
Field observations in New Zealand suggested that selenium deficiency
may also lead to myopathy in the horse (Dodd et al., 1960; Hartley and
Grant, 1961~. Scott and Thompson (1968) demonstrated that selenium
is essential for the Japanese quad! (Coturnix coturnix) even in the pres-
ence of high dietary levels of vitamin E ( 100 mg d-a-tocopheryl acetate
per kilogram of diet). Schwarz (196S) reported that administration of
selenium to two children with kwashiorkor stimulated growth. Similar
results have been reported by Majaj and Hopkins (1966), while Burk et
al. (1967) noted low blood selenium levels in children with untreated
kwashiorkor and an enhanced in vitro uptake of radioselenite by the
erythrocytes of these affected children.
One of the biochemical functions of selenium in higher animals was
defined by Rotruck et al. (1973), who discovered that selenium was an
integral part of the enzyme glutathione peroxidase (ECI.M.l9~. This
enzyme destroys lipid peroxides and thus functions in protecting cell
membranes against peroxidative damage. However, selenium has been
shown to be a constituent of other enzyme systems in microorganisms
(Stadtmanj 1974), and this element may eventually be shown to have
OCR for page 394
394 MINERAL TOLERANCE OF DOMESTIC ANIMALS
aticlitional roles In mammalian metabolism. Diplock and Lucy (1973)
have proposed that selenide may occupy an active site in certain non-
heme iron proteins. Levander et al. (1973, 1974) suggested that
selenium plays a role In the electron transport chain, and Whanger e'
al. (1973) found a selenoprote~n in lamb muscle containing a heme
group identical with that of cytochrome c.
METABOLISM
Selenium absorption from the gastrointestinal tract and its retention
and distribution within the body varies with the chemical form and
amount ingested. The amounts, forests, and routes of excretion are also
affected by these factors and may be greatly influenced by other ele-
ments, notably arsenic.
At toxic or near-toxic levels, selenium is absorbed rapidly and e~-
ciently from naturally seleniferous diets and from soluble selenium
salts. Rats consuming a seleniferous wheat diet (18 ppm selenium)
retained 63 percent of the ingested selenium within the first week and
a similar proportion Tom the same concentration of selenium as sodium
selen~te (Moxon, 1937; Anderson and Moxon, 1941~. Toxicity studies
with rats suggest a higher absorption from seleniferous grains than from
selen~tes and selenates and a very low absorption from selenides and
elements selenium (Franke and Painter, 1938; Smith et al., 1938~.
Some organic compounds, such as selenodiacetic and selenopropionic
acids, are markedly less toxic to rats (per unit of selenium) than is
selenite, probably as a consequence of lower absorption (Moxon et at.,
1938).
Studies with physiological levels of radioselenium indicate that the
duodenum is the main site of absorption, with no absorption from the
rumen or abomasum of sheep or the stomach of pigs (Wright and BeD,
1966~. Net absorption was about 35 percent in sheep and 85 percent in
pigs when the diets contained 0.35 and 0.50 ppm selenium,
respectively.
Absorbed selenium is at first ca'Tied mostly in plasma (Buescher et
al., 1960) In association with plasma proteins (McConneU and Levy,
1962) and is then deposited in all tissues.
Much of the tissue selenium is highly labile, and, following transfer
from selenium-adequate or seleniferous diets to low-selenium diets,
losses are rapid initially and then slower. The urine is a major pathway
of excretion in both ruminants (Lopez et al., 1969) and monogastric
species (McConnell, 1941, 1942, 1948~. Most of the selenium in the
feces is that which has not been absorbed from the diet, plus smog
OCR for page 395
Selenium
395
amounts excreted in biliary, pancreatic, and intestinal secretions.
Levander and Baumann (1966a,b) have shown that biliary selenium
excretion is markedly increased when subacute injections of arsenic are
given with the selenium. Exhalation of selenium is an important route
of excretion at high dietary intakes, but is much less so at low intakes
(Olson et al., 1963; Gantheret al., 1966; Handreck and Godwin, 1970~.
SOURCES
Selenium exists in several oxidation states (-2, 0, +4, +6), and its
chemical properties are similar to those of super. In its -2 state, it
occurs as hydrogen selenide, a highly toxic and reactive gas, that
quickly decomposes in the presence of oxygen to elemental selenium
and water. Heavy metal serenades are insoluble, and a number of or-
gan~c selemdes have been identified in biological materials, some of
which are very volatile. In elemental form (0 oxidation state), selenium
is insoluble, not toxic, and not readily oxidized or reduced in nature.
When burned, it is oxidized to selenium dioxide, which sublimes, and,
when dissolved In water, forms selenious acid. In the +4 state, sele-
Hum occurs as inorganic selen~tes. Those that are soluble are highly
toxic. Selenite has an amity for iron and aluminum sesquioxides and
forms stable adsorption complexes with them In soil. In addition,
selenite is easily reduced to the elemental form under acid and reducing
conditions, and, thus, selen~te added to soil may become quite unavail-
able to plants and is unlikely to pollute water supplies. The formation
and stability of selenates (+6 oxidation state) is favored by alkaline and
oxidizing conditions. Most selenates are quite soluble and highly toxic.
Selenates are not tightly complexed by sesquioxides and, in soils, are
available to plants and easily leached.
Biological processes are involved in the reduction of selenium, but
reduction also results from bunting. Biological reduction can produce
volatile organic selenides or hydrogen selenide. Burning can produce
particulate elemental selenium or selenium dioxide, and these are the
most likely forms In the atmosphere. Oxidation apparently occurs in
alkaline soils by chemical weathering.
TOXICOSIS
Soon after the relationship between high selenium intakes and livestock
losses was established, it became apparent that selenium poisoning has
more than one form. Rosenfeld and Beath (1946) suggested that three
OCR for page 396
396 MINERAL TOLERANCE OF DOMESTIC ANIMALS
types of selenium toxicosis occur in the field: low level of the blind
staggers type' low level of the alkali disease type, and high level.
LOW LEVELS
Selenium poisoning of the blind staggers type has been ascribed to
consumption of limited amounts of accumulator plants over several
weeks or months (Rosenfeld and Beath, 19461. Included among the
accumulators are many species of Astragalus, and some species of
Machaeranthera, Haplopappus, and Stanieya. Affected animals
wander aimlessly, stumble, have impaired vision, and exhibit some
signs of respiratory failure. Since water extracts of accumulator plants
will produce this condition, while pure selenium compounds will not, it
is probable that alkaloids rather than selenium may be responsible
(Maag and Glenn, 1967~.
Low-level selenium toxicosis of the alkali disease type has been
described in detail by Moxon (1937) and Rosenfeld and Beath (1946~. It
is a consequence of consuming feeds ranging from about 5 to 40 ppm
selenium over periods of weeks or months. The most prominent signs
in cattle and horses include lameness, hoof malformations, loss of hair
from mane or tail, and emaciation. Sheep do not usually exhibit hoof or
wool lesions, but reproduction is adversely affected, as it may be also
in cattle (Minyard, 1961), swine (WahIstrom and Olson, 1959), and rats
(Franke and Potter, 1935~. Swine exhibit lameness, hoof malformation,
loss of body hair, and emaciation. Poultry show decreased egg hatch-
ability associated with teratogenic effects. Duhamel (1913) described a
hemorrhagic exudate in lung alveoli, dilated capillaries, and bronchial
exudate. Necrosis, hemorrhage, and fibrosis were seen as hepatic cir-
rhosis developed. The kidneys exhibited a mild tubular degeneration
with acute glomerular injury. Ascites and edema are common. The
vascular effects are apparent even in goldfish (Ellis et al., 1937), where
marked edema, particularly of gastric submucosa and of perivascular
tissues in the kidneys and liver, has been seen.
Herigstad et al. (1973) fed selenium as sodium selenite or seleno-
methionine to pigs at concentrations of 20 to 600 ppm. They noted
emesis, anorexia, weight loss, cachexia, central nervous system de-
pression, respiratory distress, coma, subnormal body temperature, and
death. Lesions at necropsy were similar for swine given both selenium
compounds and included hepatic fatty metamorphosis and centrilobu-
lar necrosis; congestion of the renal medulla; necrosis in Iymphoid
follicles; edema and degenerative changes in cerebrum, cerebellum,
and spinal cord; edema and hemorrhagic necrosis of the pancreas;
OCR for page 397
Seier~ium
397
depletion of hematopoietic cells in bone marrow; hemorrhagic necrosis
of the adrenal cortex; serous atrophy of body fat; and degenerative
changes in diaphragm and skeletal muscles.
Loew e' al. (1975) accidentally fed 10 ppm selenium (from sodium
selenite) in the diet of cynomolgus monkeys and noted erosions on the
tongue, hemorrhagic dermatosis on the tail, loss of nails
(onychoptosis), anorexia, lassitude, and leukopenia. These signs devel-
oped over 40 days and disappeared when the selenium level was re-
stored to normal.
Suggestions that selenium might induce neoplasia (Nelson et al.,
1943), and interest in nutritional requirements for selenium, led to an
extensive study at Oregon State University in which 1,437 rats were fed
varying levels of selenite or selenate selenium for up to 30 months (Herr
et al., 1967; Tinsley et a]., 19671. The basal semipurif~ed diet contained
0.1 ppm, and selenium was added at 0.5, 2, 4, 6, 8, or 16 ppm. Acute
toxic hepatitis was noted in rats receiving 4 to 16 ppm. These rats were
emaciated and pale, and exhibited ascites, edema, and poor-quality hair
coats. Most lived less than 100 days. Chronic toxic hepatitis and hyper-
plastic hepatocytes were reported in rats receiving selenium supple-
ments of 0.5 to 2 ppm. These rats lived 24 to 30 months and many had
developed murine pneumonia. Unfortunately, necropsy findings in rats
on the basal diet were not adequately described. Although 63 neo-
plasms were observed in the entire study, none could be attributed to
added selenium.
HIGH LEVELS
In the field, acute poisoning occurs when grazing animals eat sufficient
amounts of selenium accumulator plants to cause sudden death or signs
of severe distress (labored breathing, ataxia, abnormal posture, pros-
tration, and diarrhea). This type of poisoning is rare, since animals
usually avoid these plants. However, when pasture is limited, accumu-
lators may be nearly the only food available, and occasional large losses
among sheep and cattle may occur. Acute poisoning has also been
produced accidentally or experimentally by the administration of large
amounts of selenium compounds to farm animals (Caravaggi and Clark,
1969; Caravaggi et al., 1970; Shortridge et al., 1971; Herigstad e! al.,
1973).
Rosenfeld and Beath (1946) described vascular manifestations, in-
cluding petechial hemorrhages in the endocardium and acute conges-
tion and disuse hemorrhages in the lungs. In ruminants, the omasum
was congested and hemorrhagic, and there was desquamation of the
OCR for page 398
398 MINERAL TOLERANCE OF DOMESTIC ANIMALS
mucous epithelium. There was enteritis, intestinal hemorrhage, and
occasionally colitis and proctitis. The liver was passively congested,
hemorrhagic, and exhibited parenchymatous degeneration with focal
necrosis. The kidneys exhibited parenchymatous degeneration,
hemorrhages, and nephritis. Steele and Wilhelm (1967) showed that
high levels of selenite produced remarkable increases in vascular per-
meability in the guinea pig.
When Her~gstad et al. ( 1973) intravenously injected 3 mg of selenium
per kilogram of body weight into two pigs, fatal selenium toxicosis
developed in 2~2 or 14 hours. The pig dying first received selenium as
sodium selenite and exhibited pulmonary edema at necropsy. The pig
dying at 14 hours received selenomethionine, and postmortem signs
included a yellow-brown mottled liver, pale renal cortex, and congested
renal medulla. The clinical course of the toxicosis included vomiting,
profound central nervous system depression, weakness, respiratory
distress, coma, and death.
FACTORS INFLUENCING TOXICITY
Halverson e' al. (1962) have demonstrated that dietary sulfate can
decrease the toxicity of selenate but not of selenite or organic selenium.
Sellers et al (1950) demonstrated that methionine could protect against
selenium toxicity, but only when adequate vitamin E was present in the
diet. This was confirmed by Levander and Morris (1970), who also
found that several fat-soluble antioxidants could replace vitamin E in
potentiating the methionine response.
Starting with the discovery of Moxon (1938) that arsenic could
counteract the toxicity of seleniferous grains, a number of interactions
between selenium and other elements have been found that render
selenium much less toxic than when it is present alone. Levander and
Baumann (1966b) found that arsenic functioned by increasing biliary
excretion of selenium into the intestine. Moxon and DuBois (1939)
reported that tungsten as well as arsenic counteracted the toxicity of
selenium. Hill (1975) reported that mercury, cadmium, and copper
reduce selenium toxicosis in the chick, and Jensen (1975) found that
silver was also effective.
Linseed meal has a unique protective activity against chronic sele-
nium toxicosis (Moxon, 1941), which is not associated with protein and
which can be extracted with hot aqueous ethanol (Halverson et al.,
1955~. Levander e! al. (1970) showed that this feedstuff resulted in
higher and more tightly bound hepatic selenium levels. Recently,
OCR for page 399
Selenium
399
Palmer et al. (1980) presented data suggesting that the cyanogenic
glycosides, linustatin and neolinustatin' are responsible for the protec-
tive action of linseed meal.
Harr e! al. (1967) noted that rats fed commercial diets showed 2 to 3
times greater resistance to selenium toxicity than when fed a semi-
purif~ed diet.
Although a number of dietary factors will ameliorate the develop-
ment of selenium toxicosis, treatment of the poisoned animal is not
very satisfactory. Oral administration of 4 to 5 g naphthalene daily for
5 days has been used for chronic selenosis in cattle and horses to
increase urinary selenium loss. The dosage is repeated after a 5-day
dosage-free interval. Removal of the source of selenium will result in a
gradual decline in tissue concentration if kidney function has not been
seriously impaired.
TISSUE LEVELS
Much of the selenium in tissues is highly labile, and transfer of animals
from seleniferous to nonseleniferous diets is followed by rapid, and
then slow, loss of selenium from the tissues via bile, urine, and/or
expired air. Selenium concentrations in tissues tend to reflect dietary
selenium concentrations, particularly when provided by natural dietary
ingredients as compared to selenate or selenite. Ku et al. (1972) found
the selenium concentration of swine skeletal muscle (0.03~0.521 ppm,
wet basis) was highly correlated (r = 0.95) with that in natural swine
diets (0.027-0.493 ppm, air dry) from 13 different U.S. locations. When
these workers (Ku et al., 1973) added sufficient selenium (0.4 ppm)
from sodium selenite to raise a low-selenium (0.04 ppm) swine diet to
the level found in a South Dakota swine diet (0.44 ppm from natural
sources), respective skeletal muscle selenium concentrations were 0.12
and 0.48 ppm, wet basis. Corresponding liver selenium concentrations
were 0.61 and 0.84 ppm, wet basis. Kidney selenium concentrations
were 2.14 and 2.17 ppm, wet basis. When swine diets were selenium-
deficient (0.05 ppm), the following tissue selenium concentrations
(ppm, wet basis) have been found: longissimus muscle, 0.05; myo-
cardium, 0.11;liver, 0.14; kidney, 1.37(Groce et al., 1973~. A similar
pattern of tissue selenium concentrations has been found in cattle and
sheep (Ullrey et al., 1977) and in chicks and poults (Scott and Thomp-
son, 19711. -
Selenium in serum of swine receiving an unsupplemented natural diet
OCR for page 400
400 MINERAL TOLERANCE OF DOMESTIC ANIMALS
(0.04 ppm selenium) or this diet supplemented with 0.05, 0.1, or 0.2 ppm
selenium from sodium selenite was 0.046, 0.150, 0.164, or 0.168 ppm.
Respective erythrocyte selenium concentrations were 0.088, 0.181,
0.193, or 0.207 ppm (Groce e' al., 1973~.
Cows with hair selenium concentrations between 0.06 and 0.23 ppm
produced calves with white muscle disease, while no lesions were seen
in calves from cows with hair selenium greater than 0.25 ppm
(Hidiroglou et al., 1965~. Selenium In hair of yearling cattle on sele-
niferous range averaged over 10 ppm (Olson et al., 1954~.
Areaway et al. (1968) reported that cow's milk from a low-selenium
area in the United States contained less than 20 ng/ml, compared with
50 ng/ml from a high-selenium area in South Dakota.
Normally, hen's eggs contain a total of 10 to 12 fig selenium, with
most in the yolk (Taussky et al., 1963, 1965~. Whole-egg selenium
concentrations on an adequate diet are about 0.3 ppm (Latshaw, 1975~;
although very high egg selenium levels can be produced by extremely
high dietary intakes (Moxon and Foley, 19381.
MAXIMUM TOLERABLE LEVELS
Dietary requirements for selenium range from 0.1 to 0.3 ppm in dry
matter, and supplements of selenite and selenate are regularly added to
animals' diets. Signs of toxicity have been seen in some food animal
species when 5 ppm selenium were fed in relatively short-term studies.
In rats fed semipurified diets, 4 ppm were toxic. However, 2 ppm
selenium has produced no unequivocally toxic signs, and this dietary
concentration is suggested as a maximum tolerable level for all species.
SUMMARY
Selenium is a relatively rare metalloid that is similar to sulfur in its
chemical properties. Although early interest among nutritionists was
concerned with its potential toxicity, selenium has been established as
an essential nutrient and is a constituent of glutathione peroxidase.
Selenium toxicity in high selenium areas has been divided into three
types. The low-level, blind staggers type results from consumption of
limited amounts of selenium accumulator plants over several weeks or
months and is probably due to toxic alkaloids. The low-level alkali
disease type results from consuming feeds containing 5 to 40 ppm
selenium over weeks or months. High-level, acute poisoning results
OCR for page 401
Selenium
401
when Dazing animals consume large amounts of accumulator plants
sufficient to cause severe distress and sudden death. Since selenite and
selenate are now being used to supplement deficient animal diets, a
potential for accidental poisoning by this route also exists. Dietary
selenium requirements are approximately 0.1 to 0.3 ppm, and toxic
dietary levels are about 10 to 50 times greater.
OCR for page 402
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416 MINERAL TOLERANCE OF DOMESTIC ANIMALS
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Representative terms from entire chapter:
sodium selenite
