6 Minerals

6.1 Functions of minerals

6.2 Natural and supplementary sources of minerals
6.3 Acid–base balance
6.4 Major elements
6.5 Trace elements
6.6 Other elements

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6.1 FUNCTIONS OF MINERALS
Although most of the naturally occurring mineral elements are found in animal tis-
sues, many are thought to be present merely because they are constituents of the
animal’s food and may not have an essential function in the animal’s metabolism.
The term ‘essential mineral element’ is restricted to a mineral element that has been
proven to have a metabolic role in the body. Before an element can be classed as
essential it is generally considered necessary to prove that purified diets lacking
the element cause deficiency symptoms in animals and that those symptoms can be
eradicated or prevented by adding the element to the experimental diet. Most
research on mineral nutrition has been carried out in this way. However, some of the
mineral elements required by animals for normal health and growth are needed in
such minute amounts that the construction of deficient diets is often difficult to
achieve and deficiency has been demonstrated only in laboratory animals under spe-
cial conditions. In such studies it is necessary not only to monitor food and water
supplies but also to ensure that animals do not obtain the element under investiga-
tion from cages, troughs, attendants or dust in the atmosphere.
Requirements or allowances for minerals may be derived factorially from the
amounts required to meet endogenous losses and the mineral retained or excreted in
products, or, more usually for the trace elements, empirically from dose responses to
levels in the diet. The main problem for the minerals with more than one function is
deciding on the criterion for adequacy. Dietary levels of mineral that are sufficient
for one function may be inadequate for another. Adequacy for the short period of
growth of animals slaughtered for meat may not cover the long-term needs of breed-
ing and longevity of adult stock. Also, for the minerals involved in bone formation,
there are many criteria, such as bone dimensions, strength, histology and composi-
tion. Depletion of body reserves in times of undernutrition will supply the mineral

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Chapter 6 Minerals

for its metabolic functions, and this needs to be considered if requirements are to be
measured accurately.
Until 1950, 13 mineral elements were classified as essential: these comprised
the major elements (calcium, phosphorus, potassium, sodium, chlorine, sulphur,
magnesium) and the micro or trace elements (iron, iodine, copper, manganese, zinc
and cobalt). By 1970, molybdenum, selenium, chromium and fluorine had been
added to the list; subsequently, arsenic, boron, lead, lithium, nickel, silicon, tin,
vanadium, rubidium and aluminium have also been included, the list varying
slightly according to the different authorities. Plant and animal tissues contain a
further 30 mineral elements, in small quantities, for which no essential function
has been found. They may be acquired from the environment, but it has been sug-
gested that as many as 40 or more elements may have metabolic roles in mam-
malian tissues. Fortunately, many of these trace elements, especially those of more
recent discovery, are required in such minute quantities, or are so widely distrib-
uted in foods for animals, that deficiencies are likely to be extremely rare under
normal practical conditions.
The classification of the essential minerals into major elements and trace ele-
ments depends upon their concentration in the animal or amounts required in
the diet. Normally trace elements are present in the animal body in a concentration
not greater than 50 mg/kg and are required at less than 100 mg/kg diet. Those es-
sential mineral elements that are of particular nutritional importance together with
their approximate concentrations in the animal body are shown in Table 6.1.
The minerals are held in different forms in the body, which can be considered as
compartments. There is a central reserve or interchange compartment, which is usu-
ally blood plasma, and one or more compartments that interchange the mineral with
the central compartment at various rates, e.g. compartments easy or difficult to mo-
bilise. Metabolic processes take place via the central reserve (plasma), which re-
ceives minerals from other compartments, the digestive tract and the difficult to
mobilise compartment. The central reserve secretes mineral into the readily mo-
bilised compartments, the difficult to mobilise compartment, the gastrointestinal
tract, the kidneys and milk.The flux between the compartments can be measured by
a combination of balance trials and injection of radioactive marker followed by sam-
pling the tissues over time. An example of the body compartments of copper is
shown in Fig. 6.1.

Table 6.1 Nutritionally important essential mineral elements and their

approximate concentration in the animal

Major elements g/kg Trace elements mg/kg

Calcium 15 Iron 20–80
Phosphorus 10 Zinc 10–50
Potassium 2 Copper 1–5
Sodium 1.6 Molybdenum 1–4
Chlorine 1.1 Selenium 1–2
Sulphur 1.5 Iodine 0.3–0.6
Magnesium 0.4 Manganese 0.2–0.5
Cobalt 0.02–0.1

104
 Functions of minerals

Dietary
copper
Tissue Foetus
Milk

Absorbed
Blood Kidney
Endogenous
loss
(i) I
' r - - - - ~ ·I
Bile (ii) Liver Liver Liver I
I
A B C I
I
I
I
_____ ..,!
Faecal (iii)
copper
(unabsorbed
dietary and Urine
endogenous)

Fig. 6.1 Diagram of the possible routes of movement of copper in the ruminant
body. A is a temporary storage compartment for copper in the liver destined for
exchange with blood and excretion into bile, B represents a temporary storage
for incorporation into caeruloplasmin and C represents a long-term storage
compartment.
Adapted from Symonds H W and Forbes J M 1993 Mineral metabolism. In: Forbes J M and France J (eds)
Quantitative Aspects of Ruminant Digestion and Metabolism, Wallingford, CABI.

Nearly all the essential mineral elements, both major and trace, are believed to
have one or more catalytic functions in the cell. Some mineral elements are firmly
bound to the proteins of enzymes (see Box 6.1), while others are present in pros-
thetic groups in chelated form. A chelate is a cyclic compound that is formed be-
tween an organic molecule and a metallic ion, the latter being held within the
organic molecule as if by a claw (‘chelate’ is derived from the Greek work meaning
‘claw’). Examples of naturally occurring chelates are the chlorophylls, cytochromes,
haemoglobin and vitamin B12.
Elements such as sodium, potassium and chlorine have primarily an electrochem-
ical or physiological function and are concerned with the maintenance of acid–base
balance, membrane permeability and the osmotic control of water distribution
within the body. Some elements have a structural role, for example calcium and
phosphorus are essential components of the skeleton and sulphur is necessary for
the synthesis of structural proteins. Finally, certain elements have a regulatory func-
tion in controlling cell replication and differentiation; zinc acts in this way by influ-
encing the transcription process, in which genetic information in the nucleotide
sequence of DNA is transferred to that of an RNA molecule. It is not uncommon for
an element to have a number of different roles; for example, magnesium functions
catalytically, electrochemically and structurally.
A number of elements have unique functions. Iron is important as a constituent
of haem, which is an essential part of a number of cytochromes important in respira-
tion. Cobalt is a component of vitamin B12 and iodine forms part of the hormone
thyroxine.

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Chapter 6 Minerals

BOX 6.1 Mineral elements and enzymes

Below are some examples of the involvement of minerals in enzymes (summarised from Underwood
and Suttle – see Further reading).

Mineral Enzyme Function

Iron Succinate dehydrogenase Aerobic oxidation of carbohydrates
Cytochromes a, b and c Electron transfer
Copper Cytochrome oxidase Terminal oxidase
Ceruloplasmin (ferroxidase) Iron utilisation: copper transport
Superoxide dismutase Dismutation of superoxide radical O*2 -
Zinc Carbonic anhydrase CO2 formation
Alcohol dehydrogenase Alcohol metabolism
Carboxypeptidase A Protein digestion
Alkaline phosphatase Hydrolysis of phosphate esters
Manganese Pyruvate carboxylase Pyruvate metabolism
Superoxide dismutase Antioxidant by removing O*2 -
Molybdenum Xanthine dehydrogenase Purine metabolism
Sulphite oxidase Sulphite oxidation
Selenium Glutathione peroxidases Removal of H2O2 and hydroperoxides
Type I and III deiodinases Conversion of thyroxine to active form

Some elements, for example calcium and molybdenum, may interfere with the
absorption, transport, function, storage or excretion of other elements. There are
many ways in which minerals may interact, but the three major ways involve the
formation of unabsorbable compounds, competition for metabolic pathways and
the induction of metal-binding proteins.The interaction of minerals with each other
is an important factor in animal nutrition, and an imbalance of mineral elements –
as distinct from a simple deficiency – is important in the aetiology of certain nutri-
tional disorders of farm animals. The use of radioactive isotopes in recent years has
advanced our knowledge of mineral nutrition, although there are many nutritional
diseases associated with minerals whose exact causes are still unknown.
Although we have been considering the essential role of minerals in animal
nutrition, it is important to realise that many are toxic – causing illness or death – if
given to the animal in excessive quantities. This is particularly true of copper, sele-
nium, molybdenum, fluorine, vanadium and arsenic. Copper is a cumulative poison,
the animal body being unable to excrete it efficiently; small amounts of copper
given in excess of the animal’s daily needs will, in time, produce toxic symptoms.
This also applies to the element fluorine. Supplementation of any diet with miner-
als should always be carried out with great care, and the indiscriminate use of trace
elements in particular must be avoided. Ideally, the supplement should be tailored
to the target animal and a blanket oversupply should be avoided as it is wasteful
and potentially dangerous. Minerals should be added to concentrate foods via a
premix and thoroughly mixed to avoid ‘hot spots’ of high concentration and poten-
tial toxicity.

106
 Natural and supplementary sources of minerals

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6.2 NATURAL AND SUPPLEMENTARY SOURCES OF MINERALS
Plants and plant products form the main supply of nutrients to animals, and the compo-
sition of plants will influence the animal’s mineral intake.Thus, the species and stage of
maturity of the plant, the type of soil and climate, and the seasonal conditions are im-
portant factors. Legumes tend to be richer in the major minerals and certain trace ele-
ments than are grasses, and this is also the case with the seeds of legumes compared
with the seeds of grasses and cereals. Soil conditions and mineral content affect the up-
take of minerals by plants, and this can be further influenced by fertiliser application.
One of the major influences is soil pH, the effect of which differs among the elements.
For example, molybdenum uptake by plants increases with an increase in soil pH, but
cobalt and manganese contents decrease.Therefore, adjusting soil pH with lime will in-
fluence the mineral content of plants. Herbage magnesium content and availability can
be reduced by potassium and nitrogen fertilisers.The main animal products used in ani-
mal feeding, fishmeal, whey and skimmed milk, are good sources of the major minerals.
Usually, diets for farm animals contain a mineral/trace element/vitamin supple-
ment and, on occasions, it is necessary to include extra supplies of some minerals,
e.g. calcium for laying hens. Common sources of minerals used in mineral supple-
ments are limestone for calcium, dicalcium phosphate for phosphorus, common salt
for sodium, and calcined magnesite for magnesium. Trace elements are usually sup-
plied in a salt form, e.g. selenium as sodium selenite. When considering sources of
mineral, the cost, chemical and physical form, and freedom from impurities are
taken into account. It is also necessary to take account of the availability of the ele-
ment in question (see Chapter 10). Calcium tends to have a high availability from
most sources and the phosphorus in ortho- and meta-phosphates has an availability
of 80–100 per cent.The availability of phosphorus from rock phosphates can be very
low. Magnesium from calcined magnesite has an availability of 50–60 per cent,
whereas that from magnesium sulphate is up to 70 per cent. Sulphur from sulphates
is 50–90 per cent available.The availability of trace elements in the form of sulphate,
chloride or nitrate salts is high because they are water-soluble. Table 6.2 shows the
availability of minerals in a number of sources relative to a standard source. In these
examples the criteria used to assess the relative availability of the different minerals
vary, e.g. absorption, accumulation in tissues, production of metabolically active
compounds; hence, some sources in Table 6.2 have values greater than 100 per cent
when compared with the standard source of the mineral.
Free ions from inorganic sources can form complexes with other dietary con-
stituents, resulting in low absorbability and availability to the animal. Minerals in
‘chelated’ or ‘organic’ form (where the element is in combination with an organic
molecule such as an amino acid) are protected from reaction with other constituents
and theoretically have a greater absorbability than inorganic sources. Chelates were
mentioned above and the addition of chelated minerals as supplements to diets is
currently an active area of research. One of the most potent chelating agents is the
synthetic compound ethylenediamine tetraacetic acid (EDTA), which has the prop-
erty of forming stable chelates with heavy metals. In vitro, however, chelates of
cobalt were not more effective than cobalt chloride in stimulating microbial synthe-
sis of vitamin B12, and oral supplements of cobalt EDTA and cobalt sulphate gave
similar liver and serum vitamin B12 contents. The addition of chelating agents such
as EDTA to poultry diets may in some cases improve the availability of the mineral
element. However, the bonding between the metal and EDTA is strong, and work
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Chapter 6 Minerals

Table 6.2 Examples of the relative availability (%) of mineral elements from
mineral compounds

Mineral compound Poultry Pigs Cattle Sheep

Cobaltous sulphate – – – 100
Cobalt glucoheptate – – – 85
Cobalt carbonate – – – 100
Cupric sulphate 100 100 100 100
Copper-lysine 105 – 100 –
Copper-methionine 90 110 – –
Cupric carbonate 65 85 – –
Cupric chloride 110 – 115 115
Ferrous sulphate (7H2O) 100 100 100 100
Ferric citrate 75 150 110 –
Ferric oxide 10 10 – 5
Ferrous chloride 100 – – –
Iron-methionine – 185 –
Iron-proteinate – 125 –
Manganese sulphate 100 – – 100
Manganese carbonate 55 – – 30
Manganese-methionine 120 – – 125
Manganous chloride 100 – – –
Sodium selenite 100 100 100 100
Seleno-cystine 110 – – –
Seleno-methionine 80a/115b 120a/150b – –
Seleno-yeast – – 290 100
Zinc chloride 100 100 – –
Zinc sulphate 100 – 100 100
Zinc-lysine – 100 – –
Zinc-methionine 125 100 – 100
a
Assessed from glutathione peroxidase production or incidence of exudative diathesis.
b
Assessed from whole body or tissue selenium retention or incidence of pancreatic fibrosis.
Summarised from Ammerman C B, Henry P R and Miles R D 1998 Supplemental organically-bound mineral
compounds in livestock nutrition. In: Garnsworthy P C and Wiseman J (eds) Recent Advances in Animal
Nutrition, Nottingham, Nottingham University Press, pp. 67–91.

with copper chelates in sheep has shown that the copper is no more available than in
inorganic salts. Recently the manufacture of different forms of trace element–organic
complex has increased. In 1998 the Association of American Feed Control Officials
defined four categories of such complexes:
■ Metal amino acid complex: The product resulting from complexing of a soluble
metal salt with an amino acid.
■ Metal amino acid chelate: The product of the reaction of a metal ion from a solu-
ble metal salt with amino acids with a mole ratio of one mole of metal to three
moles (preferably two) of amino acids to form coordinate covalent bonds. The
average weight of the hydrolysed amino acids must be approximately 150 and
the resulting molecular weight of the chelate must not exceed 800.
■ Metal polysaccharide complex: The product resulting from complexing of a solu-
ble salt with a polysaccharide solution.

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 Natural and supplementary sources of minerals

■ Metal proteinate: The product resulting from the chelation of a soluble salt with
amino acids and/or partially hydrolysed protein.

Amino acid and peptide chelates are absorbed efficiently, possibly because they are
taken up by the peptide absorption mechanism rather than the active transport
mechanism for minerals (see Chapter 8), although this has not been proven. Levels
of iron in the tissues of piglets and piglet growth have been improved by giving an
iron proteinate to the sow. However, the piglets also had access to the sow’s faeces
and may have obtained iron from these. Again, although zinc methionine has im-
proved tissue levels of zinc in pigs, results have not been consistent.The replacement
of sodium selenite by selenium-enriched yeast has improved the selenium content of
serum, milk and tissues of gilts and the selenium status of their offspring. Selenium-
enriched yeast in diets for lactating cows has increased the transfer of selenium to
milk when compared with selenite. In the case of selenium the element is not in the
form of one of the complexes mentioned above but replaces sulphur in the amino
acids that normally contain sulphur. However, inorganic selenium supplements are
also effective and at a lower cost. Owing to the different properties of the chelating
agents and the variable reponses observed, their use as mineral supplements is con-
troversial.There are many reports in the popular press claiming increased responses.
A critical review by Underwood and Suttle (1999; see Further reading) suggests cau-
tion at this stage until evidence of consistent responses is published in scientific jour-
nals. In view of their cost, it is unlikely that they will replace inorganic sources of
mineral entirely, but they may be appropriate for special applications. It is suggested
that ‘organic’ minerals provide an extra supply of the element when there is reduced
efficiency of inorganic sources owing to interference from other minerals. These
preparations have also been advocated for use to reduce the excretion of unabsorbed
mineral and thus reduce the effect on the environment. The EU legislation on feed-
ing stuffs permits only named supplements.
Mineral supplementation of animals at pasture can be a problem. Minerals can be
incorporated into free-access feed blocks, which also provide a source of energy and
nitrogen. However, individual animal intake can be variable. Intake depends on sea-
son, weather conditions, the siting and number of blocks (to minimise competition),
frequency of renewal and availability of water. The inclusion of oil or molasses im-
proves palatability.
Spraying the pasture with soluble salts of trace elements can increase the element
content of the pasture. Alternatively, trace elements can be included in fertilisers in
order to increase the herbage content via the soil. However, if the deficiency is due to
poor availability of the element, then this type of application will not be successful.
For some of the trace elements, e.g. cobalt and copper, a solid bolus can be de-
posited into the rumen using a dosing gun. This bolus dissolves slowly over a period
of months, giving a steady release of the element. There can be problems of regurgi-
tation of the bolus and they may become coated, thereby reducing the effective re-
lease of the mineral. Recently, boluses formed from soluble glass have been
produced that are not susceptible to this coating action. The glass boluses may con-
tain more than one element (e.g. cobalt and selenium), anthelmintics, and vitamins
A, D or E. Needles of copper oxide, which have a high specific gravity and are
retained in the abomasum, have also been used in this way. For certain minerals
(e.g. copper, iodine and selenium), oral doses, drenches or injections with solutions
or pastes can be given at appropriate intervals, but the labour requirement is high.

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Chapter 6 Minerals

- 6.3 ACID–BASE BALANCE

Normally in nutrition, minerals, including those with electrolytic properties, are con-
sidered functionally as separate entities. In physiological terms, however, the elec-
trolytes need to be taken together since cells require a specific balance of anions and
cations to function efficiently. Physiological processes operate within a narrow range
of conditions, especially with respect to pH. In addition, enzyme systems, and hence
cell metabolism, are sensitive to pH. Thus, changes in acid–base status have a wide
influence on cell function and the animal must regulate the input and output of ions
to maintain acid–base homeostasis. Failure to maintain the correct electrolyte bal-
ance within the cell means that metabolic pathways are unable to function efficiently
and resources are diverted to achieving homeostasis at the expense of growth. The
diet is important in the maintenance of the correct intracellular electrolyte balance
owing to the metabolisable anions and cations that it contains and that consume or
generate acid during metabolism. Thus, an excess of anions will result in the produc-
tion of hydrogen ions to counterbalance the anions, giving metabolic acidosis,
whereas an excess of cations requires ions such as acetate and bicarbonate and
causes alkalosis. These effects are independent of the specific metabolic or physio-
logical roles of the particular element. The balance of acids and bases influences
many functions such as growth rate, appetite, amino acid and energy metabolism,
calcium utilisation, vitamin metabolism, intestinal absorption and kidney function.
Changes in cellular pH are often accompanied by changes in blood and urine pH.
Dietary influence in this respect may be assessed by measuring the dietary electrolyte
balance, defined as:

Na+ + K+ - Cl-

where Na+, K+ and Cl- are the concentrations of the elements in mequiv per unit
weight. The dietary electrolyte balance is commonly used to assess the diets of pigs
and poultry. Pigs are more susceptible to excess anions than to cations, and the opti-
mal dietary electrolyte balance is around 250 mequiv/kg. In poultry, eggshell forma-
tion has an effect on the acid–base balance as hydrogen ions are generated when
calcium carbonate is being synthesised. A dietary electrolyte balance of 200–
300 mequiv/kg is recommended for laying hens. In conditions of heat stress, elevated
respiration rate (panting) leads to respiratory alkalosis and in poultry and dairy cows
the acid–base balance of the diet has been adjusted to alleviate this. Ideally, other
elements making a contribution to electrolyte balance should be considered and a
more sophisticated assessment may be achieved by calculating (Na+ + K+ + Ca++ +
Mg++) - (Cl- + H2PO4- + HPO4- - + SO4- - ).This is termed the dietary undetermined
anion.The latter requires a substantial analytical facility and in practice the less com-
prehensive dietary electrolyte balance is generally considered to be sufficient. Re-
cently, in ruminant nutrition the cation–anion balance or dietary cation–anion
difference (DCAD) has been used to assess the electrolyte status of diets. This is
calculated as (Na+ + K+) - (Cl- + SO4- - ) or alternatively as (Na+ + K+ ) - (Cl- + S- - ).
Manipulation of the cation–anion difference is now recommended as part of the
dietary management of dairy cows in order to avoid hypocalcaemia or milk fever
(see Box 6.2).
In the above it is seen that there may be confusion with terminology and the
method of calculation (i.e. which ions are included) of the acid–base status of the

110
 Acid–base balance

BOX 6.2 Dietary cation–anion difference and milk fever

The metabolic acid–base balance affects the sensitivity of bone to parathyroid hormone (PTH) and
the synthesis of 1,25-dihydroxycholecalciferol. Therefore, acknowledging this when balancing the
mineral content of the diet can have an effect on the incidence of milk fever. Conditions that promote
an alkalotic state (high dietary cations, Na+ and K+) reduce the sensitivity of bone to PTH and can
limit the release of calcium. Conversely, an acidotic state (high dietary anions, Cl- and S- - ) increases
the sensitivity to PTH, increases 1,25-dihydroxycholecalciferol production and hence increases the
calcium supply.Through these metabolic responses, manipulation of the acid–base balance in the diet
of the pre-calving cow has been successful in reducing the incidence of milk fever.
Early work used the dietary electrolyte balance calculation (Na+ + K + - Cl-), but subsequently it
was found that the inclusion of SO4- - or S- - was beneficial. Thus, dietary cation–anion difference
(DCAD) as (Na+ + K+) - (Cl- + SO4-) or (Na+ + K+) - (Cl- + S-) is used when calculating and ma-
nipulating the acid–base balance of the diet. The recommended target for the latter calculation is
around -100 mequiv/kg. The optimal DCAD probably varies with several factors such as breed and
feeding management. Recent studies have shown that Cl- ions are more acidogenic than S- ions,
probably owing to differences in dissociation in and absorption from the digestive tract.
In practice, manipulation of the diet involves minimising foods high in potassium and sodium.
Grass silage is the major problem, often containing 30–40 g potassium/kg DM, and alkali-treated grain
and molasses should also be avoided. The cereal by-product, brewer’s grains, is a food that is low in
sodium and potassium. Unlike the low-calcium diet strategy, the DCAD strategy requires a moderate
to high calcium intake to be maintained. Supplementary anionic salts (e.g. ammonium chloride, am-
monium sulphate, magnesium chloride, calcium chloride) can be used to adjust the DCAD, but they
tend to be unpalatable. Practical application of this stategy requires knowledge of the mineral contents
of the foods.To ensure there is adequate magnesium for effective calcium absorption and mobilisation,
the magnesium content of the diet is adjusted to 3.5 g/kg DM using magnesium sulphate or magne-
sium chloride, and the sulphur content is set at 4 g/kg DM using calcium or ammonium sulphate.
Higher magnesium (up to 4 g/kg DM) may be required if the potassium content of the diet is high in
view of the latter’s effect on magnesium absorption.The DCAD can then be manipulated with ammo-
nium or calcium chloride. Calcium intake is maintained at 120–150 g/day and phosphorus at 50 g/day.
This approach to the problem of milk fever requires careful management, since the high quantities of
anionic salts involved may reduce food intake and precipitate other metabolic problems.The effective-
ness of the strategy can be checked by measuring urine pH, which should be slightly acidic at around
6.5. It is recommended that the diets are given for at least 2 weeks but no more than 4 weeks before
calving. Although pregnant heifers show the same responses as cows in terms of increased blood cal-
cium with decreasing DCAD, food intake was depressed and they did not have increased milk yields.
It is currently recommended that heifers should not be given supplementary anions. Current research
is investigating alterations to DCAD to improve food intake and milk production. Early lactation diets
contain large amounts of rumen-fermentable carbohydrate and a positive DCAD would, in theory,
help to reduce rumen and blood acidosis.

diet. Some authorities suggest the inclusion of NH4+, HCO3- and CO3- -, while others
recommend that the absorption coefficient should also be accounted for. However,
such refinement will require much more research and information before this type of
model can be applied.
Certain pathological conditions may cause disturbances in electrolyte balance,
e.g. vomiting (loss of chloride), diarrhoea (loss of bicarbonate) and excessive amino

111
Chapter 6 Minerals

acid oxidation (excess acid production). These, however, are largely outside the con-
trol of the nutritionist.

- 6.4 MAJOR ELEMENTS

Calcium
Calcium is the most abundant mineral element in the animal body. It is an important
constituent of the skeleton and teeth, in which about 99 per cent of the total body
calcium is found; in addition, it is an essential constituent of living cells and tissue
fluids. Calcium is essential for the activity of a number of enzyme systems, including
those necessary for the transmission of nerve impulses and for the contractile prop-
erties of muscle. It is also concerned in the coagulation of blood. In blood, the ele-
ment occurs in the plasma; the plasma of mammals usually contains 80–120 mg
calcium/l, but that of laying hens contains more (300–400 mg/l).

Composition of bone
Bone is highly complex in structure, the dry matter consisting of approximately 460 g
mineral matter/kg, 360 g protein/kg and 180 g fat/kg. The composition varies, how-
ever, according to the age and nutritional status of the animal. Calcium and phospho-
rus are the two most abundant mineral elements in bone; they are combined in a
form similar to that found in the mineral hydroxyapatite, 3Ca3(PO4)2.Ca(OH)2.
Bone ash contains approximately 360 g calcium/kg, 170 g phosphorus/kg and 10 g
magnesium/kg.
The skeleton is not a stable unit in the chemical sense, since large amounts of the
calcium and phosphorus in bone can be liberated by reabsorption. This takes place
particularly during lactation and egg production, although the exchange of calcium
and phosphorus between bones and soft tissue is always a continuous process. Re-
sorption of calcium is controlled by the action of the parathyroid gland. If animals
are fed on a low-calcium diet, the ionic calcium concentration in the extracellular
fluid falls, the parathyroid gland is stimulated and the hormone produced causes re-
sorption of bone, liberating calcium to meet the requirements of the animal. Since
calcium is combined with phosphorus in bone, the phosphorus is also liberated and
excreted by the animal.
The parathyroid hormone also plays an important role in regulating the amount
of the calcium absorbed from the intestine by influencing the production of 1,25-
dihydroxycholecalciferol, a derivative of vitamin D, which is concerned with the
formation of calcium-binding protein (see p. 80). Finally, the hormone stimulates the
kidney to resorb urinary calcium.

Deficiency symptoms
If calcium is deficient in the diet of young growing animals, then satisfactory bone for-
mation cannot occur and the condition known as rickets is produced. The symptoms
of rickets are misshapen bones, enlargement of the joints, lameness and stiffness. In
adult animals, calcium deficiency produces osteomalacia, in which the calcium in the

112
 Major elements

bone is withdrawn and not replaced. In osteomalacia, the bones become weak and
are easily broken. In hens, deficiency symptoms are soft beak and bones, retarded
growth and bowed legs; the eggs have thin shells and egg production may be reduced.
The symptoms described above for rickets and osteomalacia are not specific for cal-
cium and can also be produced by a deficiency of phosphorus, an abnormal calcium :
phosphorus ratio or a deficiency of vitamin D (see p. 80). A number of factors can be
responsible for subnormal calcification.
Milk fever (parturient paresis) is a condition that most commonly occurs in dairy
cows shortly after calving. It is characterised by a lowering of the serum calcium
level, muscular spasms and, in extreme cases, paralysis and unconsciousness. The
exact cause of hypocalcaemia associated with milk fever is obscure, but it is gener-
ally considered that, with the onset of lactation, the parathyroid gland is unable to
respond rapidly enough to increase calcium absorption from the intestine to meet
the extra demand. Normal levels of blood calcium can be restored by intravenous in-
jections of calcium gluconate, but this may not always have a permanent effect. It
has been shown that avoiding excessive intakes of calcium while maintaining ade-
quate dietary levels of phosphorus during the dry period reduces the incidence of
milk fever. Deliberate use of low-calcium diets to increase calcium absorption in the
practical prevention of milk fever requires a good estimate of calving date, otherwise
calcium deficiency may occur. Also low-calcium diets are hard to achieve with for-
ages unless straw is used. Recently, success in controlling milk fever has been
achieved by manipulating the acid–base balance of the diet (see Box 6.2). Adminis-
tration of large doses of vitamin D3 for a short period before parturition has also
proved beneficial, but the timing is critical. Hypocalcaemia in ewes bearing twins
often occurs before lambing.

Sources of calcium
Milk, green leafy crops, especially legumes, and sugar beet pulp are good sources of
calcium; cereals and roots are poor sources. In some lucerne crops, calcium associ-
ated with oxalates is unavailable. Animal by-products containing bone, such as fish-
meal, are excellent sources. Calcium-containing mineral supplements that are
frequently given to farm animals, especially lactating animals and laying hens, in-
clude ground limestone, steamed bone flour and dicalcium phosphate. If rock cal-
cium phosphate is given to animals it is important to ensure that fluorine is absent,
otherwise this supplement may be toxic. High levels of fat in the diet of monogastric
animals result in the formation of calcium soaps of fatty acids, which reduce the ab-
sorbability of calcium.

Calcium : phosphorus ratio

When giving calcium supplements to animals it is important to consider the calcium :
phosphorus ratio of the diet, since an abnormal ratio may be as harmful as a defi-
ciency of either element in the diet. The calcium : phosphorus ratio considered most
suitable for farm animals other than poultry is generally within the range 1 : 1 to 2 : 1,
although there is evidence that suggests that ruminants can tolerate rather higher
ratios providing that the phosphorus requirements are met. In the case of the calcium
and phosphorus requirements for ruminants published by the Agriculture and Food
Research Council’s Technical Committee on Responses to Nutrients, the requirement

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Chapter 6 Minerals

for phosphorus can exceed that of calcium in some circumstances. The proportion of
calcium for laying hens is much larger, since they require great amounts of the element
for eggshell production. The calcium is usually given to laying hens as ground lime-
stone mixed with the diet or, alternatively, calcareous grit may be given ad libitum.
Granular limestone is more effective since the large particles are retained in the
gizzard for a longer time.

Phosphorus
Phosphorus has more known functions than any other mineral element in the animal
body. The close association of phosphorus with calcium in bone has already been
mentioned. In addition, phosphorus occurs in phosphoproteins, nucleic acids and
phospholipids. The element plays a vital role in energy metabolism in the formation
of sugar-phosphates and adenosine di- and triphosphates (see Chapter 9).The impor-
tance of vitamin D in calcium and phosphorus metabolism has already been dis-
cussed in Chapter 5. The phosphorus content of the animal body is considerably less
than that of calcium content. Whereas 99 per cent of the calcium found in the body
occurs in the bones and teeth, the proportion of the phosphorus in these structures is
about 80–85 per cent of the total; the remainder is in the soft tissues and fluids,
where it serves the essential functions mentioned above. The control of phosphorus
metabolism is different from that of calcium. If it is in an available form, phosphorus
is absorbed well even when there is an excess over requirement. The excess is ex-
creted via the kidney or the gut (via saliva). In monogastric animals, the kidney is
the primary route of excretion. Plasma phosphorus diffuses into saliva and in rumi-
nants the large amount of chewing during rumination results in saliva being the
major input of phosphorus into the rumen rather than the food.

Deficiency symptoms
Extensive areas of phosphorus-deficient soils occur throughout the world, especially
in tropical and subtropical areas, and a deficiency of phosphorus can be regarded as
the most widespread and economically important of all the mineral disabilities af-
fecting grazing livestock.
Like calcium, phosphorus is required for bone formation and a deficiency can also
cause rickets or osteomalacia. Pica, or depraved appetite, has been noted in cattle
when there is a deficiency of phosphorus in the diet; the affected animals have ab-
normal appetites and chew wood, bones, rags and other foreign materials. Pica is not
specifically a sign of phosphorus deficiency, since it may be caused by other factors.
Evidence of phosphorus deficiency may be obtained from an analysis of blood
serum, which shows a phosphorus content lower than normal. In chronic phosphorus
deficiency, animals may have stiff joints and muscular weakness.
Low dietary intake of phosphorus has also been associated with poor fertility,
with apparent dysfunction of the ovaries causing inhibition, depression or irregular-
ity of oestrus.There are many examples throughout the world of phosphorus supple-
mentation increasing fertility in grazing cattle. In cows, a deficiency of this element
may also reduce milk yield. In hens, there is reduced egg yield, hatchability and shell
thickness.
Subnormal growth in young animals and low liveweight gains in mature animals
are characteristic symptoms of phosphorus deficiency in all species. Phosphorus
deficiency is usually more common in cattle than in sheep, as the latter tend to have

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 Major elements

more selective grazing habits and choose the growing parts of plants, which happen
to be richer in phosphorus.

Sources of phosphorus
Milk, cereal grains and fishmeal products containing bone are good sources of phos-
phorus; the content in hays and straws is generally very low. Considerable attention
has been paid to the availability of phosphorus. Much of the element present in
cereal grains is in the form of phytates, which are salts of phytic acid, a phosphoric
acid derivative:

H 0P
I I
C C OH
P
01c1
10
C
P 1\1
H
H

C
0P = -
I
O -P- O
I
1\?
H
P

C
1/6
H

C
P
OH

I
H 0P
Phytic acid

Insoluble calcium and magnesium phytates occur in cereals and other plant prod-
ucts. Experiments with chicks have shown that the phosphorus of calcium phytate is
utilised only 10 per cent as effectively as disodium phosphate. In studies with laying
hens, phytate phosphorus was utilised about half as well as dicalcium phosphate.
Certain plant foods, such as wheat, contain phytase and in the pig stomach some of
the phytate phosphorus is made available by the action of this enzyme. However, it
is likely that the phytase is destroyed in the acid conditions once the acid secreted
penetrates the food mass in the stomach. Intestinal phytase activity from the micro-
flora has been observed, but it appears to be of little importance in the pig. It has
been shown with sheep that hydrolysis of phytates by bacterial phytases occurs in
the rumen. Bacteria in the hind gut also have phytase activity, but the significance of
this in phosphorus supply for the monogastric is not clear. Phytate phosphorus ap-
pears therefore to be utilised by ruminants as readily as other forms of phosphorus,
although studies using radioactive isotopes indicate that the availability of phospho-
rus may range from 0.33 to 0.90. Recent studies with a fungal source of phytase
added to the diet of pigs have shown significant increases in ileal and total tract di-
gestibility of phytate phosphorus (see Chapter 24).
Feeding with high levels of phosphorus should be avoided as the excess is ex-
creted and contributes to pollution by encouraging the growth of algae in water
courses. High phosphorus intake in association with magnesium can lead to the for-
mation of mineral deposits in the bladder and urethra (urolithiasis or urinary calculi)
and blockage of the flow of urine in male sheep and cattle.

Potassium
Potassium plays a very important part, along with sodium, chlorine and bicarbonate
ions, in osmotic regulation of the body fluids and in the acid–base balance in the
animal. Whereas sodium is the main inorganic cation of extracellular tissue fluids,

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Chapter 6 Minerals

potassium functions principally as the cation of cells. Potassium plays an impor-

tant part in nerve and muscle excitability and is also involved in carbohydrate
metabolism.

Deficiency symptoms
The potassium content of plants is generally very high, that of grass, for example,
being frequently above 25 g/kg DM, so that it is normally ingested by animals in
larger amounts than any other element. Consequently, potassium deficiency is rare in
farm animals kept under natural conditions. One exception to this is provided by dis-
tiller’s grains (draff; see p. 547), which, as a result of the removal of the liquid after
fermentation, is deficient in several soluble elements, including potassium. Appropri-
ate supplementation is necessary where draff forms a large proportion of the diet.
There are certain areas in the world where soil potassium levels are naturally low.
Such areas occur in Brazil, Panama and Uganda, and it is suggested that in these trop-
ical regions, potassium deficiencies may arise in grazing animals, especially at the end
of the long dry season, when potassium levels in the mature herbage are low.
Deficiency symptoms have been produced in chicks given experimental diets low
in potassium.They include retarded growth, weakness and tetany, followed by death.
Deficiency symptoms, including severe paralysis, have also been recorded for calves
given synthetic milk diets low in potassium.
A dietary excess of potassium is normally excreted rapidly from the body, chiefly
in the urine. Some research workers believe that high intake of the element may in-
terfere with the absorption and metabolism of magnesium in the animal, which may
be an important factor in the aetiology of hypomagnesaemic tetany (see p. 119).

Sodium
Most of the sodium of the animal body is present in the soft tissues and body fluids.
Like potassium, sodium is concerned with the acid–base balance and osmotic regu-
lation of the body fluids. Sodium is the chief cation of blood plasma and other extra-
cellular fluids of the body.The sodium concentration within the cells is relatively low,
the element being replaced largely by potassium and magnesium. Sodium also plays
a role in the transmission of nerve impulses and in the absorption of sugars and
amino acids from the digestive tract (see p. 168).
Much of the sodium is ingested in the form of sodium chloride (common salt),
and it is mainly in this form that the element is excreted from the body. There is evi-
dence that sodium rather than chlorine is the chief limiting factor in salt-deficient
diets of sheep and cows.

Deficiency symptoms
Sodium deficiency in animals occurs in many parts of the world, but especially in the
tropical areas of Africa and the arid inland areas of Australia, where pastures contain
very low concentrations of the element.A deficiency of sodium in the diet leads to a
lowering of the osmotic pressure, which results in dehydration of the body. Symp-
toms of sodium deficiency include poor growth and reduced utilisation of digested
proteins and energy. In hens, egg production and growth are adversely affected. Rats
given experimental diets low in sodium had eye lesions and reproductive distur-
bances, and eventually died.

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 Major elements

Sources of sodium
Most foods of vegetable origin have comparatively low sodium contents; animal
products, especially foods of marine origin, are richer sources. The commonest min-
eral supplement given to farm animals is common salt.

Chlorine
Chlorine is associated with sodium and potassium in acid–base relationships and os-
motic regulation. Chlorine also plays an important part in the gastric secretion,
where it occurs as hydrochloric acid as well as chloride salts. Chlorine is excreted
from the body in the urine and is also lost from the body, along with sodium and
potassium, in perspiration.
A dietary deficiency of chlorine may lead to an abnormal increase of the alkali re-
serve of the blood (alkalosis) caused by an excess of bicarbonate, since inadequate
levels of chlorine in the body are partly compensated for by increases in bicarbon-
ate. Experiments with rats on chlorine-deficient diets have shown that growth was
retarded, but no other symptoms developed.

Sources of chlorine
With the exception of fishmeals, the chlorine content of most foods is comparatively
low. The chlorine content of pasture grass varies widely and figures ranging from
3 g/kg to 25 g/kg DM have been reported. The main source of this element for most
animals is common salt.

Salt
Since plants tend to be low in both sodium and chlorine, it is the usual practice to
give common salt to herbivores. Unless salt is available, deficiencies are likely to
occur in both cattle and sheep. Experiments carried out in the USA with dairy cows
on salt-deficient diets showed that animals did not exhibit immediate ill effects, but
eventually appetite declined, with subsequent loss in weight and lowered milk pro-
duction. The addition of salt to the diet produced an immediate cure.
Salt is also important in the diet of hens, and it is known to counteract feather pick-
ing and cannibalism. Salt is generally given to pigs on vegetable diets, but if fishmeal is
given the need for added salt is reduced. Swill can also be a rich source of salt, al-
though the product is very variable and can contain excessive amounts of salt. Too
much salt in the diet is definitely harmful and causes excessive thirst, muscular weak-
ness and oedema. Salt poisoning is quite common in pigs and poultry, especially where
fresh drinking water is limited. When the concentration of salt in the diet of hens ex-
ceeds 40 g/kg DM and the supply of drinking water is limited, then death may occur.
Hens can tolerate larger amounts of salt if plenty of water is available. Chicks cannot
tolerate salt as well as adults can, and 20 g/kg DM in the diet should be regarded as the
absolute maximum.This value should also not be exceeded in the diets of pigs.Turkey
poults are even less tolerant, and 10 g/kg of salt in the diet should not be exceeded.

Sulphur
Most of the sulphur in the animal body occurs in proteins containing the amino acids
cystine, cysteine and methionine. The two vitamins biotin and thiamin, the hormone
insulin and the important metabolite coenzyme A also contain sulphur.The structural

117
Chapter 6 Minerals

compound chondroitin sulphate is a component of cartilage, bone, tendons and the

walls of blood vessels. Sulphur-containing compounds are also important in elements
of the respiratory process from haemoglobin through to cytochromes. Only a small
amount of sulphur is present in the body in inorganic form, though sulphates are
known to occur in the blood in small quantities. Wool is rich in cystine and contains
about 4 per cent of sulphur.
Traditionally, little attention has been paid to the importance of sulphur in ani-
mal nutrition, since the intake of this element is mainly in the form of protein, and
a deficiency of sulphur would indicate a protein deficiency. In recent years, how-
ever, with the increasing use of urea as a partial nitrogen replacement for protein
nitrogen and as a method for treating cereal grains (see Chapter 22), it has been
realised that the amount of sulphur present in the diet may be the limiting factor for
the synthesis in the rumen of cystine, cysteine and methionine. Under these condi-
tions, the addition of sulphur to urea-containing rations is beneficial. There is evi-
dence that sulphate (as sodium sulphate) can be used by ruminal microorganisms
more efficiently than elemental sulphur. The mean of the estimates of the ratio of
sulphur to nitrogen in microbial protein is around 0.07, which, incidentally, is ap-
proximately the ratio found in animal tissue and milk protein. The UK Agricultural
Research Council has recommended that the requirement for rumen-degradable
sulphur should be calculated by multiplying the rumen-degradable nitrogen re-
quirement by 0.07 (i.e. equivalent to a N : S ratio of 14 : 1). The ratio of nitrogen to
sulphur in wool protein is narrower, at 5 : 1, and the supply of sulphur-containing
amino acids may be limiting for sheep with a high rate of wool production. This
limitation cannot be overcome by increasing the ratio of rumen-degradable sulphur
to degradable nitrogen, since this will not alter the rate of microbial protein produc-
tion. However, the limitation can be alleviated by supplying sulphur containing
amino acids in forms that bypass the rumen or in proteins that have low rumen
degradability.
Consideration of sulphur in animal nutrition is important in areas of intensive
livestock production where sulphur in soils is not replaced regularly by fertiliser
application.
Inorganic sulphur seems to be of less practical importance for monogastric
animals, although studies with pigs, chicks and poults have indicated that inorganic
sulphate can have a sparing effect on the requirement for sulphur-containing amino
acids in the diet.
Toxicity can result from excess dietary sulphur, which is converted to hydrogen
sulphide, a toxic agent, by the gastrointestinal flora.This reduces rumen motility and
causes nervous and respiratory distress.

Magnesium
Magnesium is closely associated with calcium and phosphorus. About 70 per cent
of the total magnesium is found in the skeleton but the remainder, which is distrib-
uted in the soft tissues and fluids, is of crucial importance to the well-being of the
animal. Magnesium is the commonest enzyme activator, for example in systems
with thiamin pyrophosphate as a cofactor, and oxidative phosphorylation is re-
duced in magnesium deficiency. Magnesium is an essential activator of phosphate
transferases (e.g. creatine kinase) and it activates pyruvate carboxylase, pyruvate
oxidase and reactions of the tricarboxylic acid cycle; therefore, it is essential for the

118
 Major elements

efficient metabolism of carbohydrates and lipids. In addition, magnesium is in-

volved in cellular respiration and many other cellular reactions, forming complexes
with adenosine tri-, di- and monophosphates. The formation of cyclic AMP and
other secondary messengers requires magnesium. Magnesium ions moderate neuro-
muscular activity and, through binding to phospholipid, are involved in cell mem-
brane integrity. The interaction of parathyroid hormone, which is responsible for
calcium mobilisation (see p. 112), with its receptors on bone and kidney cells in-
volves magnesium, and low blood levels of the element are associated with
hypocalcaemia. Thus, it can be seen that magnesium is a key element in cellular
biochemistry and function. Magnesium is absorbed from the small and large intes-
tine of monogastric animals, and requirements are usually met with cereal and soya
bean meal diets. In ruminants, absorbability can be low and potassium reduces the
efficiency of absorption by inhibiting the two active transport systems in the rumen
wall that carry magnesium against the electrochemical gradient. Potassium does not
affect absorption beyond the rumen.

Deficiency symptoms
Symptoms due to a simple deficiency of magnesium in the diet have been reported
for a number of animals. In rats fed on purified diets, the symptoms include in-
creased nervous irritability and convulsions. Experimental low-magnesium milk
diets for calves caused low serum magnesium levels, depleted bone magnesium,
tetany and death.The condition is not uncommon in milk-fed calves about 50–70 days
old. Colostrum is high in magnesium content but milk is low in magnesium, and this
is compounded by a reduction in the efficiency of absorption of magnesium as the
calf ages.
In adult ruminants, a condition known as hypomagnesaemic tetany, associated
with low blood levels of magnesium (hypomagnesaemia), has been recognised since
the early 1930s. A great deal of attention has been given to this condition in recent
years, since it is widespread and the death rate is high. Hypomagnesaemic tetany has
been known under a variety of names, including magnesium tetany, lactation tetany
and grass staggers, but most of these terms have been discarded because the disease
is not always associated with lactation or with grazing animals.The condition can af-
fect stall-fed dairy cattle, hill cattle, cattle at grass, and sheep.There is some evidence
of a breed susceptibility in the UK, where the condition appears to be more common
in Ayrshire and least common in Jersey animals. Most cases occur in grazing animals
and, in Europe and North America, the trouble is particularly common in the spring
when the animals are turned out on to young, succulent pasture. Because the tetany
can develop within a day or two of animals being turned out to graze, the condition
has been referred to as the acute form. In this acute type, blood magnesium levels
fall so rapidly that the reserve of magnesium within the body cannot be mobilised
rapidly enough. In the chronic form of the disease, plasma magnesium levels fall over
a period of time to low concentrations. This type is not uncommon in suckler herds.
Clinical signs of the disease are often brought on by stress factors such as cold, wet
and windy weather. In adult animals, bone magnesium is not as readily available as
it is in the young calf.
In New Zealand, where cows are pastured throughout the year, hypomagne-
saemic tetany occurs most frequently in late winter and early spring. In Australia, a
high incidence of the disease has been associated with periods of rapid winter
growth of pastures.

119
Chapter 6 Minerals

The normal magnesium content of blood serum in cattle is within the range of
17–40 mg magnesium/litre, but levels below 17 mg/l frequently occur without
clinical symptoms of disease. Tetany is usually preceded by a fall in blood serum
magnesium to about 5 mg/l. Urine magnesium is a better indicator of deficiency
than serum magnesium because levels of the latter do not fall until there is a
severe deficiency. However, a lack of magnesium is immediately reflected in urine
levels, for which 10 mg/100 ml is satisfactory, 2–10 mg/100 ml is inadequate and
less than 2 mg/100 ml indicates a severe deficiency. Subcutaneous injection of
magnesium sulphate, or preferably magnesium lactate, can generally be expected
to cure the animal if given early, but in practice this is sometimes difficult. Treat-
ment of this kind is not a permanent cure and oral treatment with magnesium
oxide, as described below, should be started immediately. Typical symptoms of
tetany are nervousness, tremors, twitching of the facial muscles, staggering gait
and convulsions.
The exact cause of hypomagnesaemic tetany in ruminant animals is unknown,
although a dietary deficiency of magnesium may be a contributory factor. Some
research workers consider the condition to be caused by a cation–anion imbalance
in the diet, and there is evidence of a positive relationship between tetany and
heavy dressings of pasture with nitrogenous and potassic fertilisers. It has been
suggested that the concentration of potassium in spring pasture should not exceed
25 g/kg DM and the application of potassium fertilisers should be managed
carefully.
The use of radioactive magnesium in tracer studies indicates that the magne-
sium present in food is poorly absorbed from the alimentary canal; in some cases
only 50 g/kg of the herbage magnesium can be utilised by the ruminant. Why this
is so in ruminants is not known. Since adult animals have only very small readily
available reserves of body magnesium, they are dependent upon a regular dietary
supply.
Although the exact cause of hypomagnesaemia is still uncertain, the primary fac-
tor would appear to be inadequate absorption of magnesium from the digestive
tract. A high degree of success in preventing hypomagnesaemia may be obtained by
increasing the magnesium intake. This can be effected by feeding with magnesium-
rich mineral mixtures or, alternatively, by increasing the magnesium content of pas-
ture by the application of magnesium fertilisers.

Sources of magnesium
Wheat bran, dried yeast and most vegetable protein concentrates, especially cotton
seed cake and linseed cake, are good sources of magnesium. Clovers are usually
richer in magnesium than grasses, although the magnesium content of forage crops
varies widely.As mentioned previously, draff is deficient in soluble minerals and high
levels of this food in the diet require appropriate supplementation. The mineral sup-
plement used most frequently is magnesium oxide, which is sold commercially as
calcined magnesite. When hypomagnesaemic tetany is likely to occur, it is generally
considered that about 50 g of magnesium oxide per head per day should be given to
cows as a prophylactic measure. The daily prophylactic dose for calves is 7–15 g of
the oxide, while that for lactating ewes is about 7 g. The mineral supplement can be
given mixed with the concentrate ration. Alternatively, a mixture of magnesium
acetate solution and molasses can be used, which is frequently made available on a
free-choice basis from ball feeders placed in the field.

120
 Trace elements

-
6.5 TRACE ELEMENTS
Iron
More than 90 per cent of the iron in the body is combined with proteins, the most
important being haemoglobin, which contains about 3.4 g/kg of the element. Iron
also occurs in blood serum in a protein called transferrin, which is concerned with
the transport of iron from one part of the body to another. Ferritin, a protein con-
taining up to 200 g/kg of iron, is present in the spleen, liver, kidney and bone mar-
row and provides a form of storage for iron. Haemosiderin is a similar storage
compound and may contain up to 350 g/kg of iron. Iron has a major role in a host of
biochemical reactions, particularly in connection with enzymes of the electron trans-
port chain (cytochromes). Electrons are transported by the oxidation and reduction
activity of bound iron. Among the enzymes containing or activated by iron are cata-
lase, peroxidases, phenylalanine hydroxylase and many others, including all the tri-
carboxylic acid cycle enzymes.

Deficiency symptoms
Since more than half the iron present in the body occurs as haemoglobin, a dietary de-
ficiency of iron would clearly be expected to affect the formation of this compound.
The red blood corpuscles contain haemoglobin, and these cells are continually being
produced in the bone marrow to replace those red cells destroyed in the animal body
as a result of catabolism. Although the haemoglobin molecule is destroyed in the ca-
tabolism of these red blood corpuscles, the iron liberated is made use of in the resyn-
thesis of haemoglobin, and because of this the daily requirement of iron by a healthy
animal is usually small. If the need for iron increases, as it does after prolonged haem-
orrhage or during pregnancy, then haemoglobin synthesis may be inadequate and
anaemia will result. Anaemia due to iron deficiency occurs most commonly in rapidly
growing sucklings, since the iron content of milk is usually very low. This can occur in
piglets housed in pens without access to soil. The piglet is born with very limited iron
reserves and sow’s milk provides only about 1 mg per day.The rapidly growing piglet’s
requirement is 15 mg per day, which, in extensive systems, could be obtained by inges-
tion of soil. Providing the sow with supplementary iron in gestation does not increase
the foetal piglet’s liver iron or the amount in the milk. Therefore, it is routinely sup-
plied by intramuscular injection as a dextran complex or gleptoferron, by 3 days of
age. Usually 200 mg of iron is injected. Alternatively, oral iron supplements are avail-
able in the form of a paste of the citrate or fumarate or granules of iron dextran, but
these may not be eaten or the iron may be lost if diarrhoea occurs.Attempts have been
made to increase the supply of iron to the piglet by supplementing the sow’s diet and
relying on the piglet’s consumption of the sow’s faeces during exploration activity.
However, this has produced uneven uptake, and injection of iron compounds is more
effective. Anaemia in piglets is characterised by poor appetite and growth. Breathing
becomes laboured and spasmodic – hence the descriptive term ‘thumps’ for this condi-
tion. Although iron deficiency is not common in older animals, increased supplemen-
tation is required when high levels of copper are used for growth promotion.
Iron-deficiency anaemia is not common in lambs and calves because in practice it
is unusual to restrict them to a milk diet without supplementary feeding. It does,
however, sometimes occur in laying hens, since egg production represents a consid-
erable drain on the body reserves.

121
Chapter 6 Minerals

Sources of iron
Iron is widely distributed in foods. Good sources of the element are green leafy ma-
terials, most leguminous plants and seed coats. Feeds of animal origin, such as blood
and fishmeals, are excellent sources of iron. As mentioned previously, milk is a poor
source of the element.
Iron is absorbed throughout the gastrointestinal tract, but mainly in the duo-
denum and jejunum. Absorption is poor and is, to a large extent, independent of the
dietary source. The efficiency of absorption is increased during periods of iron need
and decreased during periods of iron overload. The mechanisms whereby the body
carries this out are not fully understood. A number of theories have been advanced
and one of these, the ‘mucosal block’ theory, propounded in 1943, is still widely held
by many to explain the mechanism. According to this theory, the mucosal cells of the
gastrointestinal tract absorb iron and convert it into ferritin; when the cells become
physiologically saturated with ferritin, further absorption is impeded until the iron is
released and transferred to plasma. Another, more recent theory proposes that the
main regulator of iron uptake is the iron concentration in the epithelial cells of the
duodenal mucosa.
The adult’s need for iron is normally low, as the iron produced from the destruc-
tion of haemoglobin is made available for haemoglobin regeneration, only about
10 per cent of the element escaping from this cycle.

Iron toxicity
Iron toxicity is not a common problem in farm animals, but it can result from pro-
longed oral administration of the element. Ferrous ions are reported to generate
oxygen-based free radicals, contributing to oxidative stress in the cell (see Chapter 5).
Normally iron is protein-bound or in chemical form, which prevents it from causing
oxidation. Chronic iron toxicity results in alimentary disturbances, reduced growth
and phosphorus deficiency.

Copper
Evidence that copper is a dietary essential was obtained in 1924, when experi-
ments with rats showed that copper was necessary for haemoglobin formation. Al-
though copper is not actually a constituent of haemoglobin, it is present in certain
other plasma proteins, such as ceruloplasmin, concerned with the release of iron
from the cells into the plasma. A deficiency of copper impairs the animal’s ability
to absorb iron, mobilise it from the tissues and utilise it in haemoglobin synthesis.
Copper is also a component of other proteins in blood. One of these, erythro-
cuprein, occurs in erythrocytes, where it plays a role in oxygen metabolism. The
element is also known to play a vital role in many enzyme systems; for example,
copper is a component of cytochrome oxidase, which is important in oxidative
phosphorylation. It is also a component of superoxide dismutase, which forms part
of the cell’s antioxidant system. The element also occurs in certain pigments,
notably turacin, a pigment of feathers. Copper is necessary for the normal pigmen-
tation of hair, fur and wool. It is thought to be present in all body cells, being
particularly concentrated in the liver, which acts as the main copper storage organ
of the body. Copper has been shown to reduce the susceptibility to infection in
lambs directly.

122
 Trace elements

Deficiency symptoms
Since copper performs many functions in the animal body, there are a variety of de-
ficiency symptoms. These include anaemia, poor growth, bone disorders, scouring,
infertility, depigmentation of hair and wool, gastrointestinal disturbances, and le-
sions in the brain stem and spinal cord. The lesions are associated with muscular in-
coordination and occur, especially, in young lambs. A copper deficiency condition
known as ‘enzootic ataxia’ has been known for some time in Australia; the disorder
there is associated with pastures low in copper content (2–4 mg/kg DM) and can be
prevented by feeding with a copper salt.A similar condition that affects lambs occurs
in the UK and is known as ‘swayback’. The signs of swayback range from complete
paralysis of the newborn lamb to a swaying staggering gait that affects, in particular,
the hind limbs. The condition can occur in two forms, one congenital, in which the
signs are apparent at birth and are due to the failure of the myelin sheath of nerves
to develop, and the other in which the onset of the clinical disease is delayed for sev-
eral weeks.The congenital form of the condition is irreversible and can be prevented
only by ensuring that the ewe receives an adequate level of copper in her diet. De-
layed swayback can be prevented or retarded in copper-deficient lambs by par-
enteral injection of small doses of copper complexes.
Although the dietary level of copper is an important factor in the aetiology of
swayback, the condition does not appear to be invariably caused by a simple dietary
deficiency of the element. Swayback has been reported to occur on pastures appar-
ently normal or even high (7–15 mg/kg DM) in copper content. One important factor
is that the efficiency of absorption of dietary copper is very variable. For example,
there is about a tenfold variation in the efficiency with which Scottish Blackface ewes
absorb copper from autumn pasture (1.2 per cent) and from leafy brassicas (13.2 per
cent). It is also known that genetic factors influence the concentration of copper in the
blood, liver and brain of the sheep, and hence the incidence of swayback can be
affected by genotype. Blackface lambs given a copper-supplemented barley and
fishmeal diet retained 6 per cent of the dietary copper in the liver, whereas Texel
lambs retained 13 per cent. Finnish Landrace and Suffolk lambs were intermediate,
at 8–9 per cent retention.
Copper plays an important role in the production of ‘crimp’ in wool. The element
is present in an enzyme that is responsible for the disulphide bridge in two adjacent
cysteine molecules. In the absence of the enzyme, the protein molecules of the wool
do not form their bridge and the wool, which lacks crimp, is referred to as ‘stringy’ or
‘steely’ (see p. 375).
Nutritional anaemia resulting from copper deficiency has been produced experi-
mentally in young pigs by diets very low in the element, and this type of anaemia
could easily arise in such animals fed solely on milk. In older animals, copper defi-
ciency is unlikely to occur and copper supplementation of practical rations is gener-
ally considered unnecessary. There are, however, certain areas in the world where
copper deficiency in cattle occurs. A condition in Australia known locally as ‘falling
disease’ was found to be related to a progressive degeneration of the myocardium of
animals grazing on copper-deficient pastures.

Copper–molybdenum–sulphur interrelations
Certain pastures on calcareous soils in parts of England and Wales have been known
for over 100 years to be associated with a condition in cattle known as ‘teart’, which

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Chapter 6 Minerals

is characterised by unthriftiness and scouring.A similar disorder occurs on reclaimed

peat lands in New Zealand, where it is known as ‘peat scours’. Molybdenum levels in
teart pasture are of the order of 20–100 mg/kg DM compared with 0.5–3.0 mg/kg DM
in normal pastures, and teart was originally regarded as being a straightforward
molybdenosis. In the late 1930s, however, it was demonstrated that feeding with
copper sulphate controlled the scouring and hence a molybdenum–copper relation-
ship was established.
It is now known that the effect of molybdenum is complex, and it is considered
that the element exerts its limiting effect on copper retention in the animal only in
the presence of sulphur. Sulphide is formed by ruminal microorganisms from dietary
sulphate or organic sulphur compounds; the sulphide then reacts with molybdate to
form thiomolybdate, which in turn combines with copper to form an insoluble cop-
per thiomolybdate (CuMoS4), thereby limiting the absorption of dietary copper. In
addition, it is considered likely that if thiomolybdate is formed in excess, it may be
absorbed from the digestive tract and exert a systemic effect on copper metabolism
in the animal.

Sources of copper
Copper is widely distributed in foods, and under normal conditions the diet of farm
animals is likely to contain adequate amounts.The copper content of crops is related
to some extent to the soil copper level, but it is also affected by other factors such as
drainage conditions and the herbage species. Seeds and seed by-products are usually
rich in copper, but straws contain little.The normal copper content of pasture ranges
from about 4 mg/kg to 8 mg/kg DM. The copper content of milk is low, and hence it
is customary when dosing young animals, especially piglets, with an iron salt to in-
clude a trace of copper sulphate.

Copper toxicity
It has long been known that copper salts given in excess to animals are toxic. Con-
tinuous ingestion of copper in excess of nutritional requirements leads to an accu-
mulation of the element in the body tissues, especially in the liver. Copper can be
regarded as a cumulative poison, so that considerable care is required in administer-
ing copper salts to animals. The tolerance to copper varies considerably between
species. Pigs are highly tolerant (see Box 6.3) and cattle relatively so. On the other

BOX 6.3 Copper as growth promoter

In the late 1950s and early 1960s Barber, Braude, Mitchell and their colleagues at the National In-
stitute for Research in Dairying at Reading demonstrated that pigs given high levels of copper (up to
250 mg/kg) in the diet had faster growth rates and better food conversion efficiency than unsupple-
mented pigs. Most of this copper is not absorbed but passes through the digestive tract, achieving its
effect by altering the microbial population in much the same way as antibiotic growth promoters, al-
though its effect is independent of and in addition to that caused by antibiotics.
Concern about pollution of the environment has resulted in restrictions on the use of copper
as a growth promoter in Europe. The maximum permitted dietary level is 170 mg/kg for pigs up to
12 weeks of age, and then it must be reduced to 35 mg/kg as for other classes of pig. Furthermore, it
is essential that sheep do not have access to pasture that has recently been fertilised with pig slurry.

124
 Trace elements

hand, sheep are particularly susceptible and chronic copper poisoning has been en-
countered in housed sheep on concentrate diets. There is a gradual accumulation of
copper in the liver of sheep until the danger level of about 1000 mg/kg fat-free DM
is reached. Poisoning has been known to occur in areas where the herbage contains
copper of the order of 10–20 mg/kg DM and low levels of molybdenum. Chronic
copper poisoning results in necrosis of the liver cells, jaundice, loss of appetite and
death from hepatic coma. The slow accumulation of copper in the liver causes dam-
age to the organ without overt symptoms. There is leakage of enzymes from the
damaged cells into the blood. Eventually there is a sudden release of copper and
haemolysis, which can occur spontaneously or as a result of stressors such as partu-
rition or infection. There is a genetic variation in animals’ susceptibility to copper
poisoning related to the efficiency of retention, with the Scottish Blackface being the
least susceptible and continental breeds, such as the Texel, being highly susceptible.
The EU maximum permitted level for copper in sheep diets is 15 mg/kg – this should
not be exceeded if toxicity is to be avoided. For susceptible breeds, a dietary level of
10 mg/kg can be excessive. It is unwise to administer copper supplements to sheep
unless deficiency conditions are liable to occur – many cases of death due to copper
poisoning caused by the indiscriminate use of copper-fortified diets have been re-
ported. Chronic copper poisoning in sheep has occurred under natural conditions in
parts of Australia where the copper content of the pasture is high. Care should be
taken when sheep are given antiprotozoal compounds such as monensin, which may
eliminate the protozoa that produce the sulphide that normally reduces copper
availability.

Cobalt
A number of disorders of cattle and sheep, characterised by emaciation, anaemia
and listlessness, have been recognised for many years and have been described as
‘pining’, ‘salt sick’, ‘bush sickness’ and ‘wasting disease’. These disorders occur in
Europe, Australia, New Zealand and the USA. In the UK, ‘pining pastures’ occur in
many counties and are particularly common in the border counties of England and
Scotland.
As early as 1807, Hogg, an Ettrick shepherd, recognised pining or ‘vinquish’ as
being a dietary upset. Pining is associated with a dietary deficiency of cobalt caused
by low concentrations of the element in the soil and herbage. Pining can be pre-
vented in these areas by feeding with small amounts of cobalt.
The physiological function of cobalt was discovered only when vitamin B12 was
isolated and was shown to contain the element. Cobalt is required by microorgan-
isms in the rumen for the synthesis of vitamin B12; if the element is deficient in the
diet, then the vitamin cannot be produced in the rumen in amounts sufficient to sat-
isfy the animal’s requirements and symptoms of pining occur. Pining is therefore re-
garded as being due to a deficiency of vitamin B12. There is evidence for this, since
injections of vitamin B12 into the blood alleviate the condition, whereas cobalt injec-
tions have little beneficial effect. Although vitamin B12 therapy will prevent pining
occurring in ruminant animals, it is more convenient and cheaper in cobalt-deficient
areas to supplement the diet with the element, allowing the microorganisms in the
rumen to synthesise the vitamin for subsequent absorption by the host.
When ruminants are confined to cobalt-deficient pastures it may be several
months before any manifestations of pine occur because of body reserves of vitamin

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Chapter 6 Minerals

B12 in the liver and kidneys. When these are depleted there is a gradual decrease in
appetite, with consequent loss of weight followed by muscular wasting, pica, severe
anaemia and eventually death. If the deficiency is less severe, then a vague unthrifti-
ness, difficult to diagnose, may be the only sign. Deficiency symptoms are likely to
occur where levels of cobalt in the herbage are below 0.1 mg/kg DM. Under grazing
conditions, lambs are the most sensitive to cobalt deficiency, followed by mature
sheep, calves and mature cattle in that order.
Ruminants have a higher requirement for the element than non-ruminants be-
cause some of the element is wasted in microbial synthesis of organic compounds
with no physiological activity in the host’s tissues. Furthermore, vitamin B12 is
poorly absorbed from the digestive tract of ruminants, the availability in some cases
being as low as 0.03.The ruminant has an additional requirement for the vitamin be-
cause of its involvement in the metabolism of propionic acid (see p. 202), an impor-
tant acid absorbed from the rumen.
There is evidence that the intestinal microorganisms in non-ruminants also can
synthesise vitamin B12, although in pigs and poultry this synthesis may be insuffi-
cient to meet their requirements. It is common practice to include in pig and poultry
diets some animal protein food rich in vitamin B12 and/or a vitamin supplement, in
preference to including a cobalt salt.
Apart from the importance of cobalt as a component of vitamin B12, the element
is believed to have other functions in the animal body as an activating ion in certain
enzyme reactions.

Sources of cobalt
Most foods contain traces of cobalt. Normal pasture herbages have a cobalt content
within the range 100–250 µg/kg DM.
Cobalt deficiency in ruminants can be prevented by dosing the animals with a so-
lution of cobalt salts, although this form of treatment has to be repeated at short in-
tervals and precautions must be taken when handling the solution (see below).
Alternatively the animals can be given access to cobalt-containing salt licks. A con-
tinuous supply from a single dose can be obtained by giving a cobalt bullet contain-
ing 900 g cobaltic oxide/kg; the bullet remains in the reticulum and slowly releases
the element over a long period. Some of this cobalt is not utilised by the animal and
is excreted, and this of course has the effect of improving the cobalt status of the pas-
ture.Alternatively, deficient pastures can be treated with cobalt-containing fertilisers
or with small amounts of cobalt salt solutions.

Cobalt toxicity
Although an excess of cobalt can be toxic to animals, there is a wide margin of
safety between the nutritional requirement and the toxic level. Cobalt toxicosis is
extremely unlikely to occur under practical farming conditions. Unlike copper,
cobalt is poorly retained by the body tissues and an excess of the element is soon ex-
creted. The toxic level of cobalt for cattle is 1 mg cobalt/kg body weight daily. Sheep
are less susceptible to cobalt toxicosis than cattle and have been shown to tolerate
levels up to 3.5 mg/kg. Excessive cobalt supplementation of ruminant diets can lead
to the production of analogues of vitamin B12 and a reduction in the quantity of the
true vitamin. Cobalt compounds pose a risk to human health as they cause cancer if
inhaled and they irritate the skin; for this reason, their use has been restricted in the

126
 Trace elements

EU, where materials with more than 100 mg Co/kg must be labelled as hazardous
and should be handled only with appropriate personal protection equipment. The
European Food Safety Authority has recommended that the supplementation of
diets for farm animals with cobalt be limited to ruminants (except milk replacers),
horses and rabbits at a level of 0.3 mg/kg DM of supplemental cobalt, and the max-
imum amount permitted in the complete diet in the EU is 2 mg/kg DM.

Iodine
The concentration of iodine present in the animal body is very small and in the adult
is usually less than 600 µg/kg. Although the element is distributed throughout the
tissues and secretions, its only known role is in the synthesis of the two hormones,
triiodothyronine (T3) and tetraiodothyronine (T4, thyroxine) produced in the thyroid
gland (see p. 54).
Iodine is removed from iodides in the blood and combined with the amino acid ty-
rosine to form monoiodotyrosine (T1) and diiodotyrosine (T2).Two molecules of T2 are
condensed to produce T4, the physiologically inactive transport form of the hormone,
which is stored in the thyroid gland.T4 is released into the blood capillaries as required
and is activated by deiodinase enzymes to produce the physiologically active T3. The
enzymes are selenium-dependent (see p. 131) and occur in the periphery where the
hormone is needed, mainly in the liver and kidneys but also in the skin.
The thyroid hormones accelerate reactions in most organs and tissues in the body,
thus increasing the basal metabolic rate, accelerating growth and increasing the oxy-
gen consumption of the whole organism. They also control the development of the
foetus and are involved in immune defence, digestion, muscle function and seasonal-
ity of reproduction.

Deficiency symptoms
When the diet contains insufficient iodine, the production of thyroxine is de-
creased. The main indication of such a deficiency is an enlargement of the thyroid
gland, termed endemic goitre, and is caused by compensatory hypertrophy of the
gland. As the thyroid is situated in the neck, the deficiency condition in farm ani-
mals manifests itself as a swelling of the neck, so-called ‘big neck’. Reproductive ab-
normalities are one of the most outstanding consequences of reduced thyroid
function; breeding animals deficient in iodine give birth to hairless, weak or dead
young; brain development is impaired; oestrus is suppressed or irregular; and male
fertility is reduced.
A dietary deficiency of iodine is not the sole cause of goitre: it is known that cer-
tain foods contain goitrogenic compounds and cause goitre in animals if given in
large amounts. These foods include most members of the Brassica genus, especially
kale, cabbage and rape, and also soya beans, linseed, peas and groundnuts. Goitro-
gens have been reported in milk of cows fed on goitrogenic plants. A goitrogen pres-
ent in brassicas has been identified as L-5-vinyl-2-oxazolidine-2-thione (goitrin),
which inhibits the iodination of tyrosine and thus interferes with thyroxine synthe-
sis.Therefore, it cannot be overcome by adding more iodine to the diet.Thiocyanate,
which may also be present in members of the Brassica genus, is known to be goitro-
genic and may be produced in the tissues from a cyanogenetic glycoside present in
some foods. Goitrogenic activity of the thiocyanate type is prevented by supplying

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Chapter 6 Minerals

adequate iodine in the diet. It has been reported that high dietary nitrate levels in-
hibit the uptake of iodine.

Sources of iodine
Iodine occurs in traces in most foods and is present mainly as inorganic iodide, in
which form it is absorbed from the digestive tract.The richest sources of this element
are foods of marine origin, and values as high as 6 g/kg DM have been reported for
some seaweeds; fishmeal is also a rich source of iodine. The iodine content of land
plants is related to the amount of iodine present in the soil, and consequently wide
variations occur in similar crops grown in different areas.
In areas where goitre is endemic, precautions are generally taken by supplement-
ing the diet with the element, usually in the form of iodised salt. This contains the
element either as sodium or potassium iodide or as sodium iodate.

Iodine toxicity
The minimum toxic dietary level of iodine for calves of 80–112 kg body weight has
been shown to be about 50 mg/kg, although some experimental animals have been
adversely affected at lower levels. Symptoms of toxicity include depressions in
weight gain and feed intake. In studies with laying hens, diets with iodine contents of
312–5000 mg/kg DM stopped egg production within the first week at the higher
level and reduced egg production at the lower level. The fertility of the eggs pro-
duced was not affected, but early embryonic death, reduced hatchability and delayed
hatching resulted. Excessively high levels of iodine supplementation should be
avoided in diets for ewes in pregnancy because this has resulted in lambs with a re-
duced ability to absorb immunoglobulins and vitamin E from colostrum. Pigs seem
to be more tolerant of excess iodine and the minimum toxic level is considered to lie
between 400 mg/kg and 800 mg/kg.

Manganese
The amount of manganese present in the animal body is extremely small. Most tissues
contain traces of the element, the highest concentrations occurring in the bones, liver,
kidney, pancreas and pituitary gland. Manganese is important in the animal body as
an activator of many enzymes such as hydrolases and kinases and as a constituent of
arginase, pyruvate carboxylase and manganese superoxide dismutase.

Deficiency symptoms
Manganese deficiency has been found in ruminants, pigs and poultry. The effects of
acute deficiency are similar in all species and include retarded growth, skeletal ab-
normalities, ataxia of the newborn and reproductive failure. Manganese, through its
activation of glycosyl transferases, is required for the formation of the mucopolysac-
charide that forms the organic matrix of bone.
Deficiencies of manganese in grazing ruminants are likely to be rare, although the
reproductive performance of grazing Dorset Horn ewes in Australia was improved by
giving manganese over two consecutive years. Low-manganese diets for cows and
goats have been reported to depress or delay oestrus and conception, and to increase
abortion. Manganese is an important element in the diet of young chicks, a defi-
ciency leading to perosis or ‘slipped tendon’, a malformation of the leg bones. Man-
ganese deficiency is not, however, the only factor involved in the aetiology of this

128
 Trace elements

condition, as perosis in young birds may be aggravated by high dietary intakes of cal-
cium and phosphorus or a deficiency of choline. Another link between manganese
and choline deficiencies is shown in fatty infiltration of the liver and changes in the
ultrastructure of the liver.
Manganese deficiency in breeding birds reduces hatchability and shell thickness,
and in chicks causes head retraction. In pigs, lameness is a symptom. Other abnor-
malities associated with manganese deficiency include impaired glucose utilisation
and a reduced vitamin K-induced blood-clotting response.

Sources of manganese
The element is widely distributed in foods, and most forages contain 40–200 mg/kg
DM. The manganese content of pasture herbages, however, can vary over a much
wider range and in acid conditions may be as high as 500–600 mg/kg DM. Seeds and
seed products contain moderate amounts, except for maize, which is low in the ele-
ment.Yeast and most foods of animal origin are also poor sources of manganese. Rich
sources are rice bran and wheat offals. Most green foods contain adequate amounts.

Manganese toxicity
There is a wide margin of safety between the toxic dose of manganese and the nor-
mal level in foods. Levels as high as 1 g/kg DM in the diet have been given to hens
without evidence of toxicity. Growing pigs are less tolerant, levels of 0.5 g/kg DM
having been shown to depress appetite and retard growth.

Zinc
Zinc has been found in every tissue in the animal body. The element tends to accu-
mulate in the bones rather than the liver, which is the main storage organ of many of
the other trace elements. High concentrations have been found in the skin, hair and
wool of animals. Several enzymes in the animal body are known to contain zinc;
these enzymes include carbonic anhydrase, pancreatic carboxypeptidase, lactate de-
hydrogenase, alcohol dehydrogenase, alkaline phosphatase and thymidine kinase. In
addition, zinc is an activator of several enzyme systems. It is involved in cell replica-
tion and differentiation, particularly in nucleic acid metabolism. Among the other
physiological functions of zinc are the production, storage and secretion of hor-
mones, involvement in the immune system and electrolyte balance.

Deficiency symptoms
Zinc deficiency in pigs is characterised by subnormal growth, depressed appetite,
poor food conversion and parakeratosis. The latter is a reddening of the skin fol-
lowed by eruptions that develop into scabs. A deficiency of this element is particu-
larly liable to occur in young, intensively housed pigs offered a dry diet ad libitum,
though a similar diet given wet may not cause the condition. It is aggravated by high
calcium levels in the diet and reduced by decreased calcium and increased phospho-
rus levels. Pigs given a diet supplemented with high levels of copper, for growth pro-
motion, have an increased requirement for zinc. Gross signs of zinc deficiency in
chicks are retarded growth, foot abnormalities, ‘frizzled’ feathers, parakeratosis and
a bone abnormality referred to as ‘swollen hock syndrome’.
Symptoms of zinc deficiency in calves include inflammation of the nose and
mouth, stiffness of the joints, swollen feet and parakeratosis.The response of severely

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zinc-deficient calves to supplemental zinc is rapid and dramatic. Improvements in

skin condition are usually noted within 2–3 days.
Manifestations of zinc deficiency, responsive to zinc therapy, have been observed
in growing and mature cattle in parts of Guyana, Greece, Australia and Scandinavia.
As levels in the pasture herbage are apparently comparable with those of other
areas, the deficiency is believed to be conditioned by some factor in the herbage or
general environment. In dairy cows, low dietary zinc concentrations are associated
with high somatic cell counts in their milk.

Sources of zinc
The element is fairly widely distributed. Yeast is a rich source, and zinc is concen-
trated in the bran and germ of cereal grains.Animal protein by-products, such as fish-
meal, are usually richer sources of the element than are plant protein supplements.

Zinc toxicity
Although cases of zinc poisoning have been reported, most animals have a high tol-
erance for this element. Excessive amounts of zinc in the diet are known to depress
food consumption and may induce copper deficiency.

Molybdenum
The first indication of an essential metabolic role for molybdenum was obtained in
1953, when it was discovered that xanthine oxidase, important in purine metabo-
lism, was a metalloenzyme containing molybdenum. Subsequently the element was
shown to be a component of two other enzymes, aldehyde oxidase and sulphite
oxidase.The biological functions of molybdenum, apart from its reactions with copper
(see p. 123), are concerned with the formation and activities of these three enzymes.
In addition to being a component of xanthine oxidase, molybdenum participates in the
reaction of the enzyme with cytochrome C and also facilitates the reduction of
cytochrome C by aldehyde oxidase.

Deficiency symptoms
In early studies with rats, low-molybdenum diets resulted in reduced levels of xan-
thine oxidase but did not affect growth or purine metabolism. Similar molybdenum-
deficient diets have been given to chicks without adverse effects, but when tungstate
(a molybdenum antagonist) was added, growth was reduced and the chick’s ability to
oxidise xanthine to uric acid was impaired. These effects were prevented by the ad-
dition of molybdenum to the diet. A significant growth response has been obtained
in young lambs by the addition of molybdate to a semi-purified diet low in the ele-
ment. It has been suggested that this growth effect could have arisen indirectly by
stimulation of cellulose breakdown by ruminal microorganisms. Molybdenum defi-
ciency has not been observed under natural conditions in any species.

Molybdenum toxicity
The toxic role of molybdenum in the condition known as ‘teart’ is described under
the section on copper (see p. 123). All cattle are susceptible to molybdenosis, with
milking cows and young animals suffering most. Sheep are less affected and horses
are not affected on teart pastures. Scouring and weight loss are the dominant mani-
festations of the toxicity.

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 Trace elements

Selenium
The nutritional importance of selenium became evident in the 1950s, when it was
shown that most myopathies in sheep and cattle, and exudative diathesis in
chicks, could be prevented by supplementing the diet with the element or vitamin
E (see p. 85). A biochemical role of selenium in the animal body was demon-
strated in 1973, when it was discovered that the element was a component of glu-
tathione peroxidase, an enzyme that catalyses the removal of hydrogen peroxide,
thereby protecting cell membranes from oxidative damage. Glutathione peroxi-
dase contains four selenium atoms and forms a second line of defence after vita-
min E, since some peroxidases remain even if vitamin E levels are adequate.
Selenium has a sparing effect on vitamin E by ensuring normal absorption of the
vitamin. This is due to its role in preserving the integrity of the pancreas and
thereby ensuring satisfactory fat digestion. Selenium also reduces the amount of
vitamin E required to maintain the integrity of lipid membranes and aids the
retention of vitamin E in plasma. Conversely, vitamin E spares selenium by main-
taining the element in its active form and preventing its loss. It reduces the pro-
duction of hydroperoxides and thus the amount of glutathione peroxidase needed
to protect cells. However, there are limits to the mutual substitution of selenium
and vitamin E.
Vitamin E and selenium have roles in the immune system and protect against
heavy metal toxicity. Other mutual functions and effects of deficiency in farm ani-
mals are discussed in the section on vitamin E (see pp. 81–86).
The other major role of selenium is in the production of the thyroid hormones
(see p. 127), for which it is a component of the enzyme type I iodothyronine deiod-
inase (ID1), which converts T4 to the physiologically active T3. When there is a defi-
ciency of selenium the ratio of T4 : T3 increases.The enzyme is found primarily in the
liver and kidney and not in the thyroid of farm animals. Type II iodothyronine deio-
dinase (ID2) does not contain selenium and also converts T4 to T3, but as it is under
feedback control from T4 an increase in the latter, when selenium is deficient, com-
pounds the problem. The major enzyme in ruminants is ID1 and in non-ruminants
ID2.A third selenium-containing enzyme, ID3, has been found in the placenta. ID1 is
particularly important in the brown adipose tissue of newborn ruminants and
releases T3 for use in other tissues.

Deficiency symptoms
As mentioned above, the effects of selenium deficiency are often similar to those
of vitamin E. In parts of Australia and New Zealand, a condition known as ‘ill
thrift’ occurs in lambs, beef cattle and dairy cows at pasture. The clinical signs in-
clude loss of weight and sometimes death. Ill thrift can be prevented by selenium
treatment with, in some instances, dramatic increases in growth and wool yield.
Similar responses with sheep have also been noted in experiments carried out in
selenium-deficient areas of Scotland, Canada and the USA. In hens, selenium defi-
ciency reduces hatchability and egg production. The reduction in use of feed wheat
from seleniferous regions of North America and Canada has reduced the plant-
based dietary supply of selenium, especially in pig and poultry diets, resulting in
greater supplementation being required than previously. Owing to its role in thy-
roid hormone production, a lack of selenium can produce the symptoms of iodine
deficiency.

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Chapter 6 Minerals

Sources of selenium
The main form of selenium in most foods is protein-bound seleno-methionine. Sup-
plements of selenium are provided by mineral salts containing sodium selenite, slow-
release capsules and selenium-enriched yeast.

Selenium toxicity
The level of selenium in foods of plant origin is extremely variable and depends mainly
on the soil conditions under which they are grown. Normal levels of the element in pas-
ture herbage are usually in the range 100–300 µg/kg DM. Some species of plants that
grow in seleniferous areas contain very high levels of selenium. One such plant,
Astragalus racemosus, grown in Wyoming, was reported to contain 14 g selenium/kg
DM, while the legume Neptunia amplexicaulis grown on a selenised soil in Queens-
land contained over 4 g/kg DM of the element. Localised seleniferous areas have also
been identified in Ireland, Israel and South Africa. Selenium is a highly toxic element
and a concentration in a dry diet of 5 mg/kg or 500 µg/kg in milk or water may be po-
tentially dangerous to farm animals. ‘Alkali disease’ and ‘blind staggers’ are localised
names for chronic diseases of animals grazing certain seleniferous areas in the USA.
Symptoms include dullness, stiffness of the joints, loss of hair from the mane or tail,
and hoof deformities.Acute poisoning, which results in death from respiratory failure,
can arise from sudden exposure to high selenium intakes.

Fluorine
The importance of fluorine in the prevention of dental caries in humans is well es-
tablished. Fluorine was added to the list of essential elements in 1972 when it was
shown that the growth rate of rats was improved after small amounts were added to
a low-fluorine diet. Under normal conditions a straightforward deficiency syndrome
in farm animals has not been observed, and even the results of studies with rodents
are equivocal.
Most plants have a limited capacity to absorb fluorine from the soil, and normal
levels in pasture herbage range from about 2 mg/kg to 20 mg/kg DM. Cereals and
other grains usually contain about 1–3 mg/kg DM only.
Fluorine is a very toxic element, with ruminants being more susceptible than non-
ruminants. Levels of more than 20 mg/kg DM in the diet of cattle have resulted in
dental pitting and wear, leading to exposed pulp cavities. Further increases in fluo-
rine cause depression of appetite, lameness and reduced production. Bone and joint
abnormalities also occur, probably owing to ingested fluorine being deposited in the
bone crystal lattice as calcium fluoride. The commonest sources of danger from this
element are fluoride-containing water, herbage contaminated by dust from industrial
pollution, and the use of soft or raw rock phosphate supplements. Processed phos-
phates are generally safe.

Silicon
Rats previously fed on specially purified foods showed increased growth rates from
the addition to the diet of 500 mg/kg of silicon (as sodium metasilicate).
Similar results have been obtained with chicks. Silicon is essential for growth and
skeletal development in these two species. The element is believed to function as a
biological cross-linking agent, possibly as an ether derivative of silicic acid of the

132
 Trace elements

type R1—O—Si—O—R2. Such bridges are important in the strength, structure and
resilience of connective tissue. In silicon-deficient rats and chicks, bone abnormali-
ties occur because of a reduction in mucopolysaccharide synthesis in the formation
of cartilage. Silicon is required for maximal activity of the enzyme prolyl hydroxy-
lase, which is involved in collagen synthesis. It is also thought to be involved in other
processes involving mucopolysaccharides such as the growth and maintenance of ar-
terial walls and the skin.
Silicon is so widely distributed in the environment and in foods that it is difficult
to foresee any deficiencies of this element arising under practical conditions. Whole
grasses and cereals may contain as much as 14–19 g Si/kg DM, with levels of up to
28 g/kg DM in some range grasses.
Silicon toxicity (silicosis) has long been known as an illness of miners caused by
the inhalation of silical particles into the lungs. Under some conditions, part of the
silicon present in urine is deposited in the kidney, bladder or urethra to form calculi
or uroliths. Silica urolithiasis occurs in grazing wethers in Western Australia and in
grazing steers in western Canada and northwestern parts of the USA. Excessive sil-
ica in feeds, for example in rice straw, is known to depress organic matter digestibil-
ity. In mature forage, silicon is in the form of solid particles, which are harder than
dental tissue and lead to teeth wear in sheep.

Chromium
Chromium was first shown to be essential for normal glucose utilisation in rats.
Mice and rats fed on diets composed of cereals and skimmed milk and containing
100 µg chromium/kg wet weight were subsequently shown to grow faster if given
a supplement of chromium acetate. Chromium appears to have a role in glucose
tolerance, possibly forming a complex between insulin and its receptors. It has re-
stored glucose tolerance in malnourished children. Chromium may also play a role
in lipid synthesis, and experiments have shown decreased serum cholesterol and
increased high-density lipoprotein cholesterol in cases of deficiency. There is also
thought to be an involvement in protein and nucleic acid metabolism. Investiga-
tions with pigs have supported the above putative roles, with increased lean and
decreased fat deposition as a result of more efficient glucose metabolism and spar-
ing of protein catabolism. Improved reproduction in sows has been reported with
supplements of organic sources of chromium. There have been positive responses
to chromium supplements where animals are under physiological stress, for exam-
ple periparturient dairy cattle and stressed feedlot calves. Immune response, en-
ergy status, dry matter intake and milk yield have been increased in primiparous
cows and morbidity has been reduced in calves. The practical significance of the
element in the nutrition of farm animals is still being investigated and no recommen-
dations for dietary levels have been made. Chromium is not a particularly toxic
element in its trivalent form, and a wide margin of safety exists between the nor-
mal amounts ingested and those likely to produce deleterious effects. The hexava-
lent form is more toxic because it enters the cells to a greater extent and suppresses
oxygen consumption and damages DNA. Levels of 50 mg chromium/kg DM in the
diet have caused growth depression and liver and kidney damage in rats.
Chromium in the form of its insoluble oxide is often used as a marker in digestibil-
ity trials (see p. 241).

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Chapter 6 Minerals

Vanadium
No specific biochemical function has been identified for vanadium, but it may have
a role in the regulation of the activity of sodium–potassium ATPase, phosphoryl
transferase enzymes, adenyl cyclase and protein kinase. It may also act as a cofactor
for certain enzymes. Vanadium deficiency has been demonstrated in rats, goats and
chicks. Deficiency symptoms included impaired growth and reproduction, and dis-
turbed lipid metabolism. In chicks consuming diets containing less than 10 µg
vanadium/kg DM, growth of wing and tail feathers was significantly reduced. Subse-
quent studies with chicks demonstrated a significant growth response when dietary
vanadium concentrations were increased from 30 µg to 3 mg/kg DM. In goats fed on
diets containing less than 10 µg vanadium/kg there was no effect on growth, but
there was increased incidence of abortion, reduced milk fat production and a high
death rate in the kids.
There is little information about the vanadium content of foods, but levels in the
range 30–110 µg/kg DM have been reported for ryegrass. Herring meal appears to
be a relatively rich source, containing about 2.7 mg/kg DM.Vanadium is a relatively
toxic element. When diets containing 30 mg/kg DM of the element were given to
chicks, the growth rate was depressed; at levels of 200 mg/kg DM, the mortality rate
was high.

Nickel
A discrete biochemical function has not been firmly established for nickel, but it is
thought that it may be a cofactor or structural component in metalloenzymes. It may
also play a role in nucleic acid metabolism.
Physiological symptoms of nickel deficiency have been produced in chicks, rats
and pigs kept under laboratory conditions. Chicks given a diet containing nickel in a
concentration of less than 400 µg/kg DM developed skin pigmentation changes, der-
matitis and swollen hocks. Diets with a low nickel content have produced scaly and
crusty skin in pigs, similar to the parakeratosis seen in zinc deficiency, which suggests
an involvement in zinc metabolism. Supplements of nickel have increased rumen
bacterial urease activity.
Normal levels of the element in pasture herbage are 0.5–3.5 mg/kg DM, while
wheat grain contains 0.3–0.6 mg/kg DM. Nickel is a relatively non-toxic element, is
poorly absorbed from the digestive tract and does not normally present a serious
health hazard.

Tin
In 1971 it was reported that a significant growth effect, in rats maintained on puri-
fied amino acid diets in a trace-element-free environment, was obtained when
the diets were supplemented with tin. These studies suggested that tin was an es-
sential trace element for mammals. The element is normally present in foods in
amounts less than 1 mg/kg DM, the values in pasture herbage grown in Scotland,
for example, being of the order of 300–400 µg/kg DM. The nutritional importance
of this element has yet to be determined, but it is suggested that tin contributes to
the tertiary structure of protein or other macromolecules. Tin is poorly absorbed

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 Other elements

BOX 6.4 Enhanced trace element supplementation and health status and fertility
in dairy cows
Several authors have reported that when dairy cows were given dietary supplements of certain trace
elements, above the levels necessary for production, their health status (incidence of mastitis) and
fertility were improved. In a review, Cottrill and Rymer (see Further reading) concluded that for
iodine and manganese there is no evidence that feeding levels above requirements have any bene-
fits. In some studies, raised levels of copper improved fertility and udder health, but results were in-
consistent and no recommendation could be made with respect to the appropriate level of
supplementation. The authors also pointed out the complexity surrounding copper absorption
(molybdenum, sulphur and iron – see p. 123) and the potential cumulative toxicity of copper. In the
case of chromium, there were potential benefits but again there was insufficient evidence to make
recommendations. Udder health has been improved by increased levels of selenium, but the vitamin
E status influences the effect. Again with zinc, the effects on somatic cell counts and mastitis have
been too inconsistent to recommend giving zinc above requirements.
This is an area of continuing research, especially with the use of ‘organic’ mineral supplements
(see p. 107).

from the digestive tract, especially in the inorganic form, and ingested tin has a
low toxicity.

Arsenic
Arsenic is widely distributed throughout the tissues and fluids of the body but is
concentrated particularly in the skin, nails and hair. It has been shown that the
element is essential for the rat, chick, pig and goat. It is needed to form metabolites
of methionine, including cystine. Animals given an arsenic-deficient diet had rough
coats and slower growth rates than control animals given a supplement of arsenic.
A long-term study with goats showed interference with reproduction (abortion,
low birth weights) and milk production, and sudden death. The toxicity of the
element is well known; symptoms include nausea, vomiting, diarrhoea and severe
abdominal pain. The toxicity of its compounds differs widely; trivalent arsenicals,
which block lipoate-dependent enzymes, are more toxic than the pentavalent
compounds.

- 6.6 OTHER ELEMENTS

The essentiality of other elements, listed by some authorities, is the subject of de-
bate. Often the levels required to produce a deficiency are so low as to be of no prac-
tical significance in normal animal nutrition. For example, boron, which is essential
to plants, has been shown to increase growth rate and tibia weight and strength in
broilers, but the response was obtained at levels found only in boron-deficient
plants. Lithium has been shown to be essential for goats, where it prevented growth
retardation, impaired fertility and low birth weights, but again deficiency is unlikely
under practical conditions.

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Chapter 6 Minerals

SUMMARY
Minerals fulfil physiological, structural and regulatory functions. Mineral supplements take various
forms: mineral salts, rumen boluses, ‘organic’ compounds and pasture applications. The roles of
individual mineral elements, and the effects of their deficiencies, are summarised below:

Mineral element Role Effects of deficiency

Calcium Bone and teeth, transmission Rickets, osteomalacia, thin eggshells,

of nerve impulses milk fever
Phosphorus Bone and teeth, energy metabolism Rickets, osteomalacia, depraved
appetite, poor fertility
Potassium Osmoregulation, acid–base balance, Retarded growth, weakness
nerve and muscle excitation
Sodium Acid–base balance, osmoregulation Dehydration, poor growth, poor
egg production
Chlorine Acid–base balance, osmoregulation, Alkalosis
gastric secretion
Sulphur Structure of amino acids, vitamins Equivalent to protein deficiency
and hormones, chondroitin (urea-supplemented diets)
Magnesium Bone, activator of enzymes for Nervous irritability and convulsions,
carbohydrate and lipid metabolism hypomagnesaemia
Iron Haemoglobin, enzymes of electron Anaemia
transport chain
Copper Haemoglobin synthesis, enzyme Anaemia, poor growth, depigmentation
systems, pigments of hair and wool, swayback
Cobalt Component of vitamin B12 Pining (emaciation, anaemia,
listlessness)
Iodine Thyroid hormones Goitre; hairless, weak or dead young
Manganese Enzyme activation Retarded growth, skeletal
abnormality, ataxia
Zinc Enzyme component and activator Parakeratosis, poor growth,
depressed appetite
Selenium Component of glutathione peroxidase, Myopathy, exudative diathesis
iodine metabolism, immune function

FURTHER READING
Agricultural and Food Research Council 1991 Technical Committee on Responses to Nutri-
ents, Report no. 6. A reappraisal of the calcium and phosphorus requirements of sheep and
cattle. Nutrition Abstracts and Reviews, Series B 61: 573–612.
Ammerman C B, Henry P R and Miles R D 1998 Supplemental organically-bound mineral
compounds in livestock nutrition. In: Garnsworthy P C and Wiseman J (eds) Recent
Advances in Animal Nutrition, Nottingham, Nottingham University Press, 67–91.
Cottrill B and Rymer C 2001 The Effect of Enhanced Supplementation of Trace Elements on
the Health and Performance of Dairy Cows and on the Composition of Their Milk: A
Report to the Milk Development Council, project no. 99/T2/27, Cirencester, Milk
Development Council.

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 Further reading

Ewing W N and Charlton S J 2005 The Minerals Directory, Packington, Context Publications.
McDowell L R 1992 Minerals in Animal and Human Nutrition, New York, Academic Press.
National Research Council 1980 Mineral Tolerances of Domestic Animals, Washington, DC,
National Academy of Sciences.
Thompson J K and Fowler V R 1990 The evaluation of minerals in the diets of farm animals. In:
Wiseman J and Cole D J A (eds) Feedstuff Evaluation, London, Butterworth, 235–59.
Underwood E J and Suttle N F 1999 The Mineral Nutrition of Livestock, 3rd edn,Wallingford,
CABI.

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