Vitamins are unique among dietary nutrients fed to ruminants. In addition to being vital, vitamins are required in adequate amounts to enable animals to efficiently utilize other nutrients. Many metabolic processes are initiated and controlled by specific vitamins during various stages of life.
Calves from adequately fed mothers have minimal stores of vitamins at birth. Unlike the adult ruminant, a young calf does not have a fully functional rumen and active microflora, which typically contribute to vitamin synthesis. Colostrum is rich in vitamins, particularly vitamin A, provided that vitamins have been adequately supplied to the dam. Thus, a dietary supply of vitamins is typically provided to the newborn calf through colostrum. However, deficiencies of the B vitamins have been produced experimentally in calves prior to rumen development (Miller, 1979).
Intensive production systems have placed an increased emphasis on the importance of supplying adequate vitamin concentrations to meet animal requirements. Ruminants may become more susceptible to vitamin deficiencies in confinement feeding situations and when increased levels of production increase metabolic requirements for vitamins. Determining optimal vitamin concentrations—specific to age, breed, environment, and a multiplicity of other factors—facilitates management and production.
Vitamin A is likely the vitamin of most practical importance in cattle feed. The function of vitamin A at the molecular level includes production of retinaldehyde in the chromophoric group of the visual pigment or a component of the visual purple required for dim light vision (Moore, 1939, 1941). Vitamin A is also essential for normal growth and reproduction, maintenance of epithelial tissues, and bone development.
Vitamin A does not occur, as such, in plant material; however, its precursors, carotenes or carotenoids, are present in plants in various forms (a-carotene, ß-carotene, ?-carotene, and cryptoxanthin). Efficiency of conversion of carotenoids to retinol is variable in beef cattle and is generally lower than that for nonruminant animals (Ullrey, 1972). Retinyl acetate was degraded by ruminal fluid from concentrate-fed cattle more rapidly than from animals fed hay or straw (Rode et al., 1990).
Few grains, except for yellow corn, contain appreciable amounts of carotenoid; carotene is rapidly destroyed by exposure to sunlight and air, especially at high temperatures. Ensiling effectively preserves carotene but the availability of carotene from corn silage may be low (Jordan et al., 1963; Smith et al., 1964; Miller et al., 1967). High-quality forages provide carotenoid in large amounts but tend to be seasonal in availability.
The liver can store vitamin A, and these stores can serve to prevent vitamin-A deficiency. Unfortunately, liver stores are highly variable and cannot be assessed accurately without taking samples by biopsy. Furthermore, liver stores are in a dynamic state (Frey and Jensen, 1947; Hayes et al., 1967). Factors influencing deposition and removal are not well understood, but cattle exposed to drought, winter feeds of less than high-quality forage, or stresses such as high temperature or elevated nitrate intake are particularly susceptible. On a practical basis, no more than 2 to 4 months of protection from stored vitamin A can be expected, and cattle should be observed carefully for signs of deficiency whenever the diet is deficient.
A protective role for vitamin A and ß-carotene against diseases has been demonstrated (Chew, 1987). It has also been suggested that mechanisms that require ß-carotene protect the mammary gland from infection (Daniel et al., 1991). Furthermore, dietary vitamin A and ß-carotene sup-
Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 75
Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 6 Vitamins and Water Vitamins are unique among dietary nutrients fed to ruminants. In addition to being vital, vitamins are required in adequate amounts to enable animals to efficiently utilize other nutrients. Many metabolic processes are initiated and controlled by specific vitamins during various stages of life. Calves from adequately fed mothers have minimal stores of vitamins at birth. Unlike the adult ruminant, a young calf does not have a fully functional rumen and active microflora, which typically contribute to vitamin synthesis. Colostrum is rich in vitamins, particularly vitamin A, provided that vitamins have been adequately supplied to the dam. Thus, a dietary supply of vitamins is typically provided to the newborn calf through colostrum. However, deficiencies of the B vitamins have been produced experimentally in calves prior to rumen development (Miller, 1979). Intensive production systems have placed an increased emphasis on the importance of supplying adequate vitamin concentrations to meet animal requirements. Ruminants may become more susceptible to vitamin deficiencies in confinement feeding situations and when increased levels of production increase metabolic requirements for vitamins. Determining optimal vitamin concentrations—specific to age, breed, environment, and a multiplicity of other factors—facilitates management and production. FAT-SOLUBLE VITAMINS Vitamin A Vitamin A is likely the vitamin of most practical importance in cattle feed. The function of vitamin A at the molecular level includes production of retinaldehyde in the chromophoric group of the visual pigment or a component of the visual purple required for dim light vision (Moore, 1939, 1941). Vitamin A is also essential for normal growth and reproduction, maintenance of epithelial tissues, and bone development. Vitamin A does not occur, as such, in plant material; however, its precursors, carotenes or carotenoids, are present in plants in various forms (a-carotene, ß-carotene, ?-carotene, and cryptoxanthin). Efficiency of conversion of carotenoids to retinol is variable in beef cattle and is generally lower than that for nonruminant animals (Ullrey, 1972). Retinyl acetate was degraded by ruminal fluid from concentrate-fed cattle more rapidly than from animals fed hay or straw (Rode et al., 1990). Few grains, except for yellow corn, contain appreciable amounts of carotenoid; carotene is rapidly destroyed by exposure to sunlight and air, especially at high temperatures. Ensiling effectively preserves carotene but the availability of carotene from corn silage may be low (Jordan et al., 1963; Smith et al., 1964; Miller et al., 1967). High-quality forages provide carotenoid in large amounts but tend to be seasonal in availability. The liver can store vitamin A, and these stores can serve to prevent vitamin-A deficiency. Unfortunately, liver stores are highly variable and cannot be assessed accurately without taking samples by biopsy. Furthermore, liver stores are in a dynamic state (Frey and Jensen, 1947; Hayes et al., 1967). Factors influencing deposition and removal are not well understood, but cattle exposed to drought, winter feeds of less than high-quality forage, or stresses such as high temperature or elevated nitrate intake are particularly susceptible. On a practical basis, no more than 2 to 4 months of protection from stored vitamin A can be expected, and cattle should be observed carefully for signs of deficiency whenever the diet is deficient. A protective role for vitamin A and ß-carotene against diseases has been demonstrated (Chew, 1987). It has also been suggested that mechanisms that require ß-carotene protect the mammary gland from infection (Daniel et al., 1991). Furthermore, dietary vitamin A and ß-carotene sup-
OCR for page 75
Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 plementation (53,000 IU vitamin A plus 400 mg ß-carotene) to dairy cows 6 weeks before dry off and 2 weeks after dry off influence the responsiveness of bovine neutrophils and lymphocytes (Tjoelker et al., 1988a,b). Beef cattle requirements for vitamin A are 2,200 IU/kg dry feed for beef feedlot cattle; 2,800 IU/kg dry feed for pregnant beef heifers and cows; and 3,900 IU/kg dry feed for lactating cows and breeding bulls (Guilbert and Hart, 1935; Jones et al., 1938; Guilbert et al., 1940; Madsen et al., 1948; Church et al., 1956; Chapman et al., 1964; Cullison and Ward, 1965; Perry et al., 1965, 1968; Swanson et al., 1968; Kohlmeier and Burroughs, 1970; Meacham et al., 1970; Kirk et al., 1971; Eaton et al., 1972). These requirements are the same as those given in the sixth edition of this report (National Research Council, 1984); there has been no new research to determine requirements since then. An IU is defined as 0.300 µg of trans-vitamin A alcohol (retinol) or 0.550 µg of retinyl palmitate. SIGNS OF VITAMIN-A DEFICIENCY Vitamin-A deficiency results in tissue changes associated primarily with vision, bone development, and epithelial structure and maintenance. Signs of deficiency may be specific for vitamin-A deficiency or the clinical signs may be general. Vitamin-A deficiency is most likely to occur when cattle are fed high-concentrate diets; bleached pasture or hay grown during drought conditions; feeds that have received excess exposure to sunlight, air, and high temperature; feeds that have been heavily processed or mixed with oxidizing materials such as minerals; and feeds that have been stored for long periods of time. Most susceptible are newborn calves deprived of colostrum and cattle unable to establish or maintain liver stores because of environmental or dietary stresses. Attempts to improve the vitamin-A status of the newborn calf by supplementing the dam’s diet have been successful, but very high levels of vitamin-A or carotene have been necessary (Branstetter et al., 1973). Deficiencies can be corrected by increasing carotene intake by adding to the diet fresh, leafy, high-quality forages, which contain large amounts of vitamin-A precursors and vitamin E, or by supplying vitamin-A supplements in the feed or by injection. Since inefficient conversion of carotene to vitamin A is often a part of the problem, administering preformed vitamin A is preferred when deficiencies are present. Injected vitamin A is more efficiently utilized than vitamin A provided in the diet (Perry et al., 1967; Schelling et al., 1975), possibly because of extensive destruction of the vitamin in the rumen and abomasum (Keating et al., 1964; Klatte et al., 1964; Mitchell et al., 1967). Signs of vitamin-A deficiency include reduced feed intake, rough hair coat, edema of joints and brisket, lacrimation, xerophthalmia, night blindness, slow growth, diarrhea, convulsive seizures, improper bone growth, blindness, low conception rates, abortion, stillbirths, blind calves, abnormal semen, and other infections (Guilbert and Hart, 1935; Jones et al., 1938; Guilbert et al., 1940; Guilbert and Rochfort, 1940; Hart, 1940; Madsen and Earle, 1947; Madsen et al., 1948; Moore, 1957; Mitchell, 1967); however, only night blindness has proven unique to vitamin-A deficiency (Moore, 1939, 1941). Vitamin-A deficiency should be suspected when several of these symptoms are present. Clinical verification may include ophthalmoscopic examination, liver biopsy and assay, blood assay, testing spinal fluid pressure, conjunctival smears, and response to vitamin-A therapy. SIGNS OF VITAMIN-A TOXICITY Vitamin A has a wide margin of safety for use in ruminant animals. Ruminants appear to have a relatively high tolerance for vitamin A, presumably due in part to microbial degradation of vitamin A in the rumen (Rode et al., 1990). Extremely high concentrations of vitamin A can be toxic; however, toxicity is rarely a problem in livestock, unless unreasonably high concentrations are fed inadvertently (National Research Council, 1987). Vitamin D As a general term, vitamin D encompasses a group of closely related antirachitic compounds. There are two primary forms of vitamin D: ergocalciferol (vitamin D2), which is derived from the plant steroid, ergosterol; and cholecalciferol (vitamin D3), which is derived from the precursor 7-dehydrocholesterol and is found only in animal tissues or products. Vitamin D is required for calcium and phosphorus absorption, normal mineralization of bone, and mobilization of calcium from bone. In addition, a regulatory role in immune cell function of vitamin D (1,25-dihydroxy D) has been suggested (Reinhardt and Hustmyer, 1987). Research in laboratory animals (DeLuca, 1974) indicates that before serving these functions, vitamin D must be metabolized to active forms. Vitamin D is absorbed from the diet in the intestinal tract in association with lipids and the presence of bile salts. Once in the liver, one metabolite (25-hydroxy-vitamin-D3) is formed, which is about four times as active as vitamin D. This major circulating metabolite of vitamin D is then transported to the kidney, where another vitamin D metabolite (1,25-dihydroxy-vitamin-D3) is formed. This form is
OCR for page 75
Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 about five times as active as 25-hydroxy-vitamin-D3 (Horst and Reinhardt, 1983). How vitamin D is degraded in the rumen (Parakkasi et al., 1970; Sommerfeldt et al., 1979) may be of practical significance when considering how the vitamin D should be administered. Sommerfeldt et al. (1983) indicated that orally administered tritium-labeled vitamin D2 has one-third to one-half the activity of tritium-labeled vitamin D3. The vitamin D requirement of beef cattle is 275 IU/kg dry diet. The IU is defined as 0.025 µg of cholecalciferol (D3) or its equivalent. Ergocalciferol (D2) also is active in cattle. Unlike aquatic species that store appreciable amounts of vitamin D in the liver, most land mammals, including ruminants, do not maintain body stores of vitamin D. However, because vitamin D is synthesized by beef cattle exposed to sunlight or fed sun-cured forages, these animals rarely require vitamin D supplementation. SIGNS OF VITAMIN-D DEFICIENCY The most clearly defined sign of vitamin-D deficiency in calves is rickets, caused by the failure of bone to assimilate and use calcium and phosphorus normally. Accompanying evidence frequently includes a decrease in calcium and inorganic phosphorus in the blood, swollen and stiff joints, anorexia, irritability, tetany, and convulsions. In older animals with a vitamin-D deficiency, bones become weak and easily fractured and posterior paralysis may accompany vertebral fractures. Calves may be born dead, weak, or deformed (Rupel et al., 1933; Wallis, 1944; Warner and Sutton, 1948; Stillings et al., 1964). General clinical signs of vitamin-D deficiency include decreased appetite and growth rate, digestive disturbances, labored breathing, and weakness. SIGNS OF VITAMIN-D TOXICITY Intakes of excessive amounts of vitamin D can result in a variety of effects. Most commonly, blood calcium concentration becomes abnormally high as a result of increased bone resorption and increased intestinal absorption of calcium. This can result in widespread calcification of soft tissues and bone demineralization. Other signs of vitamin-D toxicity include loss of appetite and weight loss (National Research Council, 1987). Vitamin E Vitamin E occurs naturally in feedstuffs as a-tocopherol. Other forms exist such as ß, ?, d, ?, ?, and ?; and all may occur in feedstuffs isolated from the oils of plants. Of the several compounds that have vitamin E activity, the naturally occurring compound having the highest vitamin E activity is RRR-a-tocopherol (formerly D-a-tocopherol), with a biopotency equivalent to 1.36 moles of all-rac-a-tocopherol (U.S. Pharmacopeia, 1985). All-rac-a-tocopherol is a synthetic mixture of eight stereoisomers. Tocopherul acetate does not occur naturally, but is often used in animal diets. The alcohol group linked to the acetate prevents the tocopherol from being destroyed in the diet and, when consumed, the ester is hydrolyzed in the intestine to make the tocopherol available for absorption. Terms for expressing vitamin E activity have changed over the years. The current preferred expression of vitamin E activity is in molar concentration and conversion equivalents for IU expression (now obsolete) are presented below: 1 mg all-rac-a-tocopheryl acetate=1 International Unit 0.74 mg RRR-a-tocopheryl acetate=1 International Unit 0.91 mg all-rac-a-tocopherol=1 International Unit 0.67 mg RRR-a-tocopherol=1 International Unit Determining vitamin E requirements of ruminants is difficult because of this vitamin’s interrelationships with other dietary components. Vitamin E requirements depend on concentrations of antioxidants, sulfur-containing amino acids, and selenium in the diet. In addition, high dietary concentrations of polyunsaturated fatty acids present in unsaturated oils such as corn oil, linseed oil, and soybean oil can significantly increase vitamin E requirements. Detrimental effects of polyunsaturated fatty acids may be somewhat reduced in the ruminant animal because ruminal microorganisms are capable of fatty acid saturation; however, some polyunsaturated fatty acids may escape ruminal hydrogenation (McMurray et al., 1980). Vitamin E is not stored in the body in large concentrations. In general, vitamin E may be found in many tissues, with the highest amounts found in liver and adipose tissue. Thymus, muscle, kidney, lung, spleen, heart, and adrenal tissues increase concentration of vitamin E when high concentrations of vitamin E are in the diet. When 300 IU vitamin E/day was fed for 266 days to finishing steers, less discoloration of the muscle tissue occurred during refrigeration storage. A short-term feeding regimen (67 days of 1,266 IU vitamin E/day or 30 days of 1,317 IU vitamin E/day) resulted in similar improvements (Arnold et al., 1992). D-a sources of tocopherol in plasma and tissues were increased after feeding 1,000 IU of either D or DL sources of acetate or alcohol for 28 days (Hidiroglou et al., 1988). Vitamin E serves various functions including its role as an inter- and intracellular antioxidant and in the formation of structural components of biological membranes. The role of vitamin E as a biological antioxidant and a free radical scavenger in the immune system and in disease resistance has been documented (Tappel, 1972; Hoekstra, 1975; McCay and King, 1980). Jersey steers fed 1,000 IU of vitamin E as DL-a-tocopherol acetate for 6 months had
OCR for page 75
Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 higher interleukin-1 in the cells than did other steers. (See also Chapter 8.) Vitamin E functions as an antioxidant in cellular membranes and has been widely used to protect and facilitate the uptake and storage of vitamin A (Perry et al., 1968). Its action in metabolism is not clearly defined but is linked closely with selenium (Muth et al., 1958; Hoekstra, 1975). Vitamin E functions in the maintenance of structural and functional integrity of skeletal muscle, cardiac muscle, smooth muscle, and the peripheral vascular system. There are many factors that influence the stability of vitamin E in feeds—heat, oxygen, moisture, unsaturated fatty acids, trace minerals, and high nitrates (Bunyan et al., 1961). Physical changes during storage also influence the stability of vitamin E in feeds; with natural drying, corn may lose 15 to 25 percent of vitamin E (Pond et al., 1971; Young et al., 1975; Bauernfeind, 1980). Also, high-moisture feeds lose vitamin E more rapidly than dry feed (Adams, 1982; Harvey and Bieber-Wlaschny, 1988). Adequate amounts of vitamin E may not be available from feedstuffs; thus, formulating diets to ensure adequate concentrations of vitamin E is more difficult. The vitamin E requirement for beef cattle has not been established but is estimated to be between 15 and 60 IU/kg dry diet for young calves. Even diets very low in vitamin E did not affect growth, reproduction, or lactation when fed to cattle for four generations (Gullickson and Calverley, 1946). A depletion and refeeding study was conducted with vitamin E, and the data indicate that the requirement for optimum growth of growing finishing steers was 50 to 100 units of vitamin E added in the feed daily (Hutcheson and Cole, 1985). SIGNS OF VITAMIN-E DEFICIENCY Vitamin-E deficiencies can be precipitated or accentuated by the intake of unsaturated fats. Signs of deficiencies in young calves are characteristic of white-muscle disease; they include general muscular dystrophy, weak leg muscles, crossover walking, impaired suckling ability caused by dystrophy of tongue muscles, heart failure, paralysis, and hepatic necrosis (Stafford et al., 1954; Muth et al., 1958). Animals exhibiting deficiency signs, particularly white-muscle disease, may respond to either selenium or vitamin E or may require both. Vitamin E supplements the action of glutathione peroxidase, a selenium-containing enzyme. (Vitamin E and selenium interactions are discussed in the selenium section in Chapter 5.) SIGNS OF VITAMIN-E TOXICITY Vitamin-E toxicity has not been demonstrated in ruminants and there seems to be a wide margin of safety regarding the use of vitamin E in most animals. Of the major fat-soluble vitamins, the risk of toxicity is less with vitamin E than with vitamins A and D (National Research Council, 1987). Vitamin K The term vitamin K is used to describe a group of quinone fat-soluble compounds that have characteristic anti-hemorrhagic effects. Vitamin K is required for the synthesis of plasma clotting factors prothrombin (factor II), proconvertin (factor VII), Christmas factor (factor IX), and Stuart-Prower factor (factor X). Two major natural sources of vitamin K are the phylloquinones (vitamin K1), found in plant sources, and the menaquinones (vitamin K2), which are produced by bacterial flora. For ruminants, vitamin K2 is the most significant source of vitamin K, since it is synthesized in large quantities by bacterial flora in the rumen. Vitamin K1 is abundant in pasture and green roughages. Both forms possess similar biological activity and function in blood clotting. SIGNS OF VITAMIN-K DEFICIENCY The only sign of deficiency to be reported in cattle is the “sweet clover disease” syndrome. This results from the metabolic antagonistic action of dicoumarol that occurs when an animal consumes moldy or improperly cured sweet clover hay. Consumption of dicoumarol, a fungal metabolite produced from substrates in sweet clover hay, leads to prolonged blood clotting and has caused death from uncontrolled hemorrhages. It is important to note that dicoumarol passes through the placenta, and thus, the fetus of pregnant animals may be affected. The initial appearance and severity of signs associated with dicoumarol poisoning are directly related to the dicoumarol content of the hay consumed. If low levels are consumed, then clinical signs may not appear for several months. Mild cases can be treated effectively with vitamin K (McElroy and Goss, 1940a; Link, 1959). SIGNS OF VITAMIN-K TOXICITY Few systematic studies of the effects of excess vitamin K have been conducted in ruminant animals. Toxicity associated with excessive oral intake of phylloquinone or menadione has not been demonstrated in beef cattle. The toxic dietary level of menadione is at least 1,000 times the dietary requirement (National Research Council, 1987). WATER-SOLUBLE VITAMINS Vitamin B12 Vitamin B12 is a generic descriptor for a group of compounds that have vitamin B12 activity. One of the unique
OCR for page 75
Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 features of vitamin B12 is that it contains 4.5 percent cobalt. The naturally occurring forms of vitamin B12 are adenosyl-cobalamin and methylcobalamin and these are found in plant and animal tissues. Cyanocobalamin, an artificially produced form of vitamin B, is used extensively because it is relatively stable and readily available. The primary functions of vitamin B12 involve metabolism of nucleic acids and proteins, in addition to metabolism of fats and carbohydrates. Specifically, this vitamin plays a role in purine and pyrimidine synthesis, transfer of methyl groups, protein formation, and metabolism of fats and carbohydrates. Vitamin B12 is of special interest in ruminant nutrition because of its role in propionate metabolism (Marston et al., 1961) and the practical incidence of vitamin-B12 deficiency as a secondary result of cobalt deficiency. The ruminant’s requirement for vitamin B12 is higher than the nonruminant’s requirement and is associated with the requirement for cobalt, since this trace mineral is a component of vitamin B12. Cobalt content of the diet is the primary limiting factor for ruminal microorganism synthesis of vitamin B12. Substantial areas of the United States, Australia, and New Zealand have soils without enough cobalt to produce adequate concentrations in plants to support optimum vitamin B12 synthesis in the rumen (Ammerman, 1970). (For additional information on cobalt, see Chapter 5.) SIGNS OF VITAMIN-B12 DEFICIENCY A vitamin-B12 deficiency is difficult to distinguish from a cobalt deficiency. The signs of deficiency may not be specific and can include poor appetite, retarded growth, and poor condition. In severe deficiencies, muscular weakness and demyelination of peripheral nerves occurs. In young ruminant animals, vitamin-B12 deficiency can occur when rumen microbial flora are not yet fully developed. Thiamin Thiamin functions in all cells as a coenzyme cocarboxylase. Thiamin is the coenzyme responsible for all enzymatic carboxylations of a-keto acids in the tricarboxylic acid cycle, which provides energy to the body. Thiamin also plays a key role in glucose metabolism, as a coenzyme in the pentose phosphate pathway. Thiamin antimetabolites have been found in raw fish products and bracken fern (Somogyi, 1973). Polioencephalomalacia (PEM), a central nervous system disorder, in grain-fed cattle and sheep has been linked to thiaminase activity or production of a thiamin antimetabolite in the rumen (Loew and Dunlop, 1972; Sapienza and Brent 1974). Affected animals have responded to intravenous administration of thiamin (2.2 mg/kg BW). Thiamin analogs produced in the rumen by thiaminase I in the presence of a cosubstrate appeared to be responsible for PEM (Brent and Bartley, 1984). Supplementation of high-concentrate diets with thiamin, however, yield inconsistent results (Grigat and Mathison, 1982, 1983). Synthesis of thiamin by rumen microflora makes it difficult to establish a ruminant requirement. Animals with a functional rumen can generally synthesize an adequate amount of thiamin. However, the synthesis of thiamin is subject to dietary factors including levels of carbohydrate and nitrogen. In addition, high sulfur diets have been associated with thiamin deficiency and PEM, a laminar softening or degeneration of brain gray matter in steers (Gould et al., 1991). Animal size, genetic factors, and physiological status also influence thiamin requirements. SIGNS OF THIAMIN DEFICIENCY In all species, a thiamin deficiency results in central nervous system disorders, since thiamin is an important component of the biochemical reactions that break down glucose to supply energy to the brain. Other signs of thiamin deficiency include weakness, retracted head, and cardiac arrhythmia. As with other water-soluble vitamins, deficiencies can result in slowed growth, anorexia, and diarrhea. Niacin Niacin functions in carbohydrate, protein and lipid metabolism as a component of the coenzyme forms of nicotinamide, nicotinamide adenine dinucleotide (NAD), and nicotinamide adenine dinucleotide phosphate (NADP). Niacin is particularly important in ruminants because it is required for liver detoxification of portal blood NH3 to urea and liver metabolism of ketones in ketosis. Niacin has been reported to enhance protein synthesis by ruminal microorganisms (Riddell et al., 1980, 1981). Niacin synthesis in the rumen seemed adequate when no niacin was added to the diet; however, when 6 g was added per day, an increase in niacin flow from the rumen occurred (Riddell et al., 1985). Supplemental niacin was more effective in increasing microbial protein synthesis with urea than soybean meal (Brent and Bartley, 1984). Responses to supplemental niacin of feedlot cattle have been variable. Niacin is supplied to the ruminant from three primary sources: dietary niacin, conversion of tryptophan to niacin, and ruminal synthesis. Although niacin is normally synthesized in adequate quantities in the rumen, there are several factors that can influence ruminant niacin requirements (Olentine, 1984). These factors include protein (amino acid) balance, dietary energy supply, dietary rancidity, de novo synthesis, and availability of niacin in feeds. Excess leucine, arginine, and glycine increase the niacin requirement; whereas increasing dietary tryptophan decreases the
OCR for page 75
Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 niacin requirement. High-energy diets and the use of particular antibiotics can increase the requirement for niacin. SIGNS OF NIACIN DEFICIENCY Young ruminants are most susceptible to niacin deficiencies, and a dietary source of niacin or tryptophan is required until the rumen is fully developed. The first signs of niacin deficiency in most species are loss of appetite, reduced growth, general muscular weakness, digestive disorders, and diarrhea. The skin may also be affected with a scaly dermatitis. Often, these signs are followed by a microcytic anemia. Choline Choline is essential for building and maintaining cell structure throughout the body and for the formation of acetylcholine, the compound responsible for transmission of nerve impulses. Abnormal accumulation of fat is prevented by the lipotropic actions of choline, and labile methyl groups are furnished by choline for formation of methionine. All naturally occurring fats contain choline, but little information is available on the biological availability of choline in feeds. Unlike most vitamins, choline can be synthesized by most animal species. Because ruminants synthesize choline, a requirement has not been determined; however, it has been recommended that milk-fed calves receive supplementation of 0.26% choline in milk replacers. Choline from dietary sources is only of value to adult animals if it can escape rumen degradation. Rumsey (1985) determined that for choline-supplemented steers fed an all-concentrate diet, supplementation did not affect feedlot performance, carcass measurements, acidosis, or products of rumen fermentation. However, increasing dietary rumen protected choline (0.24 percent) produced a linear increase in milk production for lactating dairy cows (Erdman and Sharma, 1991). SIGNS OF CHOLINE DEFICIENCY Calves fed a synthetic milk diet containing 15 percent casein exhibited apparent signs of choline deficiency. Within a week, calves developed extreme weakness, labored breathing, and were unable to stand. Supplementation with 260 mg choline/L milk replacer alleviated the signs of choline deficiency. Summary B vitamins are abundant in milk and many other feeds, and synthesis of B vitamins by ruminal microorganisms is extensive (McElroy and Goss, 1940a,b; 1941a,b; Wegner et al., 1940, 1941; Hunt et al., 1943) and begins very soon after the introduction of dry feed into the diet (Conrad and Hibbs, 1954). As the concentration in the diet increases, thiamin results in a net loss; whereas niacin increases substantially in the rumen, while the duodenal concentration of thiamin, niacin, riboflavin, and biotin does not change (Miller et al., 1986a,b). Niacin decreases in the duodenum and ileum when monensin is added (22 mg/kg diet), while thiamin, riboflavin, and biotin are not affected. Signs of insufficient intake of B complex vitamins have been clearly demonstrated for thiamin (Johnson et al., 1948), riboflavin (Wiese et al., 1947), pyridoxine (Johnson et al., 1950), pantothenic acid (Sheppard and Johnson, 1957), biotin (Wiese et al., 1946), nicotinic acid (Hopper and Johnson, 1955), vitamin B12 (Draper et al., 1952; Lassiter et al., 1953), and choline (Johnson et al., 1951) in young calves. The established metabolic functions of B vitamins are important and consequently, a physiological need for most B vitamins can be assumed for cattle of all ages. Attempts to obtain responses to other B vitamins are numerous, but the overall results are considered inconclusive. Although B vitamin synthesis is altered by diet, considerable change is possible without producing signs of deficiency (Hayes et al., 1966; Clifford et al., 1967). Supplemental riboflavin, niacin, folic acid, B12, and ascorbic acid are degraded and/or absorbed anterior to the small intestine, while biotin and pantothenic acid primarily escape the rumen (Zinn et al., 1987). As a result, practical vitamin-B deficiency is limited to young animals with immature rumen development and situations in which an antagonist is present or ruminal synthesis is limited by lack of precursors. WATER Water constitutes approximately 98 percent of all molecules in the body. Water is needed for regulation of body temperature as well as for growth, reproduction, and lactation; digestion; metabolism; excretion; hydrolysis of protein, fat, and carbohydrates; regulation of mineral homeostasis; lubrication of joints; nervous system cushioning; transporting sound; and eyesight. Water is an excellent solvent for glucose, amino acids, mineral ions, water-soluble vitamins, and metabolic waste transported in the body. Water intake from feeds plus that consumed ad libitum as free water is approximately equivalent to the water requirements of cattle. Water requirement is influenced by several factors, including rate and composition of gain, pregnancy, lactation, activity, type of diet, feed intake, and environmental temperature. Restriction of water intake reduces feed intake (Utley et al., 1970), which results in lower production. However,
OCR for page 75
Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 water restriction also tends to increase apparent digestibility and nitrogen retention. The minimum requirement of cattle for water is a reflection of that needed for body growth and for fetal growth or lactation and that lost by excretion in the urine, feces, or sweat or by evaporation from the lungs or skin. Anything influencing these needs or losses will influence the minimum requirement. Cattle lose water from the body through excretion from the kidney as urine and from the gastrointestinal tract as feces, as sweat, and by water vapor from skin and lungs. The amount of urine produced daily varies with the activity of the animal, air temperature, and water consumption as well as certain other factors. The antidiuretic hormone vasopressin controls reabsorption of water from the kidney tubules and ducts; thus, it affects excretion of urine. Under conditions of restricted water intake, the body may resorb a greater amount of water than usual, thus concentrating urine. Although this capacity to concentrate urine solutes is limited, it can reduce water requirements by a small amount. Water requirements can increase when a diet is high in protein, salt, minerals, or diuretic substances. The amount of water lost in the feces depends largely on the diet. Succulent diets and diets with high mineral content contribute to more water in the feces. The amount of water lost through evaporation from the skin or lungs is important and may even exceed that lost in TABLE 6–1 Approximate Total Daily Water Intake of Beef Cattlea Weight Temperature in °F (°C)b 40 (4.4) 50 (10.0) 60 (14.4) 70 (21.1) 80 (26.6) 90 (32.2) kg lb Liter Gal Liter Gal Liter Gal Liter Gal Liter Gal Liter Gal Growing heifers, steers, and bulls 182 400 15.1 4.0 16.3 4.3 18.9 5.0 22.0 5.8 25.4 6.7 36.0 9.5 273 600 20.1 5.3 22.0 5.8 25.0 6.6 29.5 7.8 33.7 8.9 48.1 12.7 364 800 23.0 6.3 25.7 6.8 29.9 7.9 34.8 9.2 40.1 10.6 56.8 15.0 Finishing cattle 273 600 22.7 6.0 24.6 6.5 28.0 7.4 32.9 8.7 37.9 10.0 54.1 14.3 364 800 27.6 7.3 29.9 7.9 34.4 9.1 40.5 10.7 46.6 12.3 65.9 17.4 454 1,000 32.9 8.7 35.6 9.4 40.9 10.8 47.7 12.6 54.9 14.5 78.0 20.6 Wintering pregnant cowsc 409 900 25.4 6.7 27.3 7.2 31.4 8.3 36.7 9.7 — — — — 500 1,100 22.7 6.0 24.6 6.5 28.0 7.4 32.9 8.7 — — — — Lactating cowsd 409 900 43.1 11.4 47.7 12.6 54.9 14.5 64.0 16.9 67.8 17.9 61.3 16.2 Mature bulls 636 1,400 30.3 8.0 32.6 8.6 37.5 9.9 44.3 11.7 50.7 13.4 71.9 19.0 727 1,600+ 32.9 8.7 35.6 9.4 40.9 10.8 47.7 12.6 54.9 14.5 78.0 20.6 aWinchester and Morris (1956). bWater intake of a given class of cattle in a specific management regime is a function of dry matter intake and ambient temperature. Water intake is quite constant up to 40 °F (4.4 °C). cDry matter intake has a major influence on water intake. Heavier cows are assumed to be higher in body condition and to require less dry matter and, thus, less water intake. dCows larger than 409 kg (900) lbs are included in this recommendation. the urine. If temperature and/or physical activity increase, water loss through evaporation and sweating increases. Because feeds themselves contain some water and the oxidation of certain nutrients in feeds produces water, not all water must be provided by drinking. Feeds such as silage, green chop, or growing pasture forage are usually very high in moisture, while grains, hays, and dormant pasture forage are low in moisture. High-energy feeds produce much metabolic water; low-energy feeds produce a lesser amount. These are obvious complications in the matter of assessing water requirements. Fasting animals or those fed a low-protein diet may form water from the destruction of body protein or fat, but this is of minor significance. The results of water requirement studies conducted under various conditions imply that thirst is a result of need and that animals drink to fill this need. The need results from an increase in the electrolyte concentration in the body fluids, which activates the thirst mechanism. As this discussion suggests, water requirements are affected by many factors, and it is impossible to list specific requirements with accuracy. A water equation for feedlot steers has been developed by Hicks et al. (1988):
OCR for page 75
Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 MT is the maximum temperature in degrees fahrenheit, DMI is dry matter intake in kg fed daily, PP is precipitation in cm/day, DS is the percent of dietary salt. However, the major influences on water intake in beef cattle fed typical rations are dry matter intake, environmental temperature, and stage and type of production. Table 6–1 has been designed as a guide only, and it must be used with respect to the influences of water intake. Water quality is important in maintaining water consumption of cattle. Cattle consume water from surface water sources such as ponds, lakes, and streams and from ground water sources such as wells. Beef cattle requirements for water are a function of different metabolic priorities. Restricting water intake to less than the animal’s requirement will reduce cattle performance. For more detailed information on toxic substances in water, refer to the National Research Council publication Nutrients and Toxic Substances in Water for Livestock and Poultry (National Research Council, 1974). REFERENCES Adams, C.R. 1982. Feedlot cattle need supplemental vitamin E. Feedstuffs 54(18):24–26. Ammerman, C.B. 1970. Recent developments in cobalt and copper in ruminant nutrition: A review. J. Dairy Sci. 53:1097–1107. Arnold, R.N., K.K.Scheller, S.C.Arp, S.N.Williams, D.R.Buege, and D.M.Schaefer. 1992. Effect of long- or short-term feeding of alpha-tocopherol acetate to Holstein and crossbred beef steers on performance, carcass characteristics and beef stability. J. Anim. Sci. 70:3055–3065. Bauernfeind, J. 1980. Tocopherols in food. Pp. 99–168 in Vitamin E: A Comprehensive Treatis, L.J.Machlin, ed. New York: Marcel Dekker. Branstetter, R.F., R.E.Tucker, G.E.Mitchell, Jr., J.A.Boling, and N.W.Bradley. 1973. Vitamin A transfer from cows to calves. Int. J. Vit. Nutr. Res. 2:142–146. Brent, B.E., and E.E.Bartley. 1984. Thiamin and niacin in the rumen. J. Anim. Sci. 59:813–822. Bunyan J., D.McHale, J.Green, and S.Marcinkiewicz. 1961. Forms of vitamin E and their activity. Br. J. Nutr. 15:253. Chapman, H.L., Jr., R.L.Shirley, A.Z.Palmer, C.E.Haines, J.W.Carpenter, and T.J.Cunha. 1964. Vitamins A and E in steer fattening rations on pasture. J. Anim. Sci. 23:669–673. Chew, B.P. 1987. Symposium: Immune function: Relationship of nutrition and disease control: Vitamin A and beta-carotene on host defense. J. Dairy Sci. 70:2732–2743. Church, D.C., L.S.Pope, and R.MacVicar. 1956. Effect of plane of nutrition of beef cows on depletion of liver vitamin A during gestation and on carotene requirements during lactation. J. Anim. Sci. 15:1078–1088. Clifford, A.J., R.D.Goodrich, and A.D.Tillman. 1967. Effects of supplementing ruminant all-concentrate and purified diets with vitamins of the B complex. J. Anim. Sci. 26:400–403. Conrad, H.R., and J.W.Hibbs. 1954. A high roughage system for raising calves based on early rumen development. IV. Synthesis of thiamin and riboflavin in the rumen as influenced by ratio of hay to grain fed and initiation of dry feed consumption. J. Dairy Sci. 37:512–522. Cullison, A.E., and C.S.Ward. 1965. Coastal Bermuda grass hay as a source of vitamin A for beef cattle. J. Anim. Sci. 24:969–972. Daniel, L.R., B.P.Chew, T.S.Tanaka, and L.W.Tjoelker. 1991. In vitro effects of ß-carotene and vitamin A on peripartum bovine peripheral blood mononuclear cell proliferation. J. Dairy Sci. 74:911–915. DeLuca, H.F. 1974. Vitamin D: The vitamin and the hormone. Fed. Proc. 33:2211–2219. Draper, H.H., J.T.Sime, and B.C.Johnson. 1952. A study of vitamin B12 deficiency in the calf. J. Anim. Sci. 11:332–340. Eaton, H.D., J.E.Rousseau, Jr., R.C.Hall, Jr., H.I.Frier, and J.J.Lucas. 1972. Reevaluation of the minimum vitamin A requirement of Holstein male calves based upon elevated cerebrospinal fluid pressure. J. Dairy Sci. 55:232–237. Erdman, R.A., and B.K.Sharma. 1991. Effect of dietary rumen-protected choline in lactating dairy cows. J. Dairy Sci. 74:1641–1647. Frey, R.R., and R.Jensen. 1947. Depletion of vitamin A reserves in the livers of cattle. Science 105:313. Gould, D.H., M.M.McAllister, J.C.Savage, and D.W.Hamar. 1991. High sulfide concentrations in rumen fluid associated with nutritionally induced polioencephalomalacia in calves. Am. J. Vet. Res. 52: 1164–1167. Grigat, G.A., and G.W.Mathison. 1982. Thiamin supplementation of all-concentrate diet for feedlot steers. Can. J. Anim. Sci. 62:807–819. Grigat, G.A., and G.W.Mathison. 1983. Thiamin and magnesium supplementation diets for feedlot steers. Can. J. Anim. Sci. 63:117–131. Guilbert, H.R., and G.H.Hart. 1935. Minimum vitamin A with particular reference to cattle. J. Nutr. 10:409–427. Guilbert, H.R., and L.H.Rochfort. 1940. Beef production in California. Calif. Agric. Exp. Stn. Circ. 11. Guilbert, H.R., C.E.Howell, and G.H.Hart. 1940. Minimum vitamin A and carotene requirement of mammalian species . J. Nutr. 19:91–103. Gullickson, T.W., and C.W.Calverley. 1946. Cardiac failure in cattle on the vitamin E-free rations as revealed by electrocardiograms. Science 104:312. Hart, G.H. 1940. Vitamin A deficiency and requirements of farm mammals. Nutr. Abstr. Rev. 10:261. Harvey, J.D., and M.Bieber-Wlaschny. 1988. Vitamin E availability to livestock varies dramatically. Feedstuffs:15–17. Hayes, B.W., G.E.Mitchell, Jr., C.O.Little, and N.W.Bradley. 1966. Concentrations of B vitamins in ruminal fluid of steers fed different levels and physical forms of hay and grain. J. Anim. Sci. 25:539–542. Hayes, B.W., G.E.Mitchell, Jr., C.O.Little, and H.B.Sewell. 1967. Turnover of liver vitamin A in steers. J. Anim. Sci. 26:855–857. Hicks, R.B., F.N.Owens, D.R.Gill, J.J.Martin, and C.A.Strasia. 1988. Water intake by feedlot steers. Okla. Anim. Sci. Rpt. Mp-125:208. Hidiroglou, N., L.F.Laflamme, and L.R.McDowell. 1988. Blood plasma and tissue concentrations of vitamin E in beef cattle as influenced by supplementation of various tocopherol compounds. J. Anim. Sci. 66:3227–3234. Hoekstra, W.G. 1975. Biochemical function of selenium and its relation to vitamin E. Fed. Proc. 34:2083–2089. Hopper, J.H., and B.C.Johnson. 1955. The production and study of an acute nicotinic acid deficiency in the calf. J. Nutr. 56:303–310. Horst, R.L., and T.A.Reinhardt. 1983. Vitamin D metabolism in ruminants and its relevance to the periparturient cow. J. Dairy Sci. 66:661–678. Hunt, C.H., E.W.Burroughs, R.M.Bethke, A.F.Schalk, and P. Gerlaugh. 1943. Further studies on riboflavin and thiamin in the rumen contents of cattle. II. J. Nutr. 25:207–216. Hutcheson, D.P., and N.A.Cole. 1985. Vitamin E and selenium for yearling feedlot cattle. Fed. Am. Soc. Exp. Biol. (abst.) 69:807. Johnson, B.C., T.S.Hamilton, W.B.Nevens, and L.E.Boley. 1948. Thiamin deficiency in the calf. J. Nutr. 35:137–145. Johnson, B.C., J.A.Pinkos, and K.A.Burke. 1950. Pyridoxine deficiency in the calf. J. Nutr. 40:309–322.
OCR for page 75
Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 Johnson, B.C., H.H.Mitchell, and J.A.Pinkos. 1951. Choline deficiency in the calf. J. Nutr. 43:37–48. Jones, J.H., J.K.Riggs, G.S.Fraps, J.M.Jones, H.Schmidt, R.E. Dickson, P.E.Howe, and W.H.Black. 1938. Carotene requirements for fattening beef cattle. Proc. Am. Soc. Anim. Prod. 94:102. Jordan, H.A., G.S.Smith, A.L.Neumann, J.E.Zimmerman, and G. W.Breniman. 1963. Vitamin A nutrition of beef cattle fed corn silage. J. Anim. Sci. 22:738–745. Keating, E.K., W.H.Hale, and F.Hubbert, Jr. 1964. In vitro degradation of vitamin A and carotene by rumen liquor. J. Anim. Sci. 23:111–117. Kirk, W.G., R.L.Shirley, J.F.Easley, and F.M.Peacock. 1971. Effect of carotene-deficient rations and supplemental vitamin A on gain, feed utilization and liver vitamin A of calves. J. Anim. Sci. 33:476–480. Klatte, F.J., G.E.Mitchell, Jr., and C.O.Little. 1964. In vitro destruction of vitamin A by abomasal and ruminal contents. J. Agric. Food Chem. 12:420–421. Kohlmeier, R.H., and W.Burroughs. 1970. Estimation of critical of plasma and liver vitamin A levels in feedlot cattle with observation upon influences of body stores and daily dietary requirements. J. Anim. Sci. 30:1012–1018. Lassiter, C.A., G.M.Ward, C.F.Huffman, C.W.Duncan, and H.D. Webster. 1953. Crystalline vitamin B12 requirement of the young dairy calf. J. Dairy Sci. 36:997–1005. Link, K.P. 1959. The discovery of dicumarol and its sequels. Circulation 19:97. Loew, F.M., and R.H.Dunlop. 1972. Induction of thiamin inadequacy and polioencephalomalacia in adult sheep with Amprolium. Am. J. Vet. Res. 33:2195. Madsen, L.L., and I.P.Earle. 1947. Some observations on beef cattle affected with generalized edema or anasarca due to vitamin A deficiency. J. Nutr. 34:603–619. Madsen, L.L., O.N.Eaton, L.Memmstra, R.E.Davis, C.A.Cabell, and B.Knapp, Jr. 1948. Effectiveness of carotene and failure of ascorbic acid to increase sexual activity and semen quality of vitamin A deficient beef bulls. J. Anim. Sci. 7:60–69. Marston, H.R., S.H.Allen, and R.M.Smith. 1961. Primary metabolic defect supervening on vitamin B12 deficiency in sheep. Nature 190:1085–1091. McCay, P.B., and M.M.King. 1980. Vitamin E: Its role as a biologic free radical scaveneger and its relationship to the microsomal mixed-function oxidase system. Pp. 289–317 in Vitamin E: Comprehensive Treatise, L.J.Machlin, ed. New York: Marcel Dekker. McElroy, L.W., and H.Goss. 1940a. A quantitative study of vitamins in the rumen contents of sheep and goats fed vitamin-low diets. I. Riboflavin and vitamin K. J. Nutr. 20:527–540. McElroy, L.W., and H.Goss. 1940b. A quantitative study of vitamins in the rumen contents of sheep and goats fed vitamin-low diets. II. Vitamin B6 (pyridoxine). J. Nutr. 20:541–550. McElroy, L.W., and H.Goss. 1941a. A quantitative study of vitamins in the rumen contents of sheep and cows fed vitamin-low diets. III. Thiamin. J. Nutr. 21:163–173. McElroy, L.W., and H.Goss. 1941b. A quantitative study of vitamins in the rumen contents of sheep and cows fed vitamin-low diets. IV. Pantothenic acid. J. Nutr. 21:405–409. McMurray, C.H., D.A.Rice, and W.J.Blanchflower. 1980. Changes in plasma levels of linoleic and linolenic acids in calves recently introduced to spring pasture. Proc. Nutr. Soc. 39:65. Meacham, T.N., K.P.Bovard, B.M.Priode, and J.P.Fontenot. 1970. Effect of supplemental vitamin A on the performance of beef cows and their calves. J. Anim. Sci. 31:428–433. Miller, B.L., J.C.Meiske, and R.D.Goodrich. 1986a. Effects of grain source and concentrate level on B-vitamin production and absorption in steers. J. Anim. Sci. 62:473–483. Miller, B.L., J.C.Meiske, and R.D.Goodrich. 1986b. Effects of grain source and concentrate level on B-vitamin production and absorption in steers. J. Anim. Sci. 62:484–496. Miller, R.W., R.W.Hemken, D.R.Waldo, and L.H.Moore. 1967. Vitamin A metabolism in steers fed corn silage or alfalfa hay pellets. J. Dairy Sci. 50:997. Miller, W.J. 1979. Dairy cattle feeding and nutrition. Academic Press, New York. Mitchell, G.E., Jr. 1967. Vitamin A nutrition of ruminants. J. Am. Vet. Med. Assoc. 151:430. Mitchell, G.E., Jr., C.O.Little, and B.W.Hayes. 1967. Pre-intestinal destruction of vitamin A by ruminants fed nitrates. J. Anim. Sci. 26:827–829. Moore, L.A. 1939. Carotene intake, level of blood plasma carotene, and the development of papillary edema and nyctalopia in calves. J. Dairy Sci. 22:803. Moore, L.A. 1941. Some ocular changes and deficiency manifestations in mature cows fed a ration deficient in vitamin A. J. Dairy Sci. 24:893. Moore, T. 1957. Vitamin A. Amsterdam: Elsevier. Muth, O.H., J.E.Oldfield, L.F.Remmert, and J.P.Schubert. 1958. Effect of selenium and vitamin E on white muscle disease. Science 128:1090. National Research Council. 1974. Nutrients and Toxic Substances in Water for Livestock and Poultry. Washington, D.C.: National Academy Press. National Research Council. 1987. Vitamin Tolerance of Animals. Washington, D.C.: National Academy Press. National Research Council. 1984. Nutrient Requirements of Beef Cattle, Sixth Revised Ed., Washington, D.C.: National Academy Press. Olentine, C. B vitamins for ruminants. In Feed Manag. 35(4):3775. Parakkasi, A., G.E.Mitchell, Jr., R.E.Tucker, C.O.Little, and A.W. Young. 1970. Pre-intestinal disappearance of vitamin D2 in ruminants. J. Anim. Sci. 35:273 (abst.). Perry, T.W., W.H.Smith, W.M.Beeson, and M.T.Mohler. 1965. Value of supplemental vitamin A for fattening beef cattle on pasture. J. Anim. Sci. 25:814–816. Perry, T.W., W.M.Beeson, W.H.Smith, and M.T.Mohler. 1967. Injectable vs oral vitamin A for fattening steer calves. J. Anim. Sci. 26:115–118. Perry, T.W., W.M.Beeson, W.H.Smith, R.B.Harrington, and M.T. Mohler. 1968. Interrelationships among vitamins A, E, and K when added to the rations of fattening beef cattle. J. Anim. Sci. 27:190–194. Pond, W.G., W.H.Allaway, E.F.Walker, Jr., and K.Krook. 1971. Effects of corn selenium content and drying temperature and of supplemental vitamin E on growth, liver selenium, and blood vitamin E of chicks. J. Anim. Sci. 33:996–1000. Rakes, A.H., M.P.Owens, J.H.Britt, and L.W.Whitlow. 1985. Effects of adding beta-carotene to rations of lactating cows consuming different forages. J. Dairy Sci. 68:1732–1737. Reinhardt, T.A., and F.G.Hustmyer. 1987. Role of vitamin D in the immune system. J. Dairy Sci. 66:1520. Riddell, D.O., E.E.Bartley, and A.D.Dayton. 1980. Effect of nicotinic acid on rumen fermentation in vitro and in vivo. J. Dairy Sci. 63:1429–1436. Riddell, D.O., E.E.Bartley, and A.D.Dayton. 1981. Effect of nicotinic acid on microbial protein synthesis in vitro and on dairy cattle growth and milk production. J. Dairy Sci. 64:782–791. Riddell, D.O., E.E.Bartley, J.J.Arambel, T.G.Nagaraja, A.D.Dayton, and G.W.Miller. 1985. Effect of niacin supplementation on ruminal niacin synthesis and degradation in cattle. Nutr. Rpt. Int. 31:407. Rode, L.M., T.A.McAllister, and K.J.Cheng. 1990. Microbial degradation of vitamin A in rumen fluid from steers fed concentrate, hay, or straw diets. Can. J. Anim. Sci. 70:227–233. Rumsey, T.S. 1985. Effect of choline in all concentrate diets of feedlot steers and on rumen acidosis. Can. J. Anim. Sci. 65:135–146.
OCR for page 75
Nutrient Requirements of Beef Cattle: Seventh Revised Edition, 1996 Rupel, I.W., W.G.Bohstedt, and E.B.Hart. 1933. Vitamin D in the nutrition of the dairy calf. Wise. Agric. Exp. Stn. Bull. 115. Sapienza, D.A., and B.E.Brent. 1974. Ruminal thiaminases vs. concentrate adaptation. J. Anim. Sci. 39:251 (abstr.). Schelling, G.T., L.W.Chittenden, T.C.Jackson, Jr., S.A.Koch, R.L. Stuart, R.E.Tucker, and G.E.Mitchell, Jr. 1975. Liver storage of oral and intramuscular vitamin A. J. Anim. Sci. 40:199 (abstr.). Sheppard, J.J., and B.C.Johnson. 1957. Pantothenic acid deficiency in growing calf. J. Nutr. 61:195–205. Smith, G.W., W.M.Durdle, J.E.Zimmerman, and A.L.Neumann. 1964. Relationships of carotene intake, thyro-active substances and soil fertility to vitamin A depletion of feeder cattle fed corn silages. J. Anim. Sci. 23:625–632. Sommerfeldt, J.L., R.L.Horst, E.T.Littledike, and D.C.Beitz. 1979. In vitro degradation of cholecalciferol in rumen fluid. J. Dairy Sci. 62(Suppl. 1):192 (abstr.). Sommerfeldt, J.L., J.L.Napoli, E.T.Littledike, D.C.Beitz, and R.L. Horst. 1983. Metabolism of orally administered [3H]ergocalciferol and [3H]cholecalciferol by dairy calves. J. Nutr. 113:2595–2600. Somogyi, J.C. 1973. Antivitamins. Pp. 254–275 in Toxicants Occurring Naturally in Foods. Washington, D.C.: National Academy Press. Stabel, J.R., T.A.Reinhart, M.A.Stevens, M.E.Kehrli, Jr., and B.J. Nonnecke. 1992. Vitamin E effects on in vitro immunoglobulin M and interleukin-1ß production and transcription in dairy cattle. J. Dairy Sci. 75:2190–2198. Stafford, J.W., K.F.Swingle, and H.Marsh. 1954. Experimental tocopherol deficiency in young calves. Am. J. Vet. Res. 15:373. Stillings, B.R., J.W.Bratzler, L.F.Marriott, and R.C.Miller. 1964. Utilization of magnesium and other minerals by ruminants consuming low and high nitrogen-containing forages and vitamin D. J. Anim. Sci. 23:1148–1154. Swanson, E.W., G.G.Martin, F.E.Pardue, and G.M.Gorman. 1968. Milk production of cows fed diets deficient in vitamin A. J. Anim. Sci. 27:541–548. Tappel, A.L. 1972. Vitamin E and free radical peroxidation of lipids. Vitamin E and its role in cellular metabolism. Ann. N.Y. Acad. Sci. 203:12–23. Tjoelker, L.W., B.P.Chew, T.S.Tanaka, and L.R.Daniel. 1988. Bovine vitamin A and ß-carotene intake and lactational status. 1. Responsiveness of peripheral blood polymorphonuclear leukocytes to vitamin A and ß-carotene challenge in vitro. J. Dairy Sci. 75:3112–3119. Tjoelker, L.W., B.P.Chew, T.S.Tanaka, and L.R.Daniel. 1988. Bovine vitamin A and ß-carotene intake and lactational status. 2. Responsiveness of mitogen-stimulated peripheral blood lymphocytes to vitamin A and ß-carotene challenge in vitro . J. Dairy Sci. 75:3120–3127. U.S. Pharmacopeia. 1985. U.S. Pharmacopeia, 21st Rev. XXI:1118–1119. Ullrey, D.E. 1972. Symposium-Biological Availability of Nutrients in Feeds. Biological availability of fat-soluble vitamins: Vitamin A and carotene. J. Anim. Sci. 35:648–657. Utley, P.R., N.W.Bradley, and J.A.Boling. 1970. Effect of restricting water intake on feed intake, nutrient digestibility and nitrogen metabolism in steers. J. Anim. Sci. 31:130–135. Wallis, G.C. 1944. Vitamin D deficiency in dairy cows: Symptoms, causes, and treatment. S. Dak. Agric. Exp. Stn. Bull. 372. Warner, R.G., and T.S.Sutton. 1948. The nutrition of the newborn dairy calf. III. The response to a photolyzed milk diet. J. Dairy Sci. 31:976. Wegner, M.I., A.N.Booth, C.A.Elvehjem, and E.B.Hart. 1940. Rumen synthesis of the vitamin B complex. Proc. Soc. Exp. Biol. Med. 45:769. Wegner, M.I., A.N.Booth, C.A.Elvehjem, and E.B.Hart. 1941. Rumen synthesis of the vitamin B complex on natural rations. Proc. Soc. Exp. Biol. Med. 47:9. Wiese, A.C., B.C.Johnson, and W.B.Nevens. 1946. Biotin deficiency in the dairy calf. Proc. Soc. Exp. Biol. Med. 63:521. Wiese, A.C., B.C.Johnson, H.H.Mitchell, and W.B.Nevens. 1947. Riboflavin deficiency in the dairy calf. J. Nutr. 33:263–270. Winchester, C.F., and M.J.Morris. 1956. Water intake rates of cattle. J. Anim. Sci. 15:722–740. Young, L.G., A.Lun, J.Pos, R.P.Forshaw, and D.Edmeades. 1975. Vitamin E stability in corn and mixed feed. J. Anim. Sci. 40:495–499. Zinn, R.A., F.N.Owens, R.L.Stuart, J.R.Dunbar, and B.B.Norman. 1987. B-vitamins supplementation of diets for feedlot calves. J. Anim. Sci. 65:267–277.