als, requirements are not listed because research data are inadequate to determine requirements.
Many of the essential minerals are usually found in sufficient concentrations in practical feedstuffs. Other minerals are frequently insufficient in diets fed to cattle, and supplementation is necessary to optimize animal performance or health. Supplementing diets at concentrations in excess of requirements greatly increases mineral loss in cattle waste. Oversupplementation of minerals should be avoided to prevent possible environmental problems associated with runoff from waste or application of cattle waste to soil.
A number of elements that are not required (or at least required only in very small amounts) can cause toxicity in beef cattle. Maximum tolerable concentrations of several elements known to be toxic to cattle are given in Table 5–2. The maximum tolerable concentration for a mineral has been defined as “that dietary level that, when fed for
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 5 Minerals At least 17 minerals are required by beef cattle. This chapter presents information about not only mineral requirements but also the function, signs of deficiency, factors affecting requirements, sources, and toxicity of each essential mineral. Macrominerals required include calcium, magnesium, phosphorus, potassium, sodium and chlorine, and sulfur. The microminerals required are chromium, cobalt, copper, iodine, iron, manganese, molybdenum, nickel, selenium, and zinc. Others, including arsenic, boron, lead, silicon, and vanadium have been shown to be essential for one or more animal species, but there is no evidence that these minerals are of practical importance in beef cattle, and therefore are not discussed. Calcium and phosphorus requirements discussed in the subsequent sections are included in the computer models. Requirements and maximum tolerable concentrations for other minerals are shown in Table 5–1. For certain miner TABLE 5–1 Mineral Requirements and Maximum Tolerable Concentrations Mineral Unit Requirement Maximum Tolerable Concentration Growing and Finishing Cattle Cows Gestating Early Lactation Calcium % See Chapter 9 Chlorine % — — — — Chromium mg/kg — — — 1,000.00 Cobalt mg/kg 0.10 0.10 0.10 10.00 Copper mg/kg 10.00 10.00 10.00 100.00 Iodine mg/kg 0.50 0.50 0.50 50.00 Iron mg/kg 50.00 50.00 50.00 1,000.00 Magnesium % 0.10 0.12 0.20 0.40 Manganese mg/kg 20.00 40.00 40.00 1,000.00 Molybdenum mg/kg — — — 5.00 Nickel mg/kg — — — 50.00 Phosphorus % See Chapter 9 Potassium % 0.60 0.60 0.70 3.00 Selenium mg/kg 0.10 0.10 0.10 2.00 Sodium % 0.06–0.08 0.06–0.08 0.10 — Sulfur % 0.15 0.15 0.15 0.40 Zinc mg/kg 30.00 30.00 30.00 500.00 als, requirements are not listed because research data are inadequate to determine requirements. Many of the essential minerals are usually found in sufficient concentrations in practical feedstuffs. Other minerals are frequently insufficient in diets fed to cattle, and supplementation is necessary to optimize animal performance or health. Supplementing diets at concentrations in excess of requirements greatly increases mineral loss in cattle waste. Oversupplementation of minerals should be avoided to prevent possible environmental problems associated with runoff from waste or application of cattle waste to soil. A number of elements that are not required (or at least required only in very small amounts) can cause toxicity in beef cattle. Maximum tolerable concentrations of several elements known to be toxic to cattle are given in Table 5–2. The maximum tolerable concentration for a mineral has been defined as “that dietary level that, when fed for
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 TABLE 5–2 Maximum Tolerable Concentrations of Mineral Elements Toxic to Cattle Element mg/kg Aluminum 1,000.00 Arsenic 50.00 (100.00 for organic forms) Bromine 200.00 Cadmium 00.5 Fluorine 40.00 to 100.00 Lead 30.00 Mercury 2.00 Strontium 2,000.00 Source: Adapted from Table 1 in National Research Council. 1980. Mineral Tolerance of Domestic Animals. Washington, D.C.: National Academy of Sciences. a limited period, will not impair animal performance and should not produce unsafe residues in human food derived from the animal” (National Research Council, 1980: p. 3). MACROMINERALS Calcium Calcium is the most abundant mineral in the body; approximately 98 percent functions as a structural component of bones and teeth. The remaining 2 percent is distributed in extracellular fluids and soft tissues, and is involved in such vital functions as blood clotting, membrane permeability, muscle contraction, transmission of nerve impulses, cardiac regulation, secretion of certain hormones, and activation and stabilization of certain enzymes. CALCIUM REQUIREMENTS Estimated requirements for calcium were calculated by adding the available calcium needed for maintenance, growth, pregnancy, and lactation and correcting for the percentage of dietary calcium absorbed. Calcium requirements are similar to those in the previous edition of this volume (National Research Council, 1984) because new information is not sufficient to justify a change. The maintenance requirement was calculated as 15.4 mg Ca/kg body weight (Hansard et al., 1954, 1957). Retained needs in excess of maintenance requirements were calculated as 7.1 g Ca/100 g protein gain. Calcium content of gain was calculated from slaughter data (Ellenberger et al., 1950). The calcium requirement for lactation in excess of maintenance needs was calculated as 1.23 g Ca/kg milk produced. Fetal calcium content was assumed to be 13.7 g Ca/kg fetal weight. This requirement was distributed over the last 3 months of pregnancy. Absolute calcium requirements were converted to dietary calcium requirements assuming a true absorption for dietary calcium of 50 percent. Lower absorption values have been obtained in older cattle, but in many instances calcium intake may have exceeded dietary requirements in these animals (Hansard et al., 1954, 1957; Martz et al., 1990). Absorption of calcium is largely determined by requirement relative to intake. True calcium absorption is reduced when intake exceeds the animal’s need. The Agricultural and Food Research Council (AFRC) recently used a value of 68 percent absorption to calculate calcium requirements of cattle (TCORN, 1991). FACTORS AFFECTING CALCIUM REQUIREMENTS Calcium is absorbed primarily from the duodenum and jejunum by both active transport and passive diffusion (McDowell, 1992). It should be noted that diets high in fat may decrease calcium absorption through the formation of soaps (Oltjen, 1975). Vitamin D is required for active absorption of calcium (DeLuca, 1979). The amount of calcium absorbed is affected by the chemical form and source of the calcium, the interrelationships with other nutrients, and the animal’s requirement. Requirement is influenced by such factors as age, weight, and type and stage of production. In natural feedstuffs, calcium occurs in oxalate or phytate form. In alfalfa hay, 20 to 33 percent was present as insoluble calcium oxalate and apparently unavailable to the animal (Ward et al., 1979). True absorption of alfalfa calcium was much lower than absorption of corn silage calcium when fed to dairy cows (Martz et al., 1990). In cattle fed high-concentrate diets, dietary calcium in excess of requirements improved gain or feed efficiency in some studies (Huntington, 1983; Brink et al., 1984; Bock et al., 1991). Improvements in performance were likely the result of manipulation of digestive tract function and may not represent a specific calcium requirement. Increasing calcium from 0.25 to 0.40 or 1.11 percent reduced organic matter and starch digestion in the rumen but increased postruminal digestion of organic matter and starch (Goetsch and Owens, 1985). In finishing cattle fed a high-concentrate diet, increasing calcium more than 0.3 percent increased gain in one of two trials but did not affect calcium status based on bone calcium, bone ash, and plasma ionizable calcium concentrations (Huntington, 1983). SIGNS OF CALCIUM DEFICIENCY The skeleton stores a large reserve of calcium that can be utilized to maintain critical blood calcium concentrations. Depending on their age, cattle can be fed calcium-deficient diets for extended periods without developing deficiency signs if previous calcium intake was adequate. Calcium deficiency in young animals, however, prevents normal bone growth, thus causing rickets and retarding growth and development. Rickets can be caused by a deficiency
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 of calcium, phosphorus, or vitamin D. It is characterized by improper calcification of the organic matrix of bone, which results in weak, soft bones that may be easily fractured. Signs include swollen, tender joints, enlargement of the ends of bones, an arched back, stiffness of the legs, and development of beads on the ribs. Osteomalacia is the result of demineralization of the bones of adult animals. Because calcium and phosphorus in bone are in a dynamic state, high demands on calcium and phosphorus stores, such as occur during pregnancy and lactation, may result in osteomalacia. This condition is characterized by weak, brittle bones that may break when stressed. Blood calcium concentration is not a good indicator of calcium status because plasma calcium is maintained at between 9 and 11 mg/dL by homeostatic mechanisms. Parathyroid hormone is released in response to a lowering of plasma calcium. It stimulates the production of 1,25-dihydroxy cholecalciferol (vitamin D3). The 1,25-dihydroxy cholecalciferol increases calcium absorption from the intestine and, in conjunction with parathyroid hormone, increases calcium resorption from bone. If plasma calcium concentrations become elevated, calcitonin is produced and parathyroid hormone production is inhibited. Thus, calcium absorption and bone resorption are decreased. CALCIUM SOURCES The calcium content in forage is affected by species, portion of plant consumed, maturity, quantity of exchangeable calcium in the soil, and climate (Minson, 1990). Forages are generally good sources of calcium, and legumes are higher in calcium content than grasses. Cereal grains are low in calcium, so high-grain diets require supplementation. Oilseed meals are much higher in calcium than grains. Sources of supplemental calcium include calcium carbonate, ground limestone, bone meal, dicalcium phosphate, defluorinated phosphate, monocalcium phosphate, and calcium sulfate. True absorption in young steers of calcium from different sources ranged from 45 percent for ground limestone to 64 percent for dibasic calcium phosphate (Hansard et al., 1957). SIGNS OF CALCIUM TOXICITY High concentrations of dietary calcium are tolerated well by cattle. Protein and energy digestibility were reduced when cattle were fed a diet containing 4.4 percent calcium (calcium carbonate) (Ammerman et al., 1963). High concentrations of dietary calcium may affect metabolism of phosphorus, magnesium, and certain trace elements, but the changes are relatively small (National Research Council, 1980; Alfaro et al., 1988). Magnesium More than 300 enzymes are known to be activated by magnesium (Wacker, 1980). Magnesium is essential, as the complex Mg-ATP, for all biosynthetic processes including glycolysis, energy-dependent membrane transport, formation of cyclic-AMP, and transmission of the genetic code. Magnesium also is involved in the maintenance of electrical potentials across nerve and muscle membranes and for nerve impulse transmission. Of the total percentage of magnesium in the body, 65 to 70 percent is in bone, 15 percent in muscle, 15 percent in other soft tissues, and 1 percent in extracellular fluid (Mayland, 1988). MAGNESIUM REQUIREMENTS Dietary requirements for magnesium vary depending on age, physiological state, and bioavailability from the diet. As a percentage of dry matter, recommended magnesium requirements are as follows: growing and finishing cattle, 0.10 percent; gestating cows, 0.12 percent; and lactating cows, 0.20 percent. Absolute requirements for magnesium have been estimated as follows: replenishment of endogenous loss, 3 mg Mg/kg liveweight; growth, 0.45 g Mg/kg gain; lactation, 0.12 g Mg/kg milk; and pregnancy, 0.12, 0.21, and 0.33 g Mg/day for early, mid, and late pregnancy, respectively (Grace, 1983). O’Kelly and Fontenot (1969, 1973) found that beef cows required 7 to 9 g Mg/day during gestation and 18 to 21 g Mg/day during lactation to maintain serum magnesium concentrations of 2.0 mg/dL. These daily quantities corresponded to 0.10 to 0.13 percent during gestation and 0.17 to 0.20 percent during lactation. In young calves fed milk, 12 to 16 mg Mg/kg body weight was adequate to maintain blood magnesium concentrations (Huffman et al., 1941; Blaxter and McGill, 1956). SIGNS OF MAGNESIUM DEFICIENCY Magnesium deficiency in calves results in excitability, anorexia, hyperemia, convulsions, frothing at the mouth, profuse salivation, and calcification of soft tissue (Moore et al., 1938; Blaxter et al., 1954). Grass tetany or hypomagnesemic tetany is characterized by low magnesium concentrations in plasma and cerebrospinal fluid and is a problem in lactating beef cows. Initial signs of grass tetany are nervousness, reduced feed intake, and muscular twitching around the face and ears. Animals are uncoordinated and
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 walk with a stiff gait. In the advanced stages, cows go down on their side with their head back and go into convulsions. Death usually occurs unless the animal is treated intravenously or subcutaneously with a magnesium-salt solution. Grass tetany is most common in lactating cows grazing lush spring pastures or fed harvested forages low in magnesium. With early spring pastures, the problem is more one of insufficient availability rather than low forage magnesium concentrations per se. Fertilizing pastures with fertilizers high in nitrogen and potassium is associated with increased incidence of grass tetany. Cows depend on a frequent supply of magnesium from the gastrointestinal tract to maintain normal blood magnesium concentrations because homeostatic mechanisms are not sufficient to regulate blood magnesium concentrations. Magnesium concentrations in bone are high, but mature animals lack the ability to mobilize large amounts of magnesium from bone (Rook and Storry, 1962). In young calves, at least 30 percent of the skeletal magnesium can be mobilized during magnesium deficiency (Blaxter et al., 1954). FACTORS AFFECTING MAGNESIUM REQUIREMENTS The rumen is the major site of magnesium absorption in ruminants (Grace et al., 1974; Greene et al., 1983). Magnesium absorption is high in young calves fed milk but decreases with age (Peeler, 1972). True absorption values for magnesium in mature ruminants fed hay and grass range from 10 to 37 percent (Agricultural Research Council, 1980). Magnesium in concentrates is more available than magnesium in forages (Peeler, 1972). A number of studies have shown that high-dietary potassium reduces magnesium absorption (Greene et al., 1983; Wylie et al., 1985). High dietary concentrations of nitrogen, organic acids (citric acid and trans-aconitate), long-chain fatty acids, calcium, and phosphorus also may reduce magnesium absorption or utilization (Fontenot et al., 1989). High-ruminal NH3 concentrations have been associated with hypomagnesemia in cows grazing spring pastures high in crude protein (Martens and Rayssiguier, 1980). Magnesium absorption has been enhanced by feeding soluble carbohydrates or carboxylic ionophores (Fontenot et al., 1989; Spears et al., 1989). Evidence suggests that magnesium absorption from the rumen occurs by an active sodium-linked process (Martens and Rayssiguier, 1980), and sodium supplementation in a low-sodium diet increases magnesium absorption (Martens et al., 1987). It has also been reported that different breeds absorb magnesium differently (Greene et al., 1989). Excess magnesium absorbed is excreted primarily in the urine. MAGNESIUM SOURCES Cereal grains generally contain 0.11 to 0.17 percent magnesium; plant protein sources contain approximately twice this concentration (Underwood, 1981). Magnesium concentration in forages varies greatly depending on plant species, soil magnesium, stage of growth, season and environmental temperature (Minson, 1990). Legumes are usually higher in magnesium than are grasses. Magnesium oxide and magnesium sulfate are good sources of supplemental magnesium, but magnesium in magnesite and dolomitic limestone is poorly available (Gerken and Fontenot, 1967; Ammerman et al., 1972). SIGNS OF MAGNESIUM TOXICITY Magnesium toxicity is not a problem in beef cattle. Maximum tolerable concentrations have been estimated at 0.4 percent (National Research Council, 1980). Cows fed 0.39 percent magnesium showed no adverse effects (O’Kelly and Fontenot, 1969). Young calves fed 1.3 percent magnesium had lower feed intake and weight gain and diarrhea with mucus in feces (Gentry et al., 1978). Steers fed 2.5 or 4.7 percent magnesium exhibited severe diarrhea and a lethargic appearance, while 1.4 percent magnesium reduced dry matter digestibility (Chester-Jones et al., 1990). Phosphorus Phosphorus is often discussed in conjunction with calcium because the two minerals function together in bone formation; however, the effect of the calcium:phosphorus ratio on ruminant performance has been overemphasized in the past. Several studies (Dowe et al., 1957; Wise et al., 1963; Ricketts et al., 1970; Alfaro et al., 1988) have shown that dietary calcium to phosphorus ratios of between 1:1 and 7:1 result in similar performance, provided that phosphorus intake is adequate to meet requirements. Approximately 80 percent of phosphorus in the body is found in bones and teeth with the remainder distributed in soft tissues. Phosphorus also functions in cell growth and differentiation as a component of DNA and RNA; energy utilization and transfer as a component of ATP, ADP, and AMP; phospholipid formation; and maintenance of acid-base and osmotic balance. Phosphorus is required by ruminal microorganisms for their growth and cellular metabolism. PHOSPHORUS REQUIREMENTS Requirements for phosphorus were calculated using the factorial method. Estimated requirements for maintenance, growth, pregnancy, and lactation were totaled and then corrected for the percentage of dietary phosphorus absorbed. The maintenance requirement for phosphorus was considered to be 16 mg P/kg body weight. This value is similar to fecal endogenous losses observed in cattle
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 fed phosphorus concentrations at or near requirements (Tillman and Brethour, 1958; Tillman et al., 1959; Challa and Braithwaite, 1988; Challa et al., 1989). Slightly lower fecal endogenous losses were observed for dairy cows in negative phosphorus balance (Martz et al., 1990). Retained-phosphorus needs in excess of maintenance requirements were calculated as 3.9 g P/100 g protein gain. The phosphorus content of gain was calculated from data presented by Ellenberger et al. (1950). Phosphorus needs, during lactation, in excess of maintenance, were calculated as 0.95 g P/kg milk produced. Fetal phosphorus was assumed to be 7.6 g P/kg fetal weight. This requirement was distributed over the last 3 months of pregnancy. FACTORS AFFECTING PHOSPHORUS REQUIREMENTS A true absorption of 68 percent was assumed in converting absolute phosphorus requirements to dietary requirements. This value agrees well with most studies (Tillman and Brethour, 1958; Tillman et al., 1959; Challa et al., 1989; Martz et al., 1990) of cattle where true absorption has been measured. Absorption of phosphorus was much higher in young calves fed milk (Lofgreen et al., 1952). In their estimate of requirements, AFRC (TCORN, 1991) assumed an absorption coefficient of 64 percent for phosphorus in forages and 70 percent for phosphorus in concentrates. In young calves with an initial weight of 96 kg, 0.22 percent phosphorus was adequate for maximum weight gains, but increasing phosphorus to 0.30 percent increased bone ash (Wise et al., 1958). A more recent study with dairy calves weighing approximately 70 kg indicated that 0.26 percent phosphorus was not adequate for maximum growth or bone ash (Jackson et al., 1988). Call et al. (1978) fed Hereford heifers (165 kg initial weight), beginning at approximately 7 months of age, diets containing 0.14 or 0.36 percent phosphorus for 2 years. No differences between the two groups were detected in growth, rib bone morphology and phosphorus content, age at puberty, conception rate, or calving interval. In a second study, Hereford heifers were fed low-phosphorus diets from weaning through their fifth gestation and lactation (Call et al., 1986). The low-phosphorus group received 6 to 12.1 g P/day, while controls received 20.6 to 38.1 g P/day with phosphorus intake increased as the cattle grew larger. Females fed the low-phosphorus intake remained healthy, and growth and reproduction were similar to that observed in phosphorus supplemented animals. When phosphorus intake of 6 to 12.1 g P/day was reduced to 5.1 to 6.6 g P/day, clinical signs of deficiency occurred within 6 months (Call et al., 1986). Reproduction was not impaired until cows were fed the very low phosphorus diet for more than 1 year. It was concluded that 12 g P/day throughout 1 production year was adequate for 450-kg Hereford cows (Call et al., 1986). No measurements of milk production or calf weaning weights were given in these papers (Call et al., 1978, 1986). SIGNS OF PHOSPHORUS DEFICIENCY In grazing livestock, phosphorus deficiency has been described as the most prevalent mineral deficiency throughout the world (McDowell, 1992). Studies in South Africa and Texas of cattle that grazed forages low in phosphorus showed large improvements in fertility and calf weaning weights with phosphorus supplementation (Dunn and Moss, 1992). Phosphorus deficiency results in reduced growth and feed efficiency, decreased appetite, impaired reproduction, reduced milk production, and weak, fragile bones (Underwood, 1981; Shupe et al., 1988). The skeleton provides a large reserve of phosphorus that can be drawn on during periods of inadequate phosphorus intake in mature animals. Skeletal reserves can subsequently be replaced during periods when phosphorus intake is high relative to requirements. Plasma phosphorus concentrations consistently below 4.5 mg/dL are indicative of a deficiency, but bone phosphorus is a more sensitive measure of phosphorus status (McDowell, 1992). Phosphorus absorption occurs in the small intestine. The percentage absorbed is not greatly affected by amount of phosphorus intake (TCORN, 1991). Varying endogenous fecal excretion is an important homeostatic mechanism for controlling phosphorus in cattle. Endogenous fecal losses consist largely of unabsorbed salivary phosphorus (Challa et al., 1989). Salivary phosphorus is affected by plasma phosphorus concentration, which does depend on phosphorus intake as well as factors that affect salivary flow such as dry matter intake and physical form of the diet (TCORN, 1991). Thus, fecal endogenous loss of phosphorus may vary depending on intake and other factors that affect salivary phosphorus. In estimating the maintenance requirement, it is important that endogenous fecal excretion of phosphorus be measured in cattle fed approximately their phosphorus requirement. Urinary losses of phosphorus are generally lower but may increase in cattle fed high-concentrate diets (Reed et al., 1965). PHOSPHORUS SOURCES Phosphorus-deficient soils are widespread and forages produced on these soils are low in phosphorus. Drought conditions and increased forage maturity also can result in low forage-phosphorus concentrations. Cereal grains and oilseed meals contain moderate to high concentrations of phosphorus. Animal and fish products are high in phosphorus. In terms of availability, supplemental sources of phosphorus were ranked as follows: dicalcium phosphate,
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 defluorinated phosphate, and bone meal (Peeler, 1972). More recent studies with calves have indicated that defluorinated phosphate (Miller et al., 1987) and monoammonium phosphate (Jackson et al., 1988) are equal in availability to dicalcium phosphate. Phytate phosphorus is not well utilized by nonruminants, but seems to be utilized by ruminants as readily as phosphorus from inorganic sources (McGillivray, 1974). Potassium Potassium is the third most abundant mineral in the body and the major cation in intracellular fluid. Potassium is important in acid-base balance, regulation of osmotic pressure, water balance, muscle contractions, nerve impulse transmission, and certain enzymatic reactions. POTASSIUM REQUIREMENTS Feedlot cattle require approximately 0.6 percent potassium. Studies conducted with potassium in cattle receiving no ionophore have been inconsistent. Roberts and St. Omer (1965) observed a response in gain with potassium supplementation of steer diets containing 0.50 to 0.56 percent potassium in only one of three trials. Devlin et al. (1969) noted improvements in steers’ gain and feed intake when potassium was added to diets already containing 0.5 percent potassium. More recently, however, Kelley and Preston (1984) observed no improvement in steer performance when potassium was supplemented to a basal diet containing 0.4 percent potassium. Studies with feedlot cattle fed lasalocid (Ferrell et al., 1983; Spears and Harvey, 1987) or monensin (Brink et al., 1984) indicate that potassium requirement does not exceed 0.55 percent. Potassium requirements in young dairy calves not fed an ionophore also do not exceed 0.55 percent (Weil et al., 1988; Tucker et al., 1991). Because of the lower rates of gain observed in growing cattle in range conditions, potassium requirements for range cattle may be lower than those for feedlot cattle. Clanton (1980) concluded that growing cattle in range conditions require 0.3 to 0.4 percent potassium. Potassium requirements of beef cows are not well defined. Clanton (1980) suggested that gestating beef cows require 0.5 to 0.7 percent potassium. Because of the relatively high secretion of potassium in milk (1.5 g/kg), requirements for potassium may be slightly higher in beef cows during lactation—for example, for cows producing 9 kg milk/day, approximately 13.5 g K/day or 0.13 percent of dry matter intake would be needed for milk production. SIGNS OF POTASSIUM DEFICIENCY A deficiency of potassium results in reduced feed intake and weight gain, pica, rough hair coat, and muscular weakness (Devlin et al., 1969). In beef cattle, a severe deficiency of potassium is unlikely. A marginal potassium deficiency results in decreased feed intake and retarded weight gain. Dietary potassium concentration is the best indicator of potassium status. Serum or plasma potassium is not a reliable indicator of potassium status. Reduced feed consumption appears to be an early indicator of marginal potassium deficiency, but the depression in feed intake is usually of relatively small magnitude, making it difficult to detect in field conditions. Potassium is absorbed from the rumen and omasum as well as the intestine, and absorption is very high. The major route of potassium excretion is the urine. Body stores of potassium are small; therefore, a deficiency can occur rapidly (Ward, 1966). POTASSIUM SOURCES Forages are excellent sources of potassium, usually containing between 1 and 4 percent potassium. In fact, high potassium content in lush spring pastures seems to be a major factor associated with the occurrence of grass tetany in beef cows (Mayland, 1988). As forages mature, the potassium content decreases, and low concentrations of potassium have been observed in range forage and in accumulated tall fescue during the winter (Clanton, 1980). Cereal grains are often deficient (<0.5 percent) in potassium, and high-concentrate diets may require potassium supplementation unless a high-potassium forage or protein supplement is included in the diet. Oilseed meals are good sources of potassium. Potassium can be supplemented to cattle diets as potassium chloride, potassium bicarbonate, potassium sulfate, or potassium carbonate. All forms are readily available. SIGNS OF POTASSIUM TOXICITY Increasing the potassium content of a liquid diet from 1.2 to 5.8 percent on a dry matter basis resulted in the deaths of 3 of 8 calves as a result of cardiac insufficiency (Blaxter et al., 1960). In calves, increasing dietary potassium from 2.77 to 6.77 percent reduced feed intake and retarded weight gain (Neathery et al., 1980). The maximum tolerable concentration of potassium has been set at 3 percent for cattle (National Research Council, 1980). Cattle grazing lush, spring pastures often consume more than 3 percent potassium, and other than reduced absorption of magnesium, no adverse effects have been reported. Sodium and Chlorine Sodium is the major cation, while chlorine is the major anion, in extracellular fluid. Both sodium and chlorine are involved in maintaining osmotic pressure, controlling water
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 balance, and regulating acid-base balance. Sodium also functions in muscle contractions, nerve impulse transmission, and glucose and amino acid transport. Chlorine is necessary for the formation of hydrochloric acid in gastric juice and for the activation of amylase. SODIUM AND CHLORINE REQUIREMENTS Requirements for sodium in nonlactating beef cattle do not exceed 0.06 to 0.08 percent, while lactating beef cows require approximately 0.10 percent sodium (Morris, 1980). Ruminants have an appetite for sodium, and if it is provided ad libitum, they will consume more salt than they actually require. In a 2-year study with beef cows grazing forage containing from 0.012 and 0.055 percent sodium, providing salt ad libitum did not affect calf weaning weights or cow body weights (Morris et al., 1980). Chlorine requirements are not well defined but a deficiency of chlorine does not seem likely in practical conditions (Neathery et al., 1981). Young calves fed 0.038 percent chlorine performed similar to those fed 0.5 percent chlorine (Burkhaltor et al., 1979). SIGNS OF SODIUM DEFICIENCY Signs of deficiency of sodium are rather nonspecific and include pica and reduced feed intake, growth, and milk production (Underwood, 1981). When sodium intake is low, the body conserves sodium by increasing reabsorption of sodium from the kidney in response to aldosterone (McDowell, 1992). The sodium:potassium ratio in saliva has been used as an indicator of sodium status. This ratio is normally 20:1, and a production response to sodium supplementation is likely when the sodium:potassium ratio is less than 10:1 (Morris, 1980). Serum or plasma sodium concentration is not a reliable indicator of sodium status. Dietary sodium concentration is a good measure of sodium adequacy. SODIUM AND CHLORINE SOURCES Cereal grains and oilseed meals usually provide inadequate amounts of sodium for beef cattle. Animal products are much higher in sodium and chlorine than plant products (Meyer et al., 1950). The sodium content of forages varies considerably (Minson, 1990). Sodium can be supplemented as sodium chloride or sodium bicarbonate and both forms are highly available. SIGNS OF SODIUM TOXICITY High concentrations of salt have been used to regulate feed intake and cattle can tolerate high-dietary concentrations provided that an adequate supply of water is available. Growing cattle were able to tolerate 9.33 percent salt for 84 days without adverse effects (Meyer et al., 1955). However, Leibholz et al. (1980) reported that 6.5 percent salt decreased organic matter intake and growth in calves. The maximum tolerable concentration for dietary salt in cattle was estimated at 9.0 percent in Mineral Tolerance of Domestic Animals (National Research Council, 1980). Salt is much more toxic when present in the drinking water of cattle. Growing cattle were able to tolerate 1.0 percent added salt in drinking water without adverse effects (Weeth et al., 1960; Weeth and Haverland, 1961); however, the addition of 1.25 to 2.0 percent salt resulted in anorexia, reduced weight gain or weight loss, reduced water intake and physical collapse (Weeth et al., 1960). In some areas of the western United States, soils are high in saline, resulting in groundwater that can cause saline water intoxication. Consumption of water with more than 7,000 mg Na/kg resulted in reduced feed and water intake, decreased growth, mild digestive disturbances, and diarrhea (Jenkins and Mackey, 1979). Sulfur Sulfur is a component of methionine, cysteine, and cystine, and the B-vitamins, thiamin and biotin, as well as a number of other organic compounds. Sulfate is a component of sulfated mucopolysaccharides and also functions in certain detoxification reactions in the body. All sulfur-containing compounds with the exception of biotin and thiamin can be synthesized from methionine. Ruminal microorganisms are capable of synthesizing all organic sulfur containing compounds required by mammalian tissue from inorganic sulfur (Block et al., 1951; Thomas et al., 1951). Sulfur is required also by ruminal microorganisms for their growth and normal cellular metabolism. SULFUR REQUIREMENTS Requirements of beef cattle for sulfur are not well defined. The recommended concentration in beef cattle diets is 0.15 percent. Sulfur supplementation increased gain in steers fed corn silage-corn-urea based diets containing 0.10 to 0.11 percent sulfur (Hill, 1985). In steers fed high-concentrate diets containing 0.14 percent sulfur, increasing dietary sulfur tended to reduce ruminal lactic acid accumulation and improve feed efficiency (Rumsey, 1978). Other studies have indicated that 0.11 to 0.12 percent sulfur was adequate for growing cattle (Bolsen et al., 1973; Pendlum et al., 1976). In Australia, sulfur supplementation increased gain by 12 percent in steers grazing sorghum×sudangrass containing 0.08 to 0.12 percent sulfur (Archer and Wheeler, 1978). The sulfur requirement of ruminants grazing sorghum×sudangrass may be increased because of the need for sulfur in the detoxifica-
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 tion of cyanogenic glucoside found in most sorghum forages. SIGNS OF SULFUR DEFICIENCY Severe sulfur deficiency results in anorexia, weight loss, weakness, dullness, emaciation, excessive salivation, and death (Thomas et al., 1951; Starks et al., 1953). Marginal deficiencies of sulfur can reduce feed intake, digestibility, and microbial protein synthesis. A dietary limitation of sulfur can dramatically decrease microbial numbers as well as microbial digestion and protein synthesis. Supplementation to increase the sulfur content of hay from 0.04 to 0.075 percent increased counts of ruminal bacteria, protozoa, and sporangia of anaerobic fungi in sheep (Morrison et al., 1990). Impaired utilization of lactate by ruminal microorganisms, resulting in lactate accumulation in the rumen and blood, also can occur as a result of sulfur deficiency (Whanger and Matrone, 1966). FACTORS AFFECTING SULFUR REQUIREMENTS Most rumen bacteria are able to synthesize the sulfurcontaining amino acids from sulfide (Goodrich et al., 1978). Ruminal sulfide is derived from the reduction of inorganic sulfur sources and from the degradation of sulfur-containing amino acids. Sulfide can be absorbed from the rumen and oxidized by tissues to sulfate, a less toxic form of sulfur. Sulfur is found in feedstuffs largely as a component of protein. Dietary sulfur requirements may be higher when diets high in rumen bypass protein are fed because of a limitation of sulfur for optimal ruminal fermentation. Most practical diets are adequate in sulfur. When urea or other nonprotein nitrogen sources replace preformed protein, sulfur supplementation may be needed. Mature forages, forages grown in sulfur-deficient soils, corn silage, and sorghum×sudangrass can be low in sulfur. Sorghum forages seem inherently low in sulfur relative to most forages, and the sulfur content of sorghum×sudangrass did not increase in response to sulfur fertilization (Wheeler et al., 1980). SULFUR SOURCES Sulfur can be supplemented in ruminant diets as sodium sulfate, ammonium sulfate, calcium sulfate, potassium sulfate, magnesium sulfate, or elemental sulfur. Based on in vitro microbial protein synthesis, the availability of sulfur to ruminal microorganisms from different sources has been ranked from most to least available as L-methionine, calcium sulfate, ammonium sulfate, D,L-methionine, sodium sulfate, sodium sulfide, elemental sulfur, and methionine hydroxy analog (Kahlon et al., 1975). SIGNS OF SULFUR TOXICITY Acute sulfur toxicity is characterized by restlessness, diarrhea, muscular twitching, dyspnea, and, in prolonged cases, inactivity followed by death (Coghlin, 1944). Concentrations of sulfur lower than those needed to cause clinical signs of toxicity can reduce feed intake and retard growth rate (Kandylis, 1984) and decrease copper status (Smart et al., 1986). Increasing dietary sulfur from 0.12 to 0.41 percent using ammonium sulfate reduced feed intake by 32 percent in steers fed high-concentrate diets containing urea (Bolsen et al., 1973). Consumption of water high in sulfate (5,000 mg/kg) reduced feed and water intake (Weeth and Hunter, 1971). The maximum tolerable concentration of dietary sulfur has been estimated at 0.40 percent (National Research Council, 1980). MICROMINERALS Chromium Chromium functions as a component of the glucose tolerance factor that serves to potentiate the action of insulin (Mertz, 1992). The addition of chromium as 0.4 mg chromium picolinate/kg diet (Bunting et al., 1994), or chromium polynicotinate/kg diet (Kegley and Spears, 1995), for growing cattle increased glucose clearance rate following intravenous glucose administration. Adding low concentrations (0.2 to 1.0 mg/kg) of chromium also increased immune response and growth rate in stressed cattle (Chang and Mowat, 1992; Moonsie-Shageer and Mowat, 1993). These studies suggest that in some situations supplemental chromium may be needed. Current information is not sufficient to determine chromium requirements. Based on studies with humans and laboratory animals, organic chromium is much more bioavailable than inorganic chromium. The maximum tolerable concentration of trivalent chromium in the chloride form was estimated to be 1,000 mg Cr/kg diet for cattle (National Research Council, 1980). No adverse effects were observed in steers fed 4.0 mg chromium polynicotinate complex/kg diet for 70 days (Claeys and Spears, unpublished data). Hexavalent chromium is much more toxic than the trivalent form (National Research Council, 1980). Cobalt Cobalt functions as a component of vitamin B12 (cobalamin). Cattle are not dependent on a dietary source of vitamin B12 because ruminal microorganisms are capable of synthesizing B12 from dietary cobalt. Measurements of the amount of dietary cobalt converted to vitamin B12 in the rumen have ranged from 3 to 13 percent of intake (Smith, 1987). Ruminal bacteria also produce a number
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 of B12 analogues that are active in bacteria but apparently inactive in animal tissues (Bigger et al., 1976). Two vitamin B12-dependent enzymes occur in mammalian tissues (Smith, 1987)—methylmalonyl CoA mutase is essential for the metabolism of propionate to succinate, as it catalyzes the conversion of L-methylmalonyl CoA to succinyl CoA; and 5-methyltetrahydrofolate homocysteine methyltransferase (methionine synthase) catalyzes the transfer of methyl groups from 5-methyltetrahydrofolate to homocysteine to form methionine and tetrahydrofolate. This reaction is important in the recycling of methionine following transfer of its methyl group. COBALT REQUIREMENTS The cobalt requirement of cattle is approximately 0.10 mg/kg dry matter diet (Smith, 1987). Cobalt concentrations between 0.07 and 0.11 percent have been reported to be adequate in various studies (Smith, 1987). Young, rapidly growing cattle seem more sensitive to cobalt deficiency than older cattle. Feeding a high-concentrate diet may depress ruminal synthesis of vitamin B12 and increase production of B12 analogues (Walker and Elliot, 1972; Halpin et al., 1984). However, MacPhearson and Chalmers (1984) found no evidence that cobalt requirements were higher when high-concentrate diets were consumed. SIGNS OF COBALT DEFICIENCY Decreased appetite and failure to grow or moderate weight loss are early signs of cobalt deficiency (Smith, 1987). If the deficiency is allowed to become severe, animals exhibit severe unthriftiness, rapid weight loss, fatty degeneration of the liver, and pale skin and mucous membranes as a result of anemia. Cobalt deficiency also has been reported to impair the ability of neutrophils to kill yeast and reduce disease resistance (MacPherson et al., 1989). Recent findings indicate that an inability by ruminal microorganisms to convert succinate to propionate is an early manifestation of cobalt deficiency (Kennedy et al., 1991). Ruminal and plasma succinate concentrations were greatly elevated in lambs fed cobalt-deficient diets. Liver vitamin B12 or cobalt concentrations can be used to assess cobalt status (Smith, 1987). Vitamin B12 concentrations in liver of 0.10 µg/g wet weight or less are indicative of cobalt deficiency. Measurement of serum B12 in cattle may be of limited value because of the presence of B12 analogues in bovine serum (Halpin et al., 1984). FACTORS AFFECTING COBALT REQUIREMENTS Soils deficient in cobalt occur in many areas of the world including the southeastern Atlantic coast of the United States (Ammerman, 1970). Legumes are generally higher in cobalt than grasses and availability of cobalt in soil is highly dependent on soil pH (Underwood, 1981). Increasing soil pH from 5.4 to 6.4 reduced the cobalt content of ryegrass from 0.35 to 0.12 mg/kg (Mills, 1981). Cobalt can be supplemented to the diet in free-choice mineral mixtures. Feed-grade sources of cobalt include cobalt sulfate and cobalt carbonate. It is unclear how these two forms of cobalt compare in terms of relative bioavailability for vitamin B12 synthesis. Pellets containing cobalt oxide and finely divided iron, and controlled-release glass pellets containing cobalt have been used in grazing ruminants. Both types of pellets remain in the reticulorumen and release cobalt over an extended period. SIGNS OF COBALT TOXICITY Cobalt toxicity is not likely to occur unless an error is made in formulating a mineral supplement. Cattle can tolerate approximately 100 times the dietary requirement for cobalt (National Research Council, 1980). Signs of chronic cobalt toxicity, with the exception of elevated liver cobalt, are similar to those of cobalt deficiency and include decreased feed intake and reduced body weight gain, anemia, emaciation, hyperchromia, debility, and increased liver cobalt (National Research Council, 1980). Young dairy calves given up to 66 mg Co/kg body weight for up to 28 weeks showed no adverse effects (Keener et al., 1949). The sulfate, carbonate, and chloride forms of cobalt were similar in terms of toxicity (Keener et al., 1949). Copper Copper functions as an essential component of a number of enzymes including lysyl oxidase, cytochrome oxidase, superoxide dismutase, ceruloplasmin, and tyrosinase (McDowell, 1992). COPPER REQUIREMENTS Requirements for copper can vary from 4 to more than 15 mg/kg depending largely on the concentration of dietary molybdenum and sulfur. The recommended concentration of copper in beef cattle diets is 10 mg Cu/kg diet. This amount should provide adequate copper if the diet does not exceed 0.25 percent sulfur and 2 mg Mo/kg diet. Less than 10 mg Cu/kg diet may meet requirements of feedlot cattle because copper is more available in concentrate diets than in forage diets. Copper requirements may be affected by breed. Simmental cattle excrete more copper in their bile than Angus (Gooneratne et al., 1994). Ward et al. (1995) reported that Simmental and Charolais cows and their calves were more susceptible to copper deficiency than Angus when fed the same diet. Copper requirements are greatly increased by molybde-
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 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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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 been contaminated with copper from agricultural or industrial sources. The liver can accumulate large amounts of copper before signs of toxicity are observed. When copper is released from the liver in large amounts (hemolytic crisis), hemolysis, methemoglobinemia, hemoglobinuria, jaundice, icterus, widespread necrosis, and often death occur (National Research Council, 1980). The maximum tolerable concentration of copper for cattle has been estimated at 100 mg Cu/kg diet (National Research Council, 1980). The concentration of copper needed to cause toxicity will depend on the concentration of molybdenum, sulfur, and iron in the diet. Adult cattle are less susceptible to copper toxicity than young cattle. In young calves, feeding 115 mg Cu/kg for 91 days resulted in signs of toxicity (Shand and Lewis, 1957). Iodine Iodine functions as an essential component of the thyroid hormones thyroxine (T4) and triiodothyronine (T3), which regulate the rate of energy metabolism in the body. Between 70 and 80 percent of dietary iodine is absorbed as iodide from the rumen with considerable resecretion occurring in the abomasum (Miller et al., 1988). Iodide that is secreted into the abomasum is largely reabsorbed from the small and large intestine. Absorbed iodide is largely taken up by the thyroid gland for thyroid hormone synthesis or is excreted in the urine. In lactating cows, approximately 8 percent of dietary iodine is secreted in milk (Miller et al., 1988). When the thyroid hormones are catabolized, much of the iodine is reused by the thyroid gland. IODINE REQUIREMENTS Iodine requirements of beef cattle are not well established; 0.5 mg I/kg diet should be adequate unless the diet contains goitrogenic substances that interfere with iodine metabolism. Iodine requirements have been estimated by measuring thyroid hormone secretion rate (Agricultural Research Council, 1980). Miller et al. (1988) calculated the theoretical iodine requirement to be 0.6 mg/100 kg BW assuming a daily thyroxine secretion rate of 0.2 to 0.3 mg I/100 kgBW, 30 percent uptake of dietary iodine by the thyroid, and 15 percent recycling of thyroxine iodine. This would correspond to 0.2 to 0.3 mg I/kg in the total diet, depending on feed intake. FACTORS AFFECTING IODINE REQUIREMENTS Goitrogenic substances in the feed may increase iodine requirements substantially (2- to 4-fold) depending on the amount and type of goitrogens present. The cyanogenetic goitrogens include the thiocyanate derived from cyanide in white clover and the glucosinolates found in some Brassica forages such as kale, turnips, and rape. They impair iodine uptake by the thyroid, and their effect can be overcome by increasing dietary iodine. Soybean meal and cottonseed meal also have a goitrogenic effect (Miller et al., 1975). The thiouracil goitrogens are found in Brassica seeds and inhibit iodination of tyrosine residues in the thyroid gland. The action of thiouracil goitrogens is more difficult to reverse with iodine supplementation. SIGNS OF IODINE DEFICIENCY The first sign of iodine deficiency is usually enlargement of the thyroid (goiter) in the newborn (Miller et al., 1988). Iodine deficiency may result in calves born hairless, weak, or dead; reduced reproduction in cows characterized by irregular cycling, low conception rate, and retained placenta; and decreased libido and semen quality in males (McDowell, 1992). Deficiency signs may not appear for more than a year after cattle are fed an iodine-deficient diet. Protein-bound iodine, thyroid weight in newborns, and milk iodine have been used to assess iodine status (Underwood, 1981). IODINE SOURCES The iodine content of feeds depends on the iodine available in the soil. In the United States, much of the Northeast, the Great Lakes, and Rocky Mountain regions are deficient in iodine (Underwood, 1981). Iodine is usually supplemented in diets or in free-choice minerals as calcium iodate or ethylenediamine dihydroiodide (EDDI), an organic form of iodine. Both forms are highly available and stable in mineral supplements and diets. Iodide forms such as potassium or sodium iodide are less stable and considerable losses can occur as a result of heat, moisture, light, and exposure to other minerals. EDDI has been widely used in cattle to prevent foot rot. The amount of EDDI fed to prevent foot rot is much higher than dietary requirements. At present, 10 mg I from EDDI is the maximum concentration that can be fed per head per day. SIGNS OF IODINE TOXICITY The maximum tolerable level of iodine is 50 mg/kg diet (National Research Council, 1980). In calves, 50 mg/kg of iodine as calcium iodate reduced weight gain and feed intake, and caused coughing and excessive nasal discharge (Newton et al., 1974). Iodine in the form of EDDI has been fed at concentrations exceeding 50 mg/kg without adverse effects in calves and lactating cows (National Research Council, 1980).
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 Iron Iron is an essential component of a number of proteins involved in oxygen transport or utilization. These proteins include hemoglobin, myoglobin, and a number of cytochromes and iron-sulfur proteins involved in the electron transport chain. Several mammalian enzymes also either contain iron or are activated by iron (McDowell, 1992). More than 50 percent of the iron in the body is present in hemoglobin, with smaller amounts present in other iron-requiring proteins and enzymes, and in protein-bound stored iron. IRON REQUIREMENTS The iron requirement is approximately 50 mg/kg diet in beef cattle. Studies with young calves fed milk diets have indicated that 40 to 50 mg Fe/kg is adequate to support growth and prevent anemia (Bremner and Dalgarno, 1973; Bernier et al., 1984). Iron requirements of older cattle are not well defined. Requirements in older cattle are probably lower than in young calves because considerable recycling of iron occurs when red blood cells turn over (Underwood, 1977), and in older animals blood volume is not increasing, or at least not to the extent that it is in young animals. SIGNS OF IRON DEFICIENCY A deficiency of iron results in anemia (hypochromic microcytic), listlessness, reduced feed intake and weight gain, pale mucus membranes and atrophy of the papillae of the tongue (Blaxter et al., 1957; Bremner and Dalgarno, 1973). Iron deficiency can occur in young calves fed exclusively milk, especially if they are housed in confinement. Most practical feedstuffs are more than adequate in iron, and iron deficiency is unlikely in other classes of cattle unless parasite infestations or diseases exist that cause chronic blood loss. In the absence of blood loss, only small amounts of iron are lost in the urine and feces (McDowell, 1992). IRON SOURCES Cereal grains normally contain 30 to 60 mg Fe/kg; oilseed meals contain 100 to 200 mg Fe/kg (Underwood, 1981). With the exception of milk and milk products, feeds of animal origin are high in iron, with meat and fish meal containing 400 to 500 mg Fe/kg; blood meal usually has more than 3,000 mg Fe/kg. The iron content of forages is highly variable but most forages contain from 70 to 500 mg Fe/kg. Much of the variation in forage iron is probably caused by soil contamination. Water and soil ingestion also can be significant sources of iron for beef cattle. Availability of iron from forages appears to be lower than from most supplemental iron sources (Thompson and Raven, 1959; Raven and Thompson, 1959). Iron from soil is probably of low availability; however, research by Healy (1972) indicated that a significant amount of iron from various soil types was soluble in ruminal fluid. Iron is generally supplemented in diets as ferrous sulfate, ferrous carbonate, or ferric oxide. Availability of iron is highest for ferrous sulfate with ferrous carbonate being intermediate (Ammerman et al., 1967; McGuire et al., 1985). Ferric oxide is basically unavailable (Ammerman et al., 1967). SIGNS OF IRON TOXICITY Iron toxicity causes diarrhea, metabolic acidosis, hypothermia, and reduced gain and feed intake (National Research Council, 1980). The maximum tolerable concentration of iron for cattle has been estimated at 1,000 mg Fe/kg (National Research Council, 1980). Dietary iron concentrations as low as 250 to 500 mg/kg have caused copper depletion in cattle (Bremner et al., 1987; Phillippo et al., 1987a). In areas where drinking water or forages are high in iron, dietary copper may need to be increased to prevent copper deficiency. Manganese Manganese functions as a component of the enzymes pyruvate carboxylase, arginase, and superoxide dismutase and as an activator for a number of enzymes (Hurley and Keen, 1987). Enzymes activated by manganese include a number of hydrolases, kinases, transferases, and decarboxylases. Of the many enzymes that can be activated by manganese, only the glycosyltransferases are known to specifically require manganese. MANGANESE REQUIREMENTS The manganese requirement for growing and finishing cattle is approximately 20 mg Mn/kg diet. Skeletal abnormalities were noted in calves from cows fed diets containing 15.8 mg Mn/kg but were not present when diets were supplemented to contain 25 mg Mn/kg (Rojas et al., 1965). The quantity of manganese needed for maximum growth is less than that required for normal skeletal development. Manganese requirements for reproduction are higher than for growth and skeletal development, and the recommended concentration for breeding cattle is 40 mg/kg. Cows fed a diet containing 15.8 mg Mn/kg had lower conception rates than cows fed 25 mg Mn/kg (Rojas et al., 1965). Heifers fed 10 mg Mn/kg exhibited impaired reproduction (delayed cycling and reduced conception rate) compared to those fed 30 mg Mn/kg, but growth was similar for the two groups (Bentley and Phillips, 1951).
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 Supplementing a corn silage-based diet containing 32 mg Mn/kg with 14 mg Mn/kg, from a manganese polysaccharide complex, reduced services per conception from 1.6 to 1.1 but did not affect overall conception rate in beef cows (DiCostanzo et al., 1986). SIGNS OF MANGANESE DEFICIENCY Inadequate intake of manganese in young animals results in skeletal abnormalities that may include stiffness, twisted legs, enlarged joints, and reduced bone strength (Hurley and Keen, 1987). In older cattle, manganese deficiency causes low reproductive performance characterized by depressed or irregular estrus, low conception rate, abortion, stillbirths, and low birth weights. FACTORS AFFECTING MANGANESE REQUIREMENTS Absorption of manganese from 54MnCl in lactating dairy cows was less than 1 percent (Van Vruwaene et al., 1984) and little is known concerning dietary factors that may influence manganese absorption. Some evidence suggests that high dietary calcium and phosphorus may increase manganese requirements (Hawkins et al., 1955; Dyer et al., 1964; Lassiter et al., 1972). Biliary excretion of manganese plays an important role in manganese homeostasis but little excretion of manganese occurs via the urine (Hidiroglou, 1979). MANGANESE SOURCES The concentration of manganese in forages varies greatly depending on plant species, soil pH, and soil drainage (Minson, 1990). Forages generally contain adequate manganese, assuming that the manganese is available for absorption. Corn silage can be low, or at best marginal, in manganese content (Buchanan-Smith et al., 1974). Cereal grains usually contain between 5 and 40 mg Mn/kg with corn being especially low (Underwood, 1981). Plant protein sources normally contain 30 to 50 mg Mn/kg, whereas animal-protein sources only contain 5 to 15 mg Mn/kg. Manganese can be supplemented to ruminant diets as manganese sulfate, manganese oxide, or various organic forms (manganese methionine, manganese proteinate, manganese polysaccharide complex, or manganese amino acid chelate). Manganese sulfate is more available than manganese oxide (Wong-Ville et al., 1989; Henry et al., 1992). Compared to manganese sulfate, relative availability of manganese from manganese methionine is approximately 120 percent (Henry et al., 1992). SIGNS OF MANGANESE TOXICITY In Mineral Tolerances of Domestic Animals (National Research Council, 1980), the maximum tolerable concentration of manganese was set at 1,000 mg/kg, at least on a short-term basis. Calves fed 1,000 mg Mn/kg for 100 days showed no adverse effects (Cunningham et al., 1966); >2,000 mg Mn/kg was required in this study to reduce growth and feed intake. In young calves fed milk replacer, 1,000 mg Mn/kg reduced weight gain and feed efficiency (Jenkins and Hidiroglou, 1991). Molybdenum Molybdenum functions as a component of the enzymes xanthine oxidase, sulfite oxidase, and aldehyde oxidase (Mills and Davis, 1987). Requirements for molybdenum, however, are not established. There is no evidence that molybdenum deficiency occurs in cattle under practical conditions, but molybdenum may enhance microbial activity in the rumen in some instances. The addition of 10 mg Mo/kg to a high-roughage diet containing 1.7 mg Mo/kg increased the rate of in situ dry matter disappearance from the rumen of cattle (Shariff et al., 1990). In situ dry matter disappearance was not improved by molybdenum supplementation when steers were fed a ground barley-based diet containing 1.0 mg Mo/kg (Shariff et al., 1990). Molybdenum added to a semipurified diet containing 0.36 mg Mo/kg improved growth and cellulose digestion in lambs (Ellis et al., 1958). In three subsequent studies with lambs fed semipurified or practical diets, no responses to added molybdenum were observed (Ellis and Pfander, 1970). FACTORS AFFECTING MOLYBDENUM UTILIZATION Metabolism of molybdenum is greatly affected by copper and sulfur with both minerals acting antagonistically. Sulfide and molybdate interact in the rumen to form thiomolybdates, resulting in decreased absorption and altered postabsorptive metabolism of molybdenum (Mills and Davis, 1987). Sulfate shares common transport systems with molybdate in the intestine and kidney, thus decreasing intestinal absorption and increasing urinary excretion of molybdate (Mills and Davis, 1987). It is well documented that relatively low dietary molybdenum can cause copper deficiency and that increasing dietary copper can overcome molybdenum toxicity. SIGNS OF MOLYBDENUM TOXICITY In cattle, high concentrations of molybdenum (20 mg Mo/kg or higher) can cause toxicity characterized by diarrhea, anorexia, loss of weight, stiffness, and changes in hair color (Ward, 1978). Providing large amounts of copper will usually overcome molybdenosis. The maximum tolerable concentration of molybdenum for cattle has been estimated to be 10 mg/kg (National Research Council, 1980). Molybdenum concentrations of less than 10 mg/kg can result in
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 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). MOLYBDENUM SOURCES 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 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). Selenium 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. SELENIUM REQUIREMENTS 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 AFFECTING SELENIUM REQUIREMENTS 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
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 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). SIGNS OF SELENIUM DEFICIENCY 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. SELENIUM SOURCES 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). SIGNS OF SELENIUM TOXICITY 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 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. ZINC REQUIREMENTS 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,
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Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 1984). Zinc requirements of beef cattle fed forage-based diets and requirements for reproduction and milk production are less well defined. Zinc supplementation increased gain in nursing calves grazing mature forages that contained 7 to 17 mg Zn/kg (Mayland et al., 1980). SIGNS OF ZINC DEFICIENCY Severe zinc deficiency in cattle results in reduced growth, feed intake, and feed efficiency; listlessness; excessive salivation; reduced testicular growth; swollen feet with open, scaly lesions; parakeratotic lesions that are most severe on the legs, neck, head, and around the nostrils; failure of wounds to heal; and alopecia (Miller and Miller, 1962; Miller et al., 1965; Ott et al., 1965; Mills et al., 1967). Thymus atrophy and impaired immune response have been observed in calves with a genetic disorder that causes impaired absorption of zinc, resulting in zinc deficiency (Perryman et al., 1989). Subclinical deficiencies of zinc can reduce weight gain (Mayland et al., 1980) and perhaps reproductive performance. Plasma or liver zinc concentrations may be used to diagnose severe zinc deficiencies, but plasma zinc determination is of little value in detecting marginal deficiencies. Stress or disease causes a redistribution of zinc in the body that can temporarily result in low plasma concentrations characteristic of a severe deficiency (Hambridge et al., 1986). FACTORS AFFECTING ZINC REQUIREMENTS Absorption of zinc occurs primarily from the abomasum and small intestine (Miller and Cragle, 1965). Zinc absorption is homeostatically controlled and cattle adjust the percentage of dietary zinc absorbed based on their need for growth or lactation (Miller, 1975). Milk contains 3 to 5 mg Zn/L, but the increased demand for milk production is likely met by increased absorption, provided that dietary zinc is present in a form that can be absorbed. Dietary factors that affect zinc requirements in ruminants are not understood. In contrast to nonruminants, high-dietary calcium does not appear to increase zinc requirements greatly in ruminants (Pond, 1983; Pond and Wallace, 1986). Phytate also does not affect zinc absorption in ruminants with a functional rumen. A relatively large portion of the zinc in forages is associated with the plant cell wall (Whitehead et al., 1985), but it is not known whether zinc’s association with fiber reduces absorption. ZINC SOURCES The zinc content of forages is affected by a number of factors including plant species, maturity, and soil zinc (Minson, 1990). Legumes are generally higher in zinc than grasses. Cereal grains usually contain between 20 and 30 mg Zn/kg, whereas plant protein sources contain 50 to 70 mg Zn/kg. Feed-grade sources of bioavailable zinc include zinc oxide, zinc sulfate, zinc methionine, and zinc proteinate. Based on available data, zinc in the sulfate and oxide form are of similar bioavailability in ruminants (Kincaid, 1979; Kegley and Spears, 1992). Absorption of zinc from zinc methionine is similar to zinc oxide, but zinc methionine appears to be metabolized differently following absorption (Spears, 1989). SIGNS OF ZINC TOXICITY The amount of zinc necessary to cause toxicity is much greater than requirements. The maximum tolerable concentration of zinc is 500 mg/kg (National Research Council, 1980). Decreased weight gain was reported in calves fed 900 mg Zn/kg for 12 weeks (Ott et al., 1966). Young calves fed milk replacer tolerated 500 mg Zn/kg for 5 weeks without adverse effects; but 700 mg/kg reduced gain, feed intake, and feed efficiency (Jenkins and Hidiroglou, 1991). REFERENCES Agricultural Research Council. 1980. The Nutrient Requirements of Ruminant Livestock. Slough, U.K.: Commonwealth Agricultural Bureaux. 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Representative terms from entire chapter: