num and sulfur. The antagonistic action of molybdenum on copper metabolism is exacerbated when sulfur is also high. Considerable evidence suggests that molybdate and sulfide interact to form thiomolybdates in the rumen (Suttle, 1991). Copper is believed to react with thiomolybdates in the rumen to form insoluble complexes that are poorly absorbed. Some thiomolybdates are absorbed and affect systemic metabolism of copper (Gooneratne et al., 1989). Thiomolybdates can result in copper being tightly bound to plasma albumin and not available for biochemical functions, and they may directly inhibit certain copper-dependent enzymes. In cattle grazing pastures containing 3 to 20 mg Mo/kg, copper concentrations in the range of 7 to 14 mg/kg were inadequate (Thornton et al., 1972).

FACTORS AFFECTING COPPER REQUIREMENTS

Sulfur reduces copper absorption, perhaps via formation of copper sulfide in the gut, independent from its role in the molybdenum-copper interaction (Suttle, 1974). Reducing the sulfate content of drinking water high in sulfate from 500 to 42 mg/L by reverse osmosis increased the copper status of cattle (Smart et al., 1986). A copper concentration of 10 mg/kg was not adequate in cows receiving sulfated water, which resulted in total dietary sulfur of 0.35 percent (Smart et al., 1986). High concentrations of iron (Phillippo et al., 1987a) and zinc (Davis and Mertz, 1987) also reduce copper status and may increase copper requirements.

SIGNS OF COPPER DEFICIENCY

Copper deficiency is a widespread problem in many areas of the United States and Canada. Signs that have been attributed to copper deficiency include

  • anemia,

  • reduced growth,

  • depigmentation and changes in the growth and physical appearance of hair,

  • cardiac failure,

  • bones that are fragile and easily fractured,

  • diarrhea, and

  • low reproduction characterized by delayed or depressed estrus (Underwood, 1981).

Achromotrichia or lack of hair pigmentation is generally the earliest clinical sign of copper deficiency. Copper deficiency also reduces the ability of isolated neutrophils to kill yeast (Boyne and Arthur, 1981); and copper deficiency in grazing lambs increased susceptibility to bacterial infections (Woolliams et al., 1986). As discussed in the molybdenum section, some of the abnormalities that have been attributed to copper deficiency may be caused by molybdenosis rather than copper per se.

Copper is poorly absorbed in ruminants with a developed rumen. Absorbed copper is excreted primarily via the bile with small amounts lost in the urine (Gooneratne et al., 1989). Considerable storage of copper can occur in the liver.

COPPER SOURCES

Forage copper concentrations are of limited value in assessing copper adequacy unless forage concentrations of copper antagonists such as molybdenum, sulfur, and iron are also considered. Liver copper concentrations less than 20 mg/kg on a dry matter basis or plasma concentrations less than 50 µg/dL are indicative of deficiency (Underwood, 1981). However, in the presence of high dietary molybdenum and sulfur, copper in liver and plasma may not accurately reflect copper status because the copper can exist in tightly bound forms unavailable for biochemical functions (Suttle, 1991). Forages vary greatly in copper content depending on plant species and available copper in the soil (Minson, 1990). Legumes are usually higher in copper than grasses. Milk and milk products are low in copper. Cereal grains generally contain 4 to 8 mg Cu/kg, and oilseed meals and leguminous seeds contain 15 to 30 mg Cu/kg.

Copper is usually supplemented to diets or ad libitum minerals in the sulfate, carbonate, or oxide forms. Recent studies indicate that copper oxide is very poorly available relative to copper sulfate (Langlands et al., 1989a; Kegley and Spears, 1994). In early studies, copper carbonate was at least equal to copper sulfate (Chapman and Bell, 1963). Various organic forms of copper also are available. In calves fed diets high in molybdenum, copper proteinate was more available than copper sulfate (Kincaid et al., 1986). However, Wittenberg et al. (1990) found similar availability of copper from copper proteinate and copper sulfate in steers fed high-molybdenum diets. Studies comparing copper lysine to copper sulfate have yielded inconsistent results. Ward et al. (1993) reported that copper lysine and copper sulfate were of similar bioavailability when fed to cattle; however, Nockels et al. (1993) found that copper lysine was more avaiable than copper sulfate.

Injectable forms of copper such as copper glycinate or copper EDTA have been given at 3- to 6-month intervals to prevent copper deficiency (Underwood, 1981). Although feed-grade copper oxide is largely unavailable, copper oxide needles, which remain in the gastrointestinal tract and slowly release copper over a period of months, have been used as a copper source for cattle (Cameron et al., 1989).

SIGNS OF COPPER TOXICITY

Copper toxicity can occur in cattle as a result of excessive supplementation of copper or the use of feeds that have



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