# Copper : Copper A short course



## Sondra (Oct 25, 2007)

Copper
A short course designed by Murdoch University and The University of Sydney. 
Sponsored by Grant 1034/25 from the Committee for the Advancement of University Teaching 
(CAUT)1995.

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What is copper? 
Does it have another name? 
Do animals need copper? 
What happens if an animal gets too little copper? 
What happens if an animal gets too much copper? 
How much is enough? 
How does copper get into and around the body?

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What is copper?

Copper (Cu) is an essential element required by ruminants and deficiencies of the element occur in grazing animals in many parts of the world under a wide range of soil and climatic conditions. It should be noted that Cu, Mo and S are closely related in ruminant nutrition, And the status of the animal with respect to Cu cannot be described without reference to the other two. Mo deficiency has not been observed in animals under practical conditions, whereas Cu deficiency and toxicity is a serious problem in ruminants.

The interaction between Cu and Mo became evident when it was discovered in the 1930s that a scouring disease of cattle was caused by excess intake of Mo, and that it could be prevented by massive amounts of Cu.

Meanwhile, Cu toxicity was identified as an area problem on the east coast of Australia, and Dick in the 1950s showed this was associated with low Mo in pastures. He demonstrated that a combination of Mo salts and inorganic S would prevent the increase in Cu absorption, thus demonstrating for the first time the interactions between Cu, Mo and S.

Does it have another name? 
The trace elements copper, zinc, manganese, selenium ( and iron), as well as glutathione and sulphur amino acids are ANTIOXIDANT NUTRIENTS. Copper and zinc, and manganese are part of the METALLOENZYMES.

There are at least 10 metalloenzymes that contain Cu.. The main enzymes are:

Cytochrome oxidase 
Ceruloplasmin (Ferroxidase) 
Lysyl oxidase (amine oxidase) 
Cu-Zn superoxide dismutase 
Tyrosinase
Do animals need copper? 
Yes. The possible functions of Cu for the maintenance of ruminant health are listed below (table 1.1), together with the main enzyme involved.

Table 1.1 The functions of Cu and the associated enzymic links

Cu-Enzyme Function 
Cytochrome oxidase energy metabolism 
Ceruloplasmin iron transport 
Lysyl oxidase connective tissue 
Cu-Zn SOD anitoxidant 
Tyrosine melanin

What happens if an animal gets too little copper?

The practical problem of deficiency of Cu is almost entirely confined to the ruminant. Cu deficiency occurs naturally in grazing livestock in many parts of the world under a range of soil and climatic conditions. Some of this is due simply to low levels of Cu in soil and hence in herbage ( < 3 ppm DM), such as in parts of WA. However, much is conditioned deficiency, due for example to calcareous soils, excessive soil (Fe) intakes or to high levels of pasture Mo in the presence of normal concentrations of S. High levels of available Fe ingestion due to feed contaminated with soil (800 ppm) can markedly reduce the concentration of Cu in liver and cause deficiency. However, different soils have different effects, and there is no general effect for all soil types. Normally 4-6 ppm Cu in the diet is sufficient for grazing sheep and cattle in the absence of other antagonists. Under circumstances where interacting substances reduce Cu availability, 10 ppm Cu in the herbage may not be adequate. 
Table 1.2 Symptoms of Cu deficiency
Symptoms Species 
Depigmentation of hair and wool (achromotrichia) All species except pigs 
Defective keratinisation of hair and wool Sheep 
Scouring or diarrhoea of cattle Cattle/Goats 
Neonatal ataxia (swayback) Kids/Lambs 
Poor growth and anorexia All species 
Anaemia All species 
Bone disorders (osteoporosis). All species Not severe in sheep/cattle 
Cardiac disease Calves 
Aortic rupture Pigs/Chicks 
Infertility Cattle/Hens

What happens if an animal gets too much copper? 
Ruminants are the most susceptible to copper toxicosis because in these species Cu accumulates readily in the liver. In monogastrics the excess Cu is quickly excreted in urine and does not build up in liver until massive doses are administered. Sheep are the species mainly affected, Toxicosis occurring mainly as a result of: 
Excessive Cu fertiliser use in the presence of low pasture Mo and S 
Overdosing from drenches, Cu oxide needles and injections 
Cu-containing licks or blocks without adequate Mo 
Hepatotoxins such as lupinosis and heliotrope poisoning. 
How much is enough? 
Liver Cu concentration is currently the best indicator of a likely Cu deficiency in ruminants. Low plasma Cu concentration will reflect a simple Cu deficiency, but not one conditioned by high Mo.This is explained further in table 1.3. 
Table 1.3. Diagnosis of liver Cu concentration in sheep (from Dept of Agric, WA)
Liver Cu 
(ppm fresh wt) Interpretation 
<4 Death of adults, ataxia in lambs, 
loss of crimp in wool, illthrift. 
8-16 Occasional loss of wool quality. 
Some risk of ataxia in lambs. 
16-32 Marginal status. 
Could lead to Cu deficiency. 
32-300 Normal

In cattle, liver Cu of < 3 ppm and plasma Cu of < 0.5 ppm are indicative of Cu deficiency.

How does copper get into and around the body? 
Adult sheep absorb only 5 to 10% of dietary Cu, while young preruminant animals absorb over 70%. Cu is absorbed in the small intestine from which it is transported in plasma bound to albumin and amino acids. The liver is the main storage organ. It is also the site for ceruloplasmin synthesis and provides the major pathway of Cu excretion via the bile.

Absorption of Cu from the GI tract is influenced largely by the concentration of Mo and S in the diet. Other elements such as Zn, Fe, Cd, as well as phytate and ascorbate can also decrease Cu availability. Fe is thought to interfere by competing for sites on carrier proteins. Cd and Zn are thought to interfere by stimulating the synthesis of a Cubinding protein in the intestinal mucosa. The half life of this protein, called metallothionein, is about the same as an intestinal cell and so Cu is bound up in the intestinal mucosa and prevented from being transported into the blood.

The interaction between Cu, Mo and S is of particular importance in the ruminant. The mechanism was first postulated by Dick and others in 1975. They showed that Mo reacted with sulphide in the rumen to form a thiomolybdate complex which in turn reacted with Cu to reduce its availability for absorption. This interaction depends upon the involvement of rumen microorganisms and thus does not function in monogastrics. The reaction for the forrnation of mono, di, tri and tetrathiomolybdate is shown below.

MoO4 + S > MoO3S'> MoO2S2'> MoOS3=> MoS4' (tetrathiomolybdate)

Sulphide is produced by rumen microbes and this reacts with inorganic molybdate to form the range of thiomolybdate compounds shown. Thiomolybdates form complexes with Cu + + in the rumen and GI tract that render Cu unavailable for absorption. Unattached thiomolybdate is absorbed and reacts with Cu in tissues and interferes with the activity of Cumetalloenzymes. Initially, systemic thiomolybdate will cause elevated plasma total Cu concentrations as plasma transport mechanisms malfunction and Cu is leached from liver into the plasma. Ultimately, however, systemic thiomolybdate will lead to depletion of Cu from tissue stores and reduced plasma Cu. Because of these effects, total plasma Cu is an unreliable indicator of Cu status of ruminants where high pasture Mo is implicated. The test for the involvement of thiomolybdates is to analyse for the ratio of TCAbound to unbound plasma Cu. If Mo is not involved, all the plasma Cu will exist as TCAfree Cu (i.e. the Cu does not precipitate when plasma is treated with the protein coagulant TCA).

Dr Nick Costa, Senior Lecturer, Biochemistry and Nutrition, School of Veterinary Studies, Murdoch University. mailto:[email protected] 4 July 1996


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