Effective Copper Nutrition for Farm Animals
by Larry L. Berger, Ph.D.
Professor, Animal Sciences
University of Illinois
With copper more than any other nutrient, factors such as specie, source, mineral interactions and stress can affect farm animal's copper requirements. Recent research has shown that these factors can interact to increase the complexity of the copper nutrition story. This article examines each of these factors so that nutritionists, veterinarians and livestock producers can evaluate more accurately their copper supplementation program.
While copper compounds were used for medicinal purposes as early as 400 BC, it was not until the 1920's that copper was first recognized as an essential nutrient for animals. Today, copper deficiency is known to cause anemia, diarrhea, bone disorders, neonatal ataxia, changes in hair and wool pigmentation, infertility, cardiovascular disorders, impaired glucose and lipid metabolism and a depressed immune system (Davis and Mertz, 1987). Copper is a key component of many enzyme systems which when impaired can directly or indirectly cause many of the symptoms of copper deficiency.
Because many of the copper deficiency symptoms are general in nature, a clear diagnostic tool that accurately reflects the copper status of the animal is needed. Although serum and plasma copper concentrations are often measured, blood levels may not show the deficiency until severe symptoms develop (Hemken et al. 1993). Liver copper concentration is probably the most sensitive indicator of changes in copper status and its determination is recommended when liver biopsies can be obtained. Ceruloplasmin concentrations and superoxide dismutase activity in the blood or red blood cells can be useful indicators of copper status.
Dietary copper requirements vary greatly among species. The recommended levels for one specie may cause toxicity in another. For example, 10 ppm is the NRC recommended level for dairy cattle but under certain conditions 10 ppm can cause toxicity in sheep (Church and Pond 1988). By comparison, growing pigs are often fed 100 to 250 ppm of copper in the diet to improve growth. According to the National Reserch Council, poultry require approximately 8 ppm copper.
Sheep are unique in that they accumulate copper in the liver more readily than other farm animals. Over a period of time, 1,000 - 3,000 ppm copper on a dry basis may be achieved. Usually there are no clinical signs until there is a sudden release of copper into the blood. Plasma copper levels then increase 10 to 20 fold. These elevated blood copper concentrations (500-2000 mg/dl) usually precede clinical signs by 24 to 48 hours (Kimberling 1988). The most common symptoms are anorexia, excessive thirst and depression. Most sheep will die within 2 to 4 days after blood concentrations sky rocket.
Because of the variation in recommended copper concentrations, it is difficult to have one copper level in a trace mineralized salt for all species. One alternative is to have a low-copper product for sheep and a high-copper product for the other species. This would insure that all species would receive an appropriate amount of copper without the risk of copper toxicity in sheep. Those swine producers feeding copper as a growth promotant will continue to supplement copper in addition to that in the trace mineralized salt.
Knowing the copper concentration in a diet without knowing the source of supplemental copper is of little nutritional value. Absorption of copper can vary from zero to as high as 75% (Linder, 1991) depending on a number of factors. Copper availability in most feedstuffs fed to farm animals is between 1% and 15% (Hemken et al. 1993). Grains are lower in copper than are forages. Most forages will contain copper at levels equal to or above the NRC requirement for ruminants. However, as plants mature and the phytate and lignin content increases, bioavailability of the copper decreases rapidly.
Copper oxide and copper sulfate have been the two predominant sources of supplemental copper used in animal feeds. In the last ten years there has been considerable research comparing the bioavailability of these and other copper sources in the different species. In 1987 Ledoux et al. compared the biological availability of reagent grade copper acetate, and feed grade copper oxide, copper carbonate and copper sulfate by feeding each copper source at 0, 150, 300, and 450 ppm to broiler chicks in a corn-soy diet. Liver copper levels were used as the indicator of absorption. Using the slope-ratio technique with acetate set at 100%, the relative biological availability values were -5, 107, and 60% for the oxide, sulfate and carbonate forms, respectively.
Cromwell et al. (1989) conducted a study to determine the effects of feeding weanling pigs 0, 125, 250, and 500 ppm supplemental copper from copper oxide or copper sulfate on rate and efficiency of gain and liver copper stores. Feeding 125 or 250 ppm copper from copper sulfate increased (P<0.01) rate and efficiency of gain and liver copper levels. All dietary levels of copper oxide failed to influence performance or liver copper levels.
One criticism of the previous studies has been that feeding very high levels of copper may give a lower biological availability for copper oxide than if it were fed closer to the dietary requirement. To answer this question Clark et al. (1993b) compared adding 15 ppm copper from copper oxide or copper sulfate on the copper status of yearling Holstein cattle. Copper availability was compared by determining the liver and blood copper levels after 30, 60 and 90 days on the two copper sources. Liver copper concentrations for cattle fed copper sulfate were higher (P<0.01) than for cattle fed copper oxide or unsupplemented cattle at day 60 (196, 87, and 93 ppm) and at day 90 (268, 142 and 90 ppm, respectively). Blood copper levels were found to be a poor indicator of copper status. Copper oxide was shown to have low bioavailability and to be better than no copper supplementation only after 90 days on the deficient diet. These data are interpreted to show that the bioavailability of copper oxide is much below copper sulfate, even when fed at levels near the NRC requirement.
Several other recent studies have shown copper sulfate to be superior to copper oxide because of differences in bioavailability. Baker et al. (1991) compared cuprous oxide (Cu2O) to copper sulfate and found them to have similar bioavailabilities. Copper carbonate is considered to have intermediate availability. Copper metal is totally unavailable.
If copper nutrition was as simple as determining the copper in the basal diet and adding a highly available copper source, copper deficiency would not be a problem. However, because copper absorption and metabolism can be affected by molybdenum, sulfur, calcium, zinc, iron, manganese, cobalt, lead, cadmium, and selenium, deciding how much supplemental copper is required is not always straightforward.
For example, in sheep, dietary molybdenum levels can be the primary factor affecting copper requirements. If molybdenum levels are low (<1 ppm), sheep are more susceptible to copper toxicity. However, if molybdenum intakes exceed 10 ppm, copper deficiency may occur on diets that would normally be adequate. This has been a significant problem in sheep grazing pastures low in copper but high in molybdenum and sulfur. Newborn lambs from ewes on these pastures often exhibit neonatal ataxia and have a low survival rate.
The formation of totally unavailable thiomolybdates from the complexing of molybdenum, copper and sulfur is the reason that copper status is easily affected by molybdenum and sulfur levels. Thiomolybdate is formed in the rumen because sulfate is converted to sulfide, which is a key intermediate in forming thiomolybdate. Sulfates are stable in the monogastric stomach and so this does not occur in monogastric animals. High sulfur in combination with normal or low molybdenum concentrations can still reduce copper bioavailability by the formation of copper sulfide in the rumen. Copper sulfide is also poorly absorbed. If high sulfur is a problem, adding copper carbonate may be recommended over copper sulfate to avoid adding more sulfur to the diet.
Recent research suggests that organic-sulfur compounds may also affect copper absorption. Linder (1991) reported that feeding the sulfur amino acids methionine and homocysteine inhibited copper absorption in the rat. With the increasing use of synthetic amino acids in the swine and poultry diets copper absorption could be depressed.
In monogastrics, high levels of zinc, calcium, and iron can reduce copper absorption. Zinc has been shown to inhibit copper absorption by displacing copper from a copper-binding protein in the intestinal mucosa of the chick (Church and Pond, 1988). High calcium reduces copper absorption by increasing the pH of the intestinal contents. Iron in the form of ferrous sulfide reduces copper absorption by forming insoluble copper sulfide.
Typically nutrient requirements are determined in environments where disease and other stressors are minimized. As animal production intensifies, the requirement for nutrients involved in combating stress may also increase. For example, Orr et al. (1990) showed that blood copper levels decreased and urinary copper excretion increased as morbidity increased in calves infected with the infectious bovine rhinotracheitis (IBR) virus. With chronic disease, liver copper stores may become depleted resulting in increased susceptibility to secondary infections.
Xin et al. (1991) showed that immune function in cattle was impaired even though there was no evidence of anemia or depression in growth. Cattle that were marginally deficient in copper had reduced superoxide dismutase activity and decreased neutrophil bacteriocidal capability. These animals were less efficient at killing Staphylococcus aureus, an organism which often causes mastitis in cattle. This could explain the observation that dairy herds which are marginal in their copper status often seem to have a higher incidence of mastitis.
The stress associated with fetal development and calving may also increase the copper requirement. Recent Kentucky research showed that dairy cows had significantly lower liver copper stores at calving than at later stages of lactation (Waterman et al. 1991). Hemken et al. (1993) reported that at least 15 ppm copper in the diet is required to replenish the mothers' liver stores because the fetal liver was taking up the copper more rapidly than the mother. These data suggest that the 10 ppm copper requirement prescribed by NRC may not be adequate during late gestation when there is rapid fetal development.
Summary and Conclusions
Although there is an abundance of scientific data to show that specie, copper source, mineral interactions and stress can affect copper nutrition, do these factors actually affect production efficiency under practical conditions? The answer is "yes" as illustrated by the following scenario.
Clark et al. (1993a) reported on a field study with beef cattle that demonstrated a copper deficiency while the cattle were being supplemented with copper oxide. The deficiency symptoms observed the previous year included low fertility, diarrhea and some loss of hair pigment. Blood samples were taken and copper deficiency confirmed by the fact that plasma copper levels were 0.3-0.5 ppm. The herd was then divide into three groups of 40 to 60 cows each and supplemented with copper oxide, copper sulfate or copper proteinate. All three supplements contained 0.04% copper. After 28 days, liver copper levels were 34.3, 56.8 and 79.3 ppm for cows fed the copper oxide, copper sulfate and copper proteinate supplements respectively. Conception rates were increased to 85% for cows on copper oxide and to 94% and 90%, respectively for cows fed copper sulfate and copper proteinate. The 9 percent unit increase in conception rate (85% vs 94%) could easily result in a 100-fold return on the increased cost of supplementing with copper sulfate compared to copper oxide.
Feeding the appropriate level of a trace mineralized salt containing a highly available copper source is one of the best nutritional investments a producer can make.
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© Salt Institute, 1993