little or no absorption from the rumen or abomasum. Absorption of selenium in ruminants is much lower than in nonruminants (Wright and Bell, 1966). The lower absorption of selenium is believed to relate to the reduction of selenite to insoluble forms in the rumen. Fecal excretion is greater than urinary excretion in mature ruminants. Pulmonary excretion of selenium is important when intakes of selenium are high (Ganther et al., 1966).
White muscle disease in young ruminants is a common clinical sign of selenium deficiency that results in degeneration and necrosis in both skeletal and cardiac muscle (Underwood, 1981). Affected animals may show stiffness, lameness, or even cardiac failure. Other signs of selenium deficiency that have been observed include unthriftiness (often times with weight loss and diarrhea; Underwood, 1981), anemia with presence of heinz bodies (Morris et al., 1984), and increased mortality and reduced calf weaning weights (Spears et al., 1986). Selenium-depleted cattle have shown reduced immune responses in a number of studies (Stabel and Spears, 1993). Arthur et al. (1988) reported that selenium-deficient cattle had increased T4 and decreased T3 concentrations in plasma relative to selenium-supplemented cattle. Depressed activity of iodothyronine 5'-deiodinase may explain the unthriftiness and poor growth often observed in selenium deficiency. Decreases in glutathione peroxidase activity associated with selenium deficiency can explain the occurrence of white muscle disease, heinz body anemia, and possibly other signs of selenium deficiency.
Selenium concentrations in plasma, serum, and whole blood, and glutathione peroxidase activities in plasma, whole blood, and erythrocytes, have been used to assess selenium status. Glutathione peroxidase activities indicative of a selenium deficiency can vary from one laboratory to another depending on assay conditions. Langlands et al. (1989b) concluded from a number of on-farm studies with cattle in Australia that selenium concentrations in whole blood and plasma were poor indicators of responsiveness to selenium supplementation unless unthriftiness was apparent.
Feedstuffs grown in many areas of the United States and Canada are deficient or at least marginally deficient in selenium. Selenium-deficient areas are located in the northwestern, northeastern, and southeastern parts of the United States. The selenium content of forages and other feedstuffs varies greatly depending on plant species and particularly the selenium content of the soil. Selenium can legally be supplemented in beef cattle diets to provide 3 mg/head/day or 0.3 mg/kg in the complete diet. Alternate methods of supplementing selenium include injecting selenium every 3 to 4 months or at critical production stages and using boluses retained in the rumen that release selenium over a period of months (Hidiroglou et al., 1985; Campbell et al., 1990).
Selenium toxicity may occur as a result of excessive selenium supplementation or consumption of plants naturally high in selenium. Many plant species of Astragalus and Stanleya grow primarily on seleniferous areas and can accumulate up to 3,000 mg Se/kg. Consumption of forages containing 5 to 40 mg Se/kg results in chronic toxicosis (alkali disease). Chronic toxicity signs include lameness, anorexia, emaciation, loss of vitality, sore feet, cracked, deformed and elongated hoofs, liver cirrhosis, nephritis, and loss of hair from the tail (Rosenfeld and Beath, 1964). Acute selenium toxicity (blind staggers) causes labored breathing, diarrhea, ataxia, abnormal posture, and death from respiratory failure (National Research Council, 1980). The maximum tolerable concentration of selenium has been estimated to be 2 mg/kg (National Research Council, 1980). The addition of 10 mg Se/kg to a milk replacer for 42 days reduced gain and efficiency in young calves, but supplemented selenium at 5 mg/kg caused no noticeable effects (Jenkins and Hidiroglou, 1986).
Zinc functions as an essential component of a number of important enzymes. In addition, other enzymes are activated by zinc. Enzymes that require zinc are involved in nucleic acid, protein, and carbohydrate metabolism (Hambidge et al., 1986). Zinc also is important for normal development and functioning of the immune system.
The recommended requirement of zinc in beef cattle diets is 30 mg Zn/kg diet. This concentration should satisfy requirements in most situations. Pond and Oltjen (1988) reported no growth responses to zinc supplementation in medium- or large-framed steers fed corn silage-corn-based diets containing 22 to 26 mg Zn/kg. Growth responses to zinc supplementation were observed in two of four studies with finishing steers fed diets containing 18 to 29 mg Zn/kg (Perry et al., 1968). In later studies, zinc added to diets containing 17 to 21 mg Zn/kg improved gain in only one of seven experiments (Beeson et al., 1977). Other studies with growing and finishing cattle have indicated no response to zinc supplementation when diets contained 22 to 32 mg Zn/kg (Pringle et al., 1973; Spears and Samsell,