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OCR for page 242
Iron
Iron (Fe) and iron salts have been used as medicinal agents for cen-
turies. The ancient Greeks, Egyptians, and Hindus prescribed iron as
a treatment for general weakness, diarrhea, and constipation. The role
of iron in blood formation became apparent in the seventeenth century
when it was shown that iron salts were of value in the treatment of
chIorosis, now known as iron-deficiency anemia, in young women.
Lemery and Geoffy demonstrated in 1713 the presence of iron in blood,
and in 1746 Menghini reported that blood iron levels could be increased
by the feeding of iron-rich foods. Various iron compounds continue to
be used in the prevention and treatment of iron-deficiency anemia in
man and animals.
ESSENTIALITY
Iron is essential to every form of life from plants to man. Hemoglobin,
myogiobin, the cytochromes, and many other enzyme systems contain
iron. The conjugated proteins help maintain the vital cellular activities
of respiration and oxygen transport. The frequency of iron-deficiency
anemia in many human populations, including those in affluent coun-
tries, emphasizes the importance of dietary iron as a marginally ade-
quate nutrient. Iron-deficiency anemia in young pigs has been rec-
ognized for almost a century, and the nature and pathology of the
anemia were described more than 50 years ago (McGowan and Crich-
242
OCR for page 243
Iron
243
ton, 1923; Doyle et al., 19281. Other young animals that receive milk as
the sole diet can suffer from iron-deficiency anemia (Blaxter e! al.,
1957).
METABOLISM
Iron absorption takes place almost exclusively in the small intestine.
Ferrous iron entering the blood plasma is quickly oxidized to the ferric
state. The ferric form then immediately complexes with a specific
B~-globulin (transferr~n), in which form it is transported to various parts
of the body as required for use or storage. Iron is stored intracellularly
in the liver, spleen,- bone marrow, and other tissues as ferritin and
hemosider~n. Iron is a component of myogIobin in skeletal muscles.
The body has limited capacity to excrete iron. It is excreted mainly in
the bile and desquamated mucosal epithelial cells sloughed from the
duodenal villi (Dubach et al., 1955; Braude et al., 1962~. Small amounts
of iron are lost in urine and sweat. Various aspects of iron metabolism
are covered in the articles and reviews by Moore (1961), Bothwell and
Finch (1962), Christopher et al. (1974), Forth (1974), Jacobs (1976), and
Underwood (19771.
SOURCES
Iron is more abundant in the earth's crust than are the macronutrients
calcium, magnesium, potassium, phosphorus, sulfur, and nitrogen. All
plant materials commonly used in the feeding of animals contain var'-
able amounts of iron. The concentration of iron in plants is a reflection
of the species and soil upon which the plants grow. The iron content of
cultivated grasses and legumes ranges from 100 to 700 ppm, although
values in excess of 1,000 ppm have been reported (Beeson, 1941~. Most
cereal grains contain between 30 and 60 ppm iron (Miller, 195X). Feeds
of animal origin, other than milk and milk products, are rich sources of
iron. Many of the minerals used to supply the calcium and phosphorus
needs of animals contain iron.
Most of the iron in plant products is in the ferric form in organic
combinations from which it must be released in the gastrointestinal
tract to permit absorption. The bioavailability of iron in certain grasses
was studied by Thompson and Raven (1959) and Raven and Thompson
(19591. Inorganic iron as ferric chloride was significantly more available
than iron present in either the grasses or legumes. Assuming that ferric
OCR for page 244
244 MINERAL TOLERANCE OF DOMESTIC ANIMALS
chloride resulted in an improvement in total hemoglobin equal to 100
percent, the grasses yielded improvements of 4X to 63 percent in one
study and the legumes 47 to 57 percent in another study. Numerous iron
compounds are used as dietary sources of iron. Some iron oxide is used
in animal feeds as a coloring agent. The bioavailability of the iron in
these different compounds varies greatly (Nesbit and Elmslie, 1960;
Ammerman et al., 1967; Harmon et al., 1969; Fritz et al., 19701. Am-
merman et al. (1974) showed the bioavailability of iron in several fer-
rous carbonates was correlated with in vitro solubility.
TOXICOSIS
LOW LEVELS
Characteristic signs of chronic iron toxicosis for most species are re-
duced feed intake, growth rate, and efficiency of feed conversion.
Standish and Ammerman (1971) reported that feeding 1,600 ppm iron to
lambs reduced plasma copper. Iron levels in the range of 4,000 to 5,000
ppm in the diet produced signs of phosphorus deficiency in swine and
poultry (Deobald and Elvehjem, 1935; O'Donovan et al., 1963; [;uru-
gouri, 19721.
Standish et al. (1969) added ferrous sulfate at levels to supply either
400 or 1,600 ppm added iron in the diets of steers weighing about 235
kg. The level of 1,600 ppm added iron caused significant reductions in
daily gains and feed intake. Koonget al. (1970), using iron citrate as the
source of added iron, conducted two experiments in which six levels
(100 to 4,000 ppm) of dietary iron were fed to calves weighing about 125
kg. The animals fed 4,000 ppm performed poorly (poor gains and
diarrhea) and were changed to a level of 2,000 ppm after being on test
for 6 weeks. A level of 2,500 ppm iron significantly reduced feed intake
and daily gains. The body weight gains and feed consumption data for
calves receiving 1,000 ppm iron were not significantly different from
those receiving 100 ppm, but there was a trend towards poorer perform-
ance at dietary iron levels of 500 ppm or more. Lawlor e' al. (1965)
obtained no effects on weight gains, hemoglobin, packed cell volume,
or red blood cell values from supplementing lambs' diets with 280 ppm
iron. Following the fourth week of the experiment, diarrhea occurred
among the lambs receiving 210 and 280 ppm iron. Postmortem examina-
tion of two lambs did not attribute death to any particular causes other
than severe generalized edema. The authors point out that it is unlikely
OCR for page 245
Iron 245
that dietary levels of 210 and 280 ppm should approach toxicity levels
for lambs. Standish and Ammerman (1971) found that lambs did not
consume adequate feed to maintain body weight when fed rations con-
taining 1,600 ppm iron, which reduced plasma copper.
Furugouri (1972) reported no significant effect on body weight gains
of young pigs fed either 1,102 or 3,103 ppm iron. When the dietary iron
levels were increased to 5,102 and 7,102 ppm, body weight gains and
feed intake were decreased. Signs of phosphorus deficiency were noted
in pigs receiving either 5,102 or 7,102 ppm iron, even though the diets
contained 0.92 percent phosphorus. O'Donovan et at. (1963) reported
that 5,000 ppm iron caused a significant decrease in rate of gain, a slight
decrease in serum inorganic phosphorus, but failed to reduce femur
ash. McGhee et al. (1965) found that chicks could tolerate 1,600 ppm
iron when adequate copper was included in the diet; when the diet
contained only 5 ppm copper, decreased gains and increased mortality
were reported with dietary iron levels of 200 ppm. Growth rate ap-
peared to be depressed when diets contained 800 ppm iron and 80 ppm
copper. Deobald and EIvehjem (1935) found that 4,500 ppm iron pro-
duced rickets in young chicks. Woerpel and Balloun (1964) showed no
consistent adverse effect on the growth rate of turkey poults from the
addition of 440 ppm iron.
Goldberg et al. (1957) studied the ejects of administering a dose of
1,650 mg iron per kilogram of body weight intramuscularly to rats for
an extended period. The only significant findings were those charac-
teristic of vitamin E deficiency. Tollerz and Lannek (1964) reported
that vitamin E gave protection against iron toxicosis in mice and young
pigs.
HIGH LEVELS
The clinical signs of acute toxicosis of iron include anorexia, oliguria,
diarrhea, hypothermia, diphasic shock, metabolic acidosis, and death
(Boyd and Shanas, 1963~. Vascular congestion of the gastrointestinal
tract, liver, kidneys, heart, lungs, brain, spleen, adrenals, and thymus
are the dominant histopathologic findings. Elevated serum iron levels
are found in iron toxicosis.
Cornelius and Harmon (1976) administered oral doses of 200 mg iron
from either ferric ammonium citrate, ferrous sulfate, ferric oxide, or an
iron dextran complex to piglets within 6 hours of birth. The ferric
ammonium citrate proved highly toxic, with only 33.3 percent of the
piglets surviving to 21 days. The rate of survival in piglets given the
other three iron compounds ranged from 82 to 100 percent. Ferrous
OCR for page 246
246 MINERAL TOLERANCE OF DOMESTIC ANIMALS
sulfate given in a large oral dose to dogs caused vomiting, and the
median emetic dose was between 19 and 29 me iron per kilogram of
body weight (weaver et al., 1961~. Gastric intolerance, as indicated by
emesis, was much less for an iron polysaccharide complex than for
several other salts. When ferrous sulfate was given to dogs at levels to
supply 150 to 600 mg iron per kilogram of body weight, various dis-
orders ranging from diarrhea and vomiting to irritation of the gastro-
intestina] tract occurred (Reissman and Coleman, 1955; D'Arcy and
Howard, 19621. In rabbits, 750 mg ferrous sulfate per kilogram of body
weight caused hepatic congestion within 24 to 48 hours (L`uongo and
Bjornson, 1954~. These workers reported a dose of 2,000 mg ferrous
sulfate per kilogram of body weight caused death in all rabbits within
a few hours of administration.
FACTORS INFLUENCING TOXICITY
Iron that is added to the plasma in excess of the physiological iron-
binding capacity is bound more loosely than the B~-gIobulin iron. The
loosely bound iron is rapidly removed from the plasma, and it is this
fraction that causes toxic reactions in the organism. Because of the
limited capacity of the body to excrete iron, the toxicity of iron is
governed largely by its absorption. Although iron is absorbed by the
cells of the intestinal mucosa in the ferrous state, substances in the
gastric and intestinal secretions can reduce the ferric ions to the ferrous
state. The solubility of the iron appears to be as important as the
valence, because some insoluble ferrous compounds are less available
than the more soluble ferric compounds (Fritz et al., 1970~. In review-
ing the toxicity of iron compounds, Herbert (1965) concluded that all
iron compounds are probably equally toxic per unit of soluble iron.
Among the dietary factors that have been shown to influence iron
toxicity are levels of copper (McGhee et al., 1965), phosphorus
(O' Donovan et al., 1963), and vitamin E (Tollerz and Lannek, 1964~.
Enhanced iron absorption has been seen with certain amino acids, e.g.,
valine and histidine (E! Hawary et al., 1975~. Ascorbic acid alone or in
combination with vitamin E increased iron absorption (Greenberg et
al., 1957; Monsen and Page, 1978~. A number of organic acids, includ-
ing succinic, lactic, pyruvic, and citric are effective in increasing iron
absorption (Van Campen, 1974~. Some simple sugars such as fructose
and sorbitol increase iron absorption, whereas the effects of more come
plex carbohydrates are somewhat variable (Herndon et al., 1958;
Jacobs and Miles, 1969~. It has been postulated that some of the com-
pounds mentioned above form complexes with iron that keep the iron
.
OCR for page 247
Iron
247
in solution during transit through the upper part of the small intestine,
where absorption most rapidly occurs.
Treatment for iron poisoning aims at precipitating the iron as insolu-
ble hydroxide. Preparations such as milk of magnesia and milk of lime
are recommended (Garner, 19611. Szabuniewicz e! al. (1971) suggested
desferrioxamine (deferoxamine) as a treatment for iron toxicosis.
TISSUE LEVELS
Standish et al. (1969) reported that livers and spleens of steers fed 400
ppm iron contained significantly more iron than those from steers fed
no additional iron. The change in the level of iron in liver, spleen, and
heart in response to dietary iron was almost linear for steers fed 0, 400,
and 1,600 ppm. On a dry matter basis, the liver, spleen, kidney, heart,
and muscle from steers fed no supplemental iron contained 185, 1,219,
315, 291, and 91 ppm iron, respectively; the same organs and tissue
from steers receiving 1,600 ppm iron contained 605, 8,941, 410, 329, and
98 ppm, respectively. The iron content of the muscle was not increased
by feeding 1,600 ppm. Thoren-Tolling (1975) showed that the liver is the
main storage site in young pigs receiving oral iron. The iron deposits in
the liver were almost depleted 19 days after the oral iron treatment was
given. Estimates of the distribution of iron in various species are given
by Moore and Dubach (1962~.
MAXIMUM TOLERABLE LEVELS
Pigs are more tolerant of excess iron than cattle, sheep, or poultry.
Based on available information, the maximum tolerable levels of
dietary iron are 3,000 ppm for swine and 1,000 ppm for cattle and
poultry. The more limited data available for sheep suggest a maximum
tolerable level of 500 ppm dietary iron. The values listed above assume
that the biological availability of the dietary iron is high. All species can
probably tolerate much higher levels when the iron is supplied from
sources with low bioavailability.
SUMMARY
Iron is essential to every form of life from plants to animals. It is
concerned with the vital cellular activities of respiration and oxygen
OCR for page 248
248 MINERAL TOLERANCE OF DOMESTIC ANIMALS
transport. The frequency of iron-deficiency anemia in many human
populations, and in some young animals that rely on milk as the sole
diet, emphasizes the importance of dietary iron as a marginally ade-
quate nutrient. Although a wide variation in the susceptibility of
various species of livestock to iron toxicosis exists, most species have
a high tolerance.
OCR for page 249
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Iron
REFERENCES
253
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254 MINERAL TOLERANCE OF DOMESTIC ANIMALS
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Iron
255
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