copper deficiency, depending on the length of time the cattle are exposed and the concentration of dietary copper. Recent studies suggest that a relatively low concentration of molybdenum may exert direct effects on certain metabolic processes independent of alterations in copper status. The addition of 5 mg Mo/kg to diets containing 0.1 mg Mo/kg caused copper depletion associated with reduced growth and feed efficiency, loss of hair pigmentation, changes in hair texture, and infertility in heifers (Bremner et al., 1987; Phillippo et al., 1987a,b). In these same studies, cattle fed high dietary iron had similar copper status—based on plasma copper, liver copper, and ceruloplasmin and superoxide dismutase activity—to heifers fed molybdenum but did not show clinical signs of copper deficiency. Supplementation with 5 mg Mo/kg starting at 13 to 19 weeks of age increased age at puberty and decreased liveweight of heifers at puberty and reduced conception rate (Phillippo et al., 1987b). Feeding beef cows and their calves an additional 5 mg Mo/kg reduced calf gains from birth to weaning by 28 percent, whereas calf gains were not affected by the addition of 500 mg Fe/kg (Gengelbach et al., 1994).
Forages vary greatly in molybdenum concentration depending on soil type and soil pH. Neutral or alkaline soils coupled with high moisture and organic matter favor molybdenum uptake by forages (McDowell, 1992). Cereal grains and protein supplements are less variable in molybdenum than forages.
Nickel deficiency has been produced experimentally in a number of animals (Nielson, 1987). However, the function of nickel in mammalian metabolism is unknown. Nickel is an essential component of urease in ureolytic bacteria (Spears, 1984). Supplementation of nickel to ruminant diets has increased ruminal urease activity in a number of studies (Spears, 1984; Oscar and Spears, 1988).
Research data are not sufficient to determine nickel requirements of beef cattle. The maximum tolerable concentration of nickel was estimated to be 50 mg/kg diet (National Research Council, 1980). Growing steers fed diets supplemented with 50 mg Ni/kg in the chloride form for 84 days showed no adverse effects (Oscar and Spears, 1988).
In 1973, glutathione peroxidase was identified as the first known selenium metalloenzyme (Rotruck et al., 1973). Glutathione peroxidase catalyzes the reduction of hydrogen peroxide and lipid hydroperoxides, thus preventing oxidative damage to body tissues (Hoekstra, 1974). Recently, a second selenometalloenzyme, iodothyronine 5'-deiodinase, was identified (Arthur et al., 1990). This enzyme catalyzes the deiodination of thyroxine (T4) to the more metabolically active triiodothyronine (T3) in tissues.
Based on available research data, the selenium requirement of beef cattle can be met by 0.1 mg Se/kg. Clinical or subclinical signs of selenium deficiency have been reported in beef cows and calves receiving forages containing 0.02 to 0.05 mg Se/kg (Morris et al., 1984; Hidiroglou et al., 1985; Spears et al., 1986); however, calves housed in confinement have been fed semipurified diets containing 0.02 to 0.03 mg Se/kg for months without showing clinical signs of deficiency, despite very low activities of glutathione peroxidase (Boyne and Arthur, 1981; Siddons and Mills, 1981; Reffett et al., 1988). Even in the absence of clinical deficiency signs, calves have reduced neutrophil activity (Boyne and Arthur, 1981) and humoral immune response (Reffett et al., 1988).
Factors that affect selenium requirements are not well defined. The function of vitamin E and selenium are interrelated, and a diet low in vitamin E may increase the amount of selenium needed to prevent certain abnormalities such as nutritional muscular dystrophy (white muscle disease) (Miller et al., 1988). High dietary sulfur has resulted in an increased incidence of white muscle disease in some but not all studies (Miller et al., 1988). In sheep, the occurrence of white muscle disease is higher when legume hay rather than nonlegume hay is consumed, even when selenium contents are similar (Whanger et al., 1972). Harrison and Conrad (1984) reported that selenium absorption in dairy cows was minimal at low (0.4 percent) and high (1.4 percent) calcium intakes and maximal when dietary calcium was 0.8 percent. In young calves, varying dietary calcium from 0.17 to 2.35 percent did not significantly affect selenium absorption (Alfaro et al., 1987). High concentrations of unsaturated fatty acids in the diet or various stressors (environmental or dietary) also may increase the requirement for selenium. Form of selenium may affect dietary requirements. Selenium is generally supplemented in animal diets as sodium selenite, while selenomethionine is the predominant form of selenium in most feedstuffs. Selenium from selenomethionine or a selenium-containing yeast was approximately twice as available as sodium selenite or cobalt selenite in growing heifers (Pehrson et al., 1989). Availability of selenium from sodium selenate was similar to sodium selenite (Podoll et al., 1992).
Selenium is absorbed primarily from the duodenum with