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OCR for page 290
Manganese
Manganese (Mn) is a steel gray lustrous metal that is hard and brittle.
In chemical properties it is similar to iron; its two most important
valence states in biological systems are I! and III. Manganese con-
stitutes 0.10 percent of the earth's crust and is the twelfth most
abundant element. The most important manganese ore is pyrolusite;
however, manganese occurs in hausmann~te, manganite, manganosite,
and braun~te. Manganese is an important component of metallic
nodules that are found on the ocean floors. Manganese is used in the
manufacture of steel, cast iron, alloys of copper and aluminum, pig-
ments for glass and ceramics, dry cell battenes, and a evade range of
chemicals. In 1970, the tons of manganese ore (at least 35 percent
manganese) used in the United States were as follows: manganese
alloys and metals, 2,099,426; pig iron and steel, 107,733; and dry cells,
chemicals, and miscellaneous, 156,778 (National Research Council,
19731. Since animals and plants require manganese, it is incorporated
into poultry and livestock feeds and frequently into fertilizers.
Reviews cover venous aspects of manganese function, metabolism,
toxicity, and uses (National Research Council, 1973; Leach, 1974,
1976; HurIey, 1976; Matrone et al., 1977; Underwood, 1977; and
Leach and Lilburn, 1978~.
ESSENTIALITY
Manganese was first recognized as an essential nutrient for animals
when it was shown to be required for growth and reproduction in rats
290
OCR for page 291
Manganese
291
and mice (Kemmerer et al., 1931; Orent and McCollum, 1931~. The
principal signs of manganese deficiency in severe species include
reduced growth rate, skeletal abnormalities, abnormal reproductive
function in males and females, and atax~a in the newborn. A suscepti-
bility to convulsions has been observed in manganese deficient guinea
pigs. Righting ability was related to abnormal otoliths, resulting from
defective bone formation.
The manganese requirements vary considerably between species. In
terms of dietary concentration (ppm), the requirements of young ani-
mals have been estimated as follows: dog, 4.5; rabbit, S.5; pig, 4; calf,
40; sheep, 30; rat, 50; chick, 55, and turkey, 55.
METABOLISM
Manganese is absorbed throughout the intestinal tract. The homeo-
static mechanism for regulating tissue levels involves the excretion of
manganese via bile and the intestine. The details of these processes are
not understood. Manganese absorption is decreased by feeding isolated
soy protein or excess levels of calcium, phosphorus, and iron. The
movement of manganese within the body is highly specific for the
element. Biogenic amities can influence the metabolism of manganese,
apparently by effects of cyclic AMP.
Ike bone defects associated with manganese deficiency appear to be
related to chondrogenesis rather than osteogenesis. Manganese is the
preferred metal cofactor for a group of glucosy! transferases involved
in mucopolysacchande synthesis. There is evidence that manganese
functions in carbohydrate and lipid metabolism and in the metabolism
of the brain. The mitochondria generally contain high concentrations of
manganese. Pyruvate carboxylase and superoxide dismutase are two
important metalloenzymes that contain manganese.
SOURCES
Underwood (1977) reviewed information on manganese content of
forage and other plant sources. The manganese concentration can vary
widely in relation to species, variety, type of soil, and manganese
concentration in the soil. Typical values for various grasses, clover,
etc., ranged from 60 to more than 800 ppm on a dry basis. As with many
other elements, whole seeds contain significant concentrations of
manganese (Schroeder e! al., 1966~; however, refining processes
OCR for page 292
292 MINERAL TOLERANCE OF DOMESTIC ANIMALS
remove much of the element. Typical values for whole cereal grains are
3~50 ppm and 3~0 ppm for soybean meal. Protein supplements
obtained from animal sources are generally low in manganese, approxi-
mately 5-15 ppm.
The manganese content of surface waters collected at 140 U.S.
sampling stations averaged 29.4 ppb between 1957 and 1969 (National
Research Council, 1974~. Minimum and maximum values were 0.20 and
3,230 ppb, and the mean was 29.4 ppb. Consumption of surface water
by domestic animals would not contribute significantly on the average
to the requirement; however, consumption of water containing the
maximum manganese content could supply 300 600 percent of the
requirement of cattle. The estimated maximum amount for swine was
20~0 percent of requirement, and for poultry the amount was
negligible.
Ammerman and Miller (1972) reviewed information on bioavailability
of manganese from venous concentrated forms. Data with chicks
showed that feeding reagent grade chemicals resulted in equal bioavail-
ability of manganese from the sulfate, chloride, carbonate, and dioxide.
Manganous oxide and manganous sulfate are the two most commonly
used forms in animal feeds. The sulfate is used when greater ease of
solubility is important.
TOXICOSIS
The manganese requirements of the common domestic animals and
fowl range from 20 to 55 ppm in the diet. The effects in five species of
animals continuously fed excess levels of dietary manganese, ranging
from 35 to 7,586 ppm, are summarized in Table 23. Data for some of the
same and three additional species appear at the end of the table. For
these, the experimental conditions differed from the bulk of available
data. The basal diets fed to the animals were generally adequate but
vaned greatly in concentration of essential nutrients, other compo-
nents, and even in manganese content. Measurements of varying sensi-
tivity have been used to detect adverse effects; however, the most
common has been growth of young animals
LOW LEVELS
The data in Table 23 show that feeding excess manganese at levels as
high as 1,000 ppm produced a serious health problem in only 1 of 21
experimental groups, including several species. In one study, pigs fed
.
OCR for page 293
Manganese
293
500 ppm manganese exhibited retarded growth, limb stiffness, and a
stilted gait (Grummer et al., 19501. It is possible that these adverse
responses may have been related to other components of the manga-
nese source, which contained 65 percent manganous sulfate, or to the
composition of the diet. Similarly severe effects were not observed by
other workers in pigs fed higher manganese levels.
Metabolic deviations from control animals have been shown with
fairly low levels of excess manganese. These include slightly decreased
copper absorption by the calf fed 50 ppm manganese above 12 ppm in
the basal diet (Ivan and Grieve, 1976) and negative calcium balance
during early lactation in cows fed70 ppm manganese (Reid et al., 1947~.
Increased fecal phosphorus was observed without other changes.
The observations at these levels of manganese, 1,000 ppm or less,
were made with the rat, calf, cow, poultry, and pig. A few experiments
were long-term, including egg production of chickens and reproduction
in mammals. Similar effects were observed in sheep fed sequentially
increasing amounts of manganese up to 2,500 ppm manganese (Hart-
man et al., 1955~.
HIGH LEVELS
Beginning around 2,000 ppm excess manganese, significant adverse
health effects, such as growth depression, were observed in some
experiments. These and higher levels of manganese caused some mor-
tality and decreased levels of hemoglobin. It is remarkable that in a
Midday study with rats growth and reproduction were normal with
4,990 ppm manganese, and only growth was adversely affected at 9,980
ppm manganese. Otherwise, 4,080 ppm manganese fed to poults is the
highest level that had no effect on growth (Vohra and Kratzer, 1968~.
Effects of dietary manganese between 1,000 and 2,000 ppm have not
been studied.
Cunningham et al. (1966) investigated the effect of feeding 5,000
ppm manganese to a rumen-fistulated cow. The manganese produced a
marked change in rumen bacterial species. The in vitro production of
propionic and total volatile fatty acids was depressed in flasks innocu-
lated with flora from the manganese-fed cow as compared with a cow
fed the basal diet. The suppressive effects of manganese added in vitro
were also greater with the innoculum from the manganese-fed cow.
These data suggest that at least part of the adverse effects of excess
manganese fed to ruminants is due to effects on the rumen microflora.
Intubation of guinea pigs with a high daily dose of manganese, 4.37
mg/kg of body weight, produced some mortality and lesions of the
OCR for page 294
294 MINERAL TOLERANCE OF DOMESTIC ANIMALS
gastrointestinal tract of survivors (Chandra and Imam, 1973~. The
lowest published lethal dose of manganese, as the sulfate, was 1X2
mg/kg for hamsters (Fairchild et al., 1977~. Young rabbits that were
given large daily doses of manganese in choking water lost weight and
developed a transient paralysis and prolonged anesthesia of the ex-
tremities (Uma~i e! al., 19691- It is surprising that neurological
damage, which occurs in humans exposed to airborne manganese dusts
such as ores, has not been observed more frequently in animals.
FACTORS INFLUENCING TOXICITY
As noted above, excess manganese affected the metabolism of several
elements. Generally a mineral antagonism is characterized by re-
ciprocal effects: i.e., a deficiency of the second or antagonized element
enhances the toxicity of the first element, and, conversely, an excess
of the second element protects against toxicity of the first.
The primary antagonism of importance in manganese toxicity is the
effect on iron. Low hemoglobin levels were found by several workers
in animals fed excess manganese (Table 23~. This anemia was accom-
panied by low levels of tissue iron and elevated levels of liver copper
(Hartman et al., 19551. Matrone et al. (1959) showed that excess
manganese interfered troth hemoglobin regeneration in rabbits and baby
pigs. Data from two experiments suggested that the minimal level of
excess manganese to depress hemoglobin regeneration in baby pigs was
125 ppm manganese or less. A supplement of 400 ppm iron in the diet
completely counteracted the effect of 2,000 ppm manganese in de-
pressing hemoglobin regeneration in baby pigs. Chandra and Tandon
(1973) found that iron deficiency in rats increased manganese levels and
pathology in the liver and kidneys when excess manganese was given
orally.
With 14,000 ppm excess manganese in the diet of rats, Diez-Ewald et
al. (1968) observed decreased liver iron stores and increased absorption
of iron; however, they also found blood loss into the gastrointestinal
tract. Under more physiological conditions, increased manganese
absorption has been reported in iron deficiency (Borg and Cotzias,
1958; PolIack e' al., 1965; Diez-EwaId et al., 1968). Thomson and
Valberg (1972) showed that iron and manganese each interfered with
the absorption of the other from perfusate in open-ended duodenal
loops of iron-deficient rats. There is evidence that manganese can be
incorporated in viva into the porphyrin of red blood cells under condi-
tions of iron deficiency (Borg and Cotzias, 1958~.
These diverse studies demonstrate the importance of iron status in
OCR for page 295
Manganese
295
modifying manganese toxicity. Much remains to be learned about the
nature of the interactions and the practical relation of iron status, rang-
ing from deficiency to excess, in defining resistance to the spectrum of
excess manganese intakes.
The effect of supplemental form on toxicity has not been systemati-
cally investigated; however, it appears that inorganic salts have similar
effects. Abnormalities of reproduction in dairy cattle have been associ-
ated with 200 ppm or higher concentrations of manganese in forages of
Costa Rica (Fonseca and Davis, 1969~. Tentatively, 100 ppm or more of
manganese in forage was designated as high. The toxicity of manganese
in forage merits detailed study.
TISSUE LEVELS
Underwood (1971, 1977) reviewed data on concentrations of manga-
nese in animal tissues. The liver and pituitary contain the highest
concentrations, each with approximately 2.5 ppm. Me manganese in
hair, wool, and feathers reflects dietary levels from deficiency to excess
In a more sensitive manner than organs or internal tissues. Feeding
manganese in the diet of laying hens at 13 and 1,000 ppm resulted in
total egg yolk values of 4 and 33 ,ug, respectively. In general, tissue
manganese remains relatively constant over a wide range of intakes
(Cotzias, 19581. The efficient homeostatic mechanisms for eliminating
excess manganese from the body would seem to preclude significant
accumulation in tissues of domestic animals (Watson et al., 1973~.
Doyle and Spaulding (1978) have summarized the data on manganese
content in liver, kidney, heart, and muscle in normal cattle, sheep,
swine, and chickens.
MAXIMUM TOLERABLE LEVELS
Levels of 1,000 ppm manganese produced some metabolic deviations
from normal but almost no effects on growth or other indications of
toxicosis in most experiments. Whether the metabolic changes would
become threats to health on a long-term basis would probably depend
on the diet composition, age, or physiological status of the animal and
on the mechanism of the adverse eject.
The data with iron deficiency show clearly that small amounts of
excess manganese, as low as 12S ppm, are undesirable. Most studies of
manganese toxicity were camed out with stack diets. Whereas these
OCR for page 296
296 MINERAL TOLERANCE OF DOMESTIC ANIMALS
have practical significance, they make it impossible to assess the exact
nutrient composition of each diet, which may explain apparent dis-
crepancies between adverse effects and dose level, particularly at 2,000
ppm manganese and above. Most manganese toxicity studies were
carried out many years ago. Due to changes in diet formulation and
genetic characteristics of domestic animals, the old results may not be
entirely applicable now.
With a well-balanced, adequate diet, it appears that. 1,000 ppm
dietary manganese is the maximum tolerable level, at least under short-
term conditions, for cattle and sheep and 2,000 ppm for poultry. Some
data indicated a greater sensitivity of swine, so the maximum tolerable
level was set at 400 ppm.
SUMMARY
Manganese is an essential element for animals and plants. It functions
in mucopolysacchar~de synthesis and carbohydrate and lipid metabo-
lism. A variety of bone disorders, retarded growth, and reproductive
failure have been observed in manganese-deficient animals. Water-
soluble salts of manganese are readily available to meet the animal's
needs.
In general, adverse health effects have not occurred in most species
with dietary concentrations of 1,000 ppm manganese or less, although
some metabolic alterations have occurred. These do not appear serious
and probably would not occur in animals receiving a well-balanced
adequate diet. Swine appear to be more sensitive to manganese than
cattle, sheep, or poultry. At 2,000 ppm and above, growth retardation,
anemia, gastrointestinal lesions, and sometimes neurological signs have
been observed. Many studies have been reported in which no adverse
effects were observed at high levels of manganese intake. Manganese
and iron are mutually antagonistic. With low iron intake, animals are
much more sensitive to manganese toxicity; conversely, excess iron is
protective. The tissues, apart from skin, hair, and feathers, do not
accumulate large amounts of the element. Homeostatic mechanisms
maintain most tissue manganese concentrations within fairly narrow
limits, primarily by excretion of excess manganese via bile or the small
intestine.
OCR for page 297
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302 MINERAL TOLERANCE OF DOMESTIC ANIMALS
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Representative terms from entire chapter:
ppm manganese
