Click for next page ( 163


The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



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 162
7 vitamins Vitamins are classified as either fat-soluble or water- soluble. Vitamins A, D, E, and K are fat-soluble and the B-vitamins and vitamin C are water-soluble. Vitamins have diverse functions including involvement in many metabolic pathways, immune cell function, and gene regulation. A clinical deficiency of a vitamin results in a specific def~- ciency disease such as rickets when vitamin D is deficient. Subclinical deficiencies may occur in which clinical signs of the deficiency are not evident but performance or overall animal health is less than optimal. FAT-SOLUBLE VITAMINS Dairy cattle require vitamins A, D, E, and K; however, vitamins A and E are the only ones with an absolute dietary requirement. Vitamin K is synthesized by ruminal and intestinal bacteria. Vitamin D is synthesized by ultraviolet radiation of the skin. Many natural foodstuffs contain vita- min A precursors and vitamin E, and under certain situa- tions these will not need to be supplemented. However, relying solely on vitamins contained within foodstuffs and on synthesis of vitamin D via exposure to sunlight has risk because of the large variability in vitamin concentrations in feeds and exposure to sunlight. As management systems for dairy cattle trend toward more confinement with less exposure to sunlight and fresh forages, there is an increased need to add supplemental sources of vitamins A, D, and E. Vitamin A SOURCES Vitamin A activity is defined in retinal equivalents. An IU of vitamin A corresponds to 0.3 fig of all-trans retinal (0.344 fig of all-trans retinyl acetate or 0.550 fig of all- trans palmitate). Retinal is not found in plants, but many feeds contain p-carotene (provitamin A). Other carot- enoids can be converted to vitamin A by animals, but conversion efficiency appears to be poor and most common feeds do not contain substantial amounts of those carot- enoids. Most of the p-carotene in plants is found in vegeta- tive material; therefore, forages can contain substantial amounts of p-carotene but most grains and grain byprod- ucts are practically void of p-carotene (corn gluten meal contains moderate concentrations of p-carotene). Beta- carotene concentrations decrease as forages mature (Park et al., 19831. Beta-carotene is easily oxidized and once plants are cut, concentrations decrease quickly so that stored forages (silage and hay) have significantly lower concentrations of p-carotene than do fresh forage (Bruhn and Oliver, 1978; Park et al., 19831. The length of time forages are stored is negatively correlated with p-carotene concentrations (Bruhn and Oliver, 19781. Even when known sources of variation are considered, the p-carotene concentrations in foodstuffs are highly variable. The common forms of supplemental vitamin A used in the United States are all-trans retinyl acetate and all-trans retinyl palmitate. When these forms of vitamin A are stored properly, vitamin A activity is relatively stable with losses of about 1 percent/month. When these retinyl esters are stored in combination with minerals or other foodstuffs or are pelleted, storage losses increase to 5 to 9 percent/ month (Coelho, 19911. BIOAVAILABILITY Studies on the bioavailability of various forms of vitamin A and p-carotene for dairy cattle are extremely limited. Bioavailability of vitamin A is dependent upon the degree of ruminal destruction and on absorption efficiency by the small intestine. In addition to those factors, the bioavailabil- ity of p-carotene also depends on the efficiency of convert- ing it to retinal. Beta-carotene is converted to retinal by enzymes located in intestinal mucosal cells. Dairy cattle also absorb and store p-carotene. Blood and milk of Guern- sey and Jersey cattle contain more p-carotene than that from other breeds because they are either more efficient 162

OCR for page 162
Vitamins 163 at absorbing p-carotene or less efficient at converting p-carotene to retinal. The vitamin A activity of p-carotene for cattle is defined as 1 mg of p-carotene = 400 IU of vitamin A (equivalent to 120 fig of retinal), and is much lower for cattle than for rats (1 mg p-carotene = 1800 IU of vitamin A). The defined activity of p-carotene for cattle is based largely on experiments using lambs fed corn silage (Martin et al., 19681. Ruminal destruction of vitamin A can be extensive. Approximately 60 percent of supplemental vitamin A was destroyed in the rumen of steers fed hay and corn grain diets (Warner et al., 19701. Similar values have been obtained using in vitro rumen systems (Rode et al., 1990; Weiss et al., 19951. In vitro data suggest that ruminal destruction of vitamin A was approximately 20 percent when cattle were fed high forage diets, but it increased to about 70 percent when cattle were fed diets with 50 to 70 percent concentrate. Limited studies with p-carotene suggest that between 0 and 35 percent of dietary p-caro- tene is destroyed in the rumen (Potanski et al., 19741. Essentially no reliable data are available on the intestinal absorption of retinyl esters in cattle. Data collected from humans and rats suggest 20 to 60 percent of dietary retinyl esters are absorbed (Blomhoff et al., 19911. Absorption in those species is dependent on the amount and type of dietary fat. Apparent digestibility of p-carotene from a variety of forages averaged 77 percent in dairy steers (Wing, 1969), but Cohen-Fernandez et al. (1976) reported that fecal recovery (indigestibility) of radiolabeled p-carotene was about 90 percent in sheep. FUNCTIONS AND ANIMAL RESPONSES Vitamin A (retinaldehyde) is necessary for the produc- tion of rhodopsin (a vision pigment) that is necessary for low light vision. Vitamin A also is needed for normal growth and development (including fetal growth), spermatogene- sis, and for maintenance of skeletal tissue and epithelial tissue. Abortions, increased prevalence of retained fetal membranes, and increased calf morbidity and mortality are indicators of vitamin A deficiency in gestating cows. Ross and Ternus (1993) reported that retinoic acid indi- rectly regulates gene expression which may explain the many diverse functions of vitamin A. Vitamin A also increases disease resistance and has stimulatory effects on cell-mediated immunity (Chew, 1987; Bendich, 19931. A deficiency of vitamin A often results in increased preva- lence of infectious diseases. Beta-carotene, independent of its provitamin A function, is an antioxidant and can enhance the killing ability of neutrophils (Chew, 19931. In some (Chew, 1987) but not all (Michal et al., 1994) studies, and mastitis. These studies were conducted with cows at dry-off or peripartum cows. Vitamin A is clearly needed for good reproduction and some data suggests that p-carotene also may be involved with reproduction. In a review, Hurley and Doane (1989) reported that supplemental p-carotene (usually at 300 to 400 mg/day) improved some measure of reproductive eff~- ciency in 12 of 22 studies. When studies conducted only in North America were summarized, p-carotene had no effect on reproduction in 4 of 5 studies. FACTORS THAT AFFECT REQUIREMENTS Since the actual p-carotene content of diets is highly variable and almost never known in commercial situations, the vitamin A requirements presented in this publication are for supplemental vitamin A, not total dietary vitamin A. Fresh forage (e.g., pasture) has relatively high concen- trations of p-carotene. Therefore the amount of supple- mental vitamin A needed when fresh forage is fed will be less than for cattle consuming conserved forages. The requirements presented below assume conserved forages are fed and are probably in excess of requirements for grazing cattle. Based on a reevaluation of older data, the vitamin A requirement for growing dairy animals was increased to 80 IU/kg of body weight (BW). In the previous Nutrient Requirements of Dairy Cattle (National Research Council, 1989), the requirement for vitamin A of growing dairy animals was 42 IU/kg of BW. That requirement for growing cattle was based on the amount of vitamin A needed to maintain cerebrospinal fluid pressure below 120 mm Hg in calves (Rousseau et al., 19541. Other data (Rousseau et al., 1954; Eaton et al., 1972) using different criteria (i.e., a statistically significant increase in cerebrospinal fluid pressure or the presence of papillary edema of the eye) suggests that the vitamin A requirement for growing dairy animals was between 60 and 100 IU/kg of BW. The sub- committee decided that rather than discounting these stud- ies, a compromise using all the data was appropriate. The vitamin A requirement for adult dairy cattle has been increased to 110 IU/kg of BW. In Nutrient Require- ments of Dairy Cattle (National Research Council, 1989), the vitamin A requirement for adult animals (76 IU/kg of BW) was based largely on a long-term reproduction study (Ronning et al., 1959~. The sole source of vitamin A in that study was p-carotene, and cows were fed low concentrate diets. The previous requirement (National Research Coun- cil, 1989) also was based on data from a study (Swanson et al., 1968) that indicated the amount of vitamin A deemed adequate by Ronning et al. (1959) was adequate to maintain supplementing between 15O,OOO and 25O,OOO IU/day of- milk production. In that study, cows produced approxi- vitamin A or feeding 300 to 600 mg of p-carotene/day mately 3500 kg of milk during a 40-week lactation. Mean reduced the incidence of intramammary gland infections milk production is currently about twice as high and many

OCR for page 162
164 Nutrient Requirements of Dairy Cattle herds have mean milk production that is more than four times higher. Furthermore, in a more recent study, milk production increased from about 35 kg/day to 40 kg/day when cows in early lactation were fed diets that provided approximately 280 IU of vitamin A/kg of BW compared with cows fed approximately 75 IU/kg of BW (Oldham et al., 19911. The new requirement for lactating cows (110 IU/kg of BW) was based on data used by the previous Nutrient Requirements of Dairy Cattle (National Research Council, 1989) and on data showing that the bioavailability of vitamin A (retinyl esters) may be as much as 50 percent less than that of p-carotene when fed in high concentrate diets because of ruminal destruction. Dry cows are typically fed diets with lower amounts of concentrate and bioavail- ability of vitamin A should be higher than for lactating cows. The previous National Research Council requirement for dry cows (76 IU/kg of BW) may be adequate, but in light of potential improvements in mammary gland health and data showing increased milk production after dry cows were supplemented with vitamin A in amounts greater than National Research Council (1989) requirements, the vitamin A requirement for dry cows was kept the same as that for lactating cows (110 IU/kg of BOO). Presently available data are not adequate to define a specific requirement for p-carotene for any class of dairy cattle. Conditions that may warrant additional supplemen- tation of vitamin A include: low forage diets (more ruminal destruction and less consumption of p-carotene); diets that contain larger amounts of corn silage and smaller amounts of haycrops (lower concentrations of p-carotene and potentially lower bioavailability of basal p-carotene); diets that contain lower quality forages (lower basal concentrations of p-carotene); increased exposure to infectious pathogens (increased demands on the immune system); and times when immunocompetence maybe reduced (per- ipartum period). Vitamin A toxicosis should not be a problem under most practical situations. The presumed safe limit for vitamin A is 66,O00 IU/kg of diet for both lactating and nonlactating cattle (National Research Council, 19871. Vitamin D PHYSIOLOGY Vitamin D is a pro-hormone, a necessary precursor for the production of the calcium regulating hormone 1,25- dihydroxyvitamin D. Vitamin D can be produced within the skin of most mammals, including cattle, as a result of the photochemical conversion of 7-dehydrocholesterol to vitamin D3. In plants, ultraviolet irradiation causes photo- chemical conversion of ergosterol to vitamin D2. Vitamin D, supplied by the skin or the diet, is rapidly transported to and sequestered by the liver. The rapid removal of vitamin D from circulation prevents concentrations of vita- min D in blood from becoming very high; the normal concentration is 1 to 2 ng vitamin D/ml plasma (Horst and Littledike, 19821. Within the liver, vitamin D can be converted to 25-hydroxyvitamin D by vitamin D 25-hydrox- ylase and released into the blood. The production of 25- hydroxyvitamin D within the liver is dependent on the vitamin D content of the diet. Thus plasma 25-hydroxy- vitamin D concentration is the best indicator of vitamin D status of an animal (Horst et al., 19941. The 25-hydroxyvitamin D then circulates to the kidney where it can be converted to the hormone 1,25-dihydroxy- vitamin D. This hormone acts to increase the active trans- port of calcium and phosphorus across the intestinal epithe- lial cells, end potentiates the action of parathyroid hormone to increase bone calcium resorption. Both functions are vital for calcium and phosphorus homeostasis. In addition to calcium and phosphorus homeostasis, 1,25-dihydroxyvi- tamin D is involved in maintaining immune function (Rein- hardt and Hustmyer, 19871; generally it promotes Th2 (humoral) immunity while inhibiting Th1 (cell mediated) immunity (Daynes et al., 19951. Renal production of 1,25-dihydroxyvitamin D is tightly regulated. The 25-hydroxyvitamin D-1-`x-hydroxylase activity of the kidney is stimulated by parathyroid hormone, which is released in response to declining concentrations of calcium in blood (DeLuca, 19791. In the absence of parathyroid hormone, when an animal is in positive Ca balance, 25-hydroxyvitamin D can be hydroxylated in the kidney to 24,25-dihydroxyvitamin D as a primary step in the inactivation and catabolism of vitamin D. The vitamin D catabolic enzymes also function to deactivate 1,25-dihy- droxyvitamin D. These catabolic enzymes exist in tissues throughout the body. In these tissues the catabolic pathway is generally stimulated by 1,25-dihydroxyvitamin D as a negative feedback to reduce high concentrations of 1,25- dihydroxyvitamin D in plasma (Goff et al., 1992; Reinhardt and Horst, 19891. A low concentration of phosphorus in blood also can enhance renal production of 1,25-dihydroxyvitamin D, even when the concentration of calcium in plasma is normal or above normal (Tanaka and DeLuca, 1973; Gray and Napoli, 19831. A1SO, higher than normal concentrations of phosphorus in blood can inhibit renal production of 1,25- dihydroxyvitamin D, which can be a factor contributing to milk fever in the periparturient cow (Barton et al., 19871. Pharmacologic doses of vitamin D have been utilized with limited success to prevent milk fever. This is discussed in the section on milk fever (Chapter 91.

OCR for page 162
Vitamins 165 Vitamin D2, the form associated with plants, and vitamin D3, the form associated with vertebrates are both used for supplementation of diets. The biologic activity of the two forms is generally considered equal in cattle; however Horst and Littledike (1982) demonstrated an apparent dis- crimination against the vitamin D2 form in cattle. Presum- ably this discrimination is the result of reduced binding of vitamin D2 metabolites to vitamin D-binding proteins in blood leading to more rapid clearance of vitamin D2 metab- olites from plasma. However, the subcommittee does not recommend adjusting the vitamin D requirement based on the form of vitamin D used as a supplement. Vitamin D deficiency reduces the ability to maintain calcium and phosphorus homeostasis, resulting in a decline for phosphorus and less often a decrease for calcium in plasma. This eventually causes rickets in young animals and osteomalacia in adults; both are bone diseases in which the primary lesion is failure to mineralize the organic matrix of bone. In young animals rickets causes enlarged and painful joints; the costochondral joints of the ribs are often readily palpated. In adults, lameness and pelvic fracture are a common sequelae of vitamin D deficiency. REQUIREMENT The amount of dietary vitamin D required to provide adequate substrate for production of 1,25-dihydroxyvita- min D is difficult to define. Animals exposed to sunlight at the lower latitudes may not require any dietary vitamin D. Sun-cured hay also may provide enough vitamin D to prevent symptoms of vitamin D deficiency (Thomas and Moore, 19511. The movement away trom pasture leeching systems anct toward confinement and feeding of stored feeds and by- products has increased the need for dietary supplementa- tion of vitamin D for dairy cows. As a general rule, the contribution of sunlight and forage to the supply of vitamin D for the cow is not considered when describing the vita- min D requirement. The vitamin D requirement in this publication will consider the "requirement" to be the amount of supplemental vitamin D that should be added to the diet. Horst et al. (1994) determined that plasma 25-hydroxyvi- tamin D concentrations below 5 ng/ml are indicative of vitamin D deficiency and concentrations of 200 to 300 ng/ ml would indicate vitamin D toxicosis. Normal cows have concentrations of 25-hydroxyvitamin D in plasma between 20 and 50 ng/ml. Dry, pregnant cows housed indoors and fed a corn silage based diet had plasma concentrations of 25-hydroxyvitamin D in plasma of 19 ng/ml at 14 days prior to parturition and 10.5 ng/ml at 35 days into lactation. Supplementation of the diet with 5,000 (7.5 IU vitamin D/kg BW) or lO,OOO IU vitamin D (15 IU vitamin D/kg BW) maintained plasma concentrations between 25 and 31 ng/ml throughout the dry period and early lactation (Vines et al., 19851. Ward et al. (1971) reported that cows fed an alfalfa hay- concentrate diet receiving 30O,OOO IU vitamin D3 once each week (~ 43,000 IU/day) returned to estrus 16 days earlier than cows given no supplement. Ward et al. (1972) also demonstrated that cows receiving 30O,OOO IU vitamin D3/week had improved absorption of dietary calcium. Hibbs and Conrad (1983) summarized the results of several Ohio State University trials and concluded that cows sup- plemented with 4O,OOO IU vitamin D2/day (50 to 70 IU vitamin D/kg BW) produced more milk and generally ate more than cows fed the same diets with no vitamin D supplementation or supplemented with 8O,OOO or more IU vitamin D/day. Reduced milk production, which could be interpreted as the beginning of vitamin D intoxicosis, was observed when cows were fed 8O,OOO IU vitamin D/day (120-140 IU/kg BOO). McDermott et al. (1985) fed an orchard grass-corn silage based ration supplemented with O. lO,00O, 5O,00O, or 25O,OOO IU vitamin D3/day to Holstein cows in late gesta- tion and for the first 12 weeks of lactation. Cows had no access to sunlight from 2 weeks before calving until 4 days postpartum. Thereafter they were outside and exposed to sunlight 1 to 2 in/day. Plasma 25-hydroxyvitamin D concen- trations in unsupplemented cows were below 20 ng/ml during late gestation and the first 4 weeks of lactation. Plasma 25-hydroxyvitamin D concentrations in cows receiving lO,OOO or 5O,OOO IU vitamin D3/day (16-80 IU/ kg) were similar (between 30 and 45 ng 25-hydroxyvitamin D/ml). Cows receiving 25O,OOO IU vitamin D/day had ele- vated plasma 25-hydroxyvitamin D concentrations (60-80 ng/ml). The rapid changes in plasma concentrations of 25- hydroxyvitamin D, 24,25-dihydroxyvitamin D, and vitamin D suggested that at 25O,OOO IU/day the capacity of the liver to store vitamin D had been exceeded, which was interpreted as excessive vitamin D supplementation though no outward clinical signs of vitamin D intoxication were noted. Under most circumstances lO,OOO IU/day (16 IU vitamin D/kg BW) should provide adequate vitamin D for dairy cows during late gestation. Astrup and Nedkvitne (1987) reported that lactating cows producing about 20 kg of milk/ day required about 10 IU vitamin D/kg body weight to maintain normal concentrations of calcium and phosphorus in blood. These studies were conducted in Norway in win- ter and spring when effective sunlight exposure should have been minimal. The 1989 Nutrient Requirements of Dairy Cattle (National Research Council, 1989) requirement forvitamin D for adult dairy cows was set at 30 IU/kg body weight. This is more vitamin D than many studies suggest is neces- sary for maintenance of normal plasma concentrations of 25-hydroxyvitamin D (17 IU/kg BW) (McDermott et al.,

OCR for page 162
166 Nutrient Requirements of Dairy Cattle 1985) or calcium and phosphorus (10 IU/kg BW) (Astrup and Nedkvitne, 1987) in plasma. However, Ward et al. (1971, 1972) and Hibbs and Conrad (1983) suggested that milk production and reproductive and health benefits were potentially improved when diets were supplemented with as much as 70 IU/kg BW. Based on all available data, the requirement of 30 IU/kg BW established previously (National Research Council, 1989) seems justified. TOXICITY The maximum tolerable amount of vitamin D is inversely related to dietary concentrations of calcium and phospho- rus. The studies of McDermott et al. (1985) suggest that 5O,OOO IU D3/day (80 IU/kg BW) is well tolerated while 25O,OOO IU vitamin D3/day (400 IU/kg BW) is not. Hibbs and Conrad (1983) reported a slight decline in milk produc- tion when cows were fed 8O,OOO IU D2/day (~ 160 IU/kg BOO). The 1987 National Research Council committee on vitamin tolerance of animals (National Research Council, 1987) suggested the maximal tolerable level of vitamin D is 2,200 IU/kg diet when fed for long periods (more than 60 days) and 25,OOO IU/kg diet when fed for short periods of time. Vitamin D intoxication is associated with reduced feed intake, polyuria initially followed by anuria, dry feces, and reduced milk production. Upon necropsy calcification of kidneys, aorta, abomasum, and bronchioles is evident (Littledike and Horst, 19801. Some of the dietary vitamin D is degraded in the rumen by bacteria to inactive metabolites (Sommerfeldt et al., 1983; Gardner et al., 19881. Injection of vitamin D avoids this problem; however, the maximal tolerable dose of par- enterally administered vitamin D is at least 100-fold lower than the maximal tolerable oral dose and repeated injec- tions can be especially toxic (Littledike and Horst, 19801. Vitamin E SOURCES Vitamin E is a generic name for a series of lipid-soluble compounds called tocopherols and tocotrienols. The most biologically active form of vitamin E is oc-tocopherol; it is also the most common form of vitamin E found in feed- stuffs. Eight different stereoisomers of oc-tocopherol can exist, and the isomer that has the highest biologic activity is RRR-oc-tocopherol. The vitamin E content of foodstuffs is highly variable (coefficients of variation are often 50 percent). Depending on species and maturity (Tramontano et al., 1993; cupola et al., 1996), fresh forage plants contain between 80 and 200 IU of vitamin E/kg of DM. Alpha- tocopherol concentrations in forages decrease quickly after the plant is cut; prolonged exposure to oxygen and sunlight exacerbates the loss in vitamin E activity (Thafvelin and Oksanen, 19661. Silage and hay contain 20 to 80 percent less oc-tocopherol than does fresh forage. In general, con- centrations of vitamin E in concentrates are low; possible exceptions are raw whole soybeans and whole cottonseeds. Heat treatment of whole soybeans destroys essentially all the oc-tocopherol (Weiss, unpublished). Alpha-tocopherol concentrations in feeds generally decrease as storage . . time Increases. The commercial form of supplemental vitamin E usually fed to dairy cows is all-rac-oc-tocopheryl acetate (previously designated DL-oc-tocopheryl acetate). The esterified form of the vitamin is more stable than the alcohol form; expected losses in biologic activity from premixes contain- ing all-rac-oc-tocopheryl acetate are less than 1 percent per month under most storage conditions, but extruded products containing all-rac-oc-tocopheryl acetate may have storage losses of 6 percent per month (Coelho, 19911. RRR- oc-tocopherol is available commercially but is not com- monly fed to ruminants. BlOAVAlLABlLITY Early data (Alderson et al., 1971) suggested that signifi- cant amounts of supplemental vitamin E were destroyed in the rumen and that destruction increased as the amount of concentrate in the diet increased. More recent studies (Leedle et al., 1993; Weiss et al., 1995) found that vitamin E (all-rac-oc-tocopheryl acetate) was not destroyed during in vitro fermentation. The authors of these studies sug- gested that poor extraction of tocopherol from digesta was the reason early reports indicated that vitamin E was destroyed by ruminal fermentation. Based on the new data using better analytic techniques, ruminal metabolism of . . vitamin ~ appears mlmma . The USP defines 1 IU of vitamin as equal to 1 mg of all-rac-oc-tocopheryl acetate, and 1.49 IU of vitamin E is equal to 1 mg of RRR-oc-tocopherol. Those conversion factors are based largely on research with laboratory ani- mals. Data from cows comparing bioavailability of various tocopherol stereoisomers is contradictory. Hidiroglou et al. (1988, 1989) reported no or only slight differences in concentrations of oc-tocopherol in plasma and tissue between cows and heifers fed similar IU amounts of vita- min E as all-rac-oc-tocopherol or all-rac-oc-tocopheryl ace- tate. Concentrations of oc-tocopherol in tissue and plasma were 20 to 60 percent higher in beef cows fed RRR-'- tocopherol than those fed all-rac-oc-tocopheryl acetate (Hidiroglou et al., 19881. Based on that study 1 mg of RRR- oc-tocopherol would be equal to 1.8 to 2.4 IU of vitamin E. Different formulations of all-rac-oc-tocopheryl acetate (silica adsorbate, oil, or a microencapsulated form) did not greatly affect concentrations of oc-tocopherol in plasma suggesting equivalent bioavailability (Bald) et al., 19971. Insufficient consistent data are available currently to war-

OCR for page 162
Vitamins 167 rant changing IU conversion factors for vitamin E for rumi- nants. The current USP factors will be used for describing vitamin E requirements in this publication. FUNCTIONS AND ANIMAL RESPONSES The best understood function of vitamin E is as a lipid- soluble cellular antioxidant (Hogan et al., 19931. Via this function and perhaps other functions, vitamin E is involved in maintenance of cellular membranes, arachadonic acid metabolism, immunity, and reproductive function. White muscle disease is a classic sign of a clinical def~- ciency of vitamin E. White muscle disease was prevented in preweaned calves when 50 IU of vitamin E/day (all-rac- oc-tocopheryl acetate) were supplemented to a vitamin E- free diet based on skim milk (Blaxter et al., 19521. Presum- ably those data were used to formulate the vitamin E requirements for all classes of dairy cattle in the last Nutri- ent Requirements of Dairy Cattle (National Research Council, 19891. More recent experiments with vitamin E have focused on its relationship with reproductive disor- ders, mastitis, and immune function. Dietary or parenteral supplementation of vitamin E to dairy cows during the peripartum period has consistently improved the function of neutrophils and macrophages (Hogan et al., l99O, 1992; Politis et al., 1995, 19961. In those studies, the amount of supplemental vitamin E fed per day during the prepartum period was either 1000 IU/ day or 3000 IU/day. In three of those studies (Hogan et al., 1992; Politis et al., 1995, 1996) vitamin E also was injected (3000 or 6000 IU on approximately day 7 prepar- tum). During the postpartum phase, cows were fed either 500 or 3000 IU/day of supplemental vitamin E. Cows in all studies were fed stored forages. Clinical studies have been conducted to evaluate the effect of supplemental vitamin E on prevalence of retained fetal membranes, intramammary infections, and clinical mastitis. Feeding approximately 1000 IU/day of supple- mental vitamin E (usually all-rac-oc-tocopheryl acetate) to dry cows when adequate selenium was supplemented reduced the prevalence of retained fetal membranes in some (Harrison et al., 1984; Miller et al., 1993) but not all (Wichtel et al., 1996) studies. When vitamin E was injected (usually in combination with selenium) rather than fed, about half the time there was no effect for prevalence of retained fetal membranes and about half the time there was a positive response (Miller et al., 19931. The typical treatment was a single injection of approximately 700 IU of vitamin E and 50 mg of selenium given about 3 weeks before calving. Relative to the amount of vitamin E nor- mally consumed, 700 IU of vitamin E over 21 days is trivial. Most likely, selenium, not vitamin E, was the nutrient responsible for the positive effect. Two clinical studies conducted in Ohio (Smith et al., 1984; Hogan et al., 1993) reported that feeding supplemen- tal vitamin E significantly reduced the incidence and dura- tion of intramammary gland infections and clinical mastitis. In those studies, approximately 1000 IU/day of supplemen- tal vitamin E was fed during the 60-day prepartum period and 500 IU/day was fed during lactation. Conversely, a study conducted in Canada (Batra et al., 1992) found that similar amounts of supplemental vitamin E did not reduce the incidence of clinical mastitis. Based on the concentra- tions of selenium in the plasma (~35 ng/ml), cows in that study (Batra et al., 1992) were deficient in selenium. Another study (Weiss et al., 1997) using diets low in total selenium (0.15 ppm) but with animals in better selenium status (plasma selenium >50 ng/ml) than cows in the Batra et al. (1992) study found that feeding 1000 IU/day of vita- min E during the dry period reduced clinical mastitis at calving by 30 percent but did not affect prevalence of intramammary gland infections. In that same study, feeding 4000 IU of supplemental vitamin E/day during the last 2 weeks of the dry period resulted in an 80 percent reduction in clinical mastitis at calving and a 60 percent reduction in intramammary gland infections (Weiss et al., 19971. REQUIREMENTS AND FACTORS THAT AFFECT REQUIREMENTS The vitamin E requirement (15 IU/kg of DMI) in the previous Nutrient Requirements of Dairy Cattle (National Research Council, 1989) was for total, not supplemental, vitamin E and the basis for that requirement was not given. The previous vitamin E requirement should prevent classic signs of vitamin E deficiency. The vitamin E content of the basal diet is highly variable and will not be known in most situations; therefore, vitamin E requirements in this edition are presented for supplemental vitamin E. The requirements presented assume that cattle are consuming conserved forages. Because fresh forage is an excellent source of vitamin E the requirements for supplemental vitamin E for grazing cattle are probably substantially less than those presented for cattle fed conserved forages. Because titration studies are lacking, a specific requirement cannot be defined. The subcommittee concluded that there were adequate data available on the effect of vitamin E on mastitis and reproductive disorders to justify an increase in the vitamin E requirement. Based on health and immune function in cows, plasma concentrations of oc-tocopherol in peripartum cows should be approximately 3 ~g/ml (Weiss et al., 1994, 19971. To maintain these blood values, dry cows and heifers fed stored forages during the last 60 days of gestation require approximately 1.6 IU of supple- mental vitamin E/kg of body weight (approximately 80 IU/ kg of DMI). An additional benefit on calf health may be observed by increasing vitamin E intake by cows and heif-

OCR for page 162
168 Nutrient Requirements of Dairy CattIe ers in late gestation. Only minor amounts of vitamin E can pass the placenta (Van Saun et al., 19891; hence newborn calves rely on colostrum for vitamin E. Increased intake of vitamin E during the prepartum period significantly elevates vitamin E in colostrum. For lactating cows, the recommended amount of vitamin E (supplemental) was changed to 0.8 IU/kg of body weight (approximately 20 IU/kg of DMI) when stored forages are fed. This recom- mendation is based on a reduction in mastitis. The differ- ence between the recommendations for vitamin E for the two classes of cattle is mainly caused by expected differ- ences in intake of vitamin E from basal foodstuffs and perhaps reduced absorption of vitamin E by cows fed con- ventional dry cow diets. Based on typical feed intakes and average vitamin E concentrations in feedstuffs, the recom- mended amount of total vitamin E (supplemental plus vitamin provided by feedstuffs) is approximately 2.6 IU/ kg of body weight during late gestation and for lactating dairy cows. Of that amount, the basal diet will provide on average about 1.8 IU/kg of body weight for lactating cows (ranges from about 0.8 for cows fed diets based on severely weathered hay to about 2.8 IU/kg of body weight for cows fed diets based on pasture) and about 1 IU/kg body weight (ranges from 0.5 to about 2.3 IU/kg of body weight) for dry cows. Although several factors are known to influence vitamin E requirements, limited data make quantifying the neces- sary adjustments difficult. The amount of supplemental vitamin E fed may need to be changed during the follow- ing situations: When fresh forage is fed there should be less need for supplemental vitamin E. A diet based on fresh forage (ca. 50 percent of dietary DM) would require about 67 percent less supplemental vitamin E to meet the cows requirements compared with a diet that contained a similar amount of stored forage. Requirements for supplemental vitamin E is reduced 67 percent in the accompanying soft- ware when animals are fed pasture. The amount of supplemental vitamin E probably should be increased when low forage diets are fed (forages typically have more vitamin E than do concentrates). The requirements listed above were generated from studies using diets with 50 to 60 percent forage (lactating cows) and 60 to 80 percent forage (animals in late gestation). Cows in suboptimal selenium status probably require more vitamin E. Milk is not a major excretion route for oc-tocopherol (0.4 to 0.6 ~g/ml) but colostrum contains high concentra- tions of oc-tocopherol (3 to 6 ~g/ml). Additional vitamin E may be useful during colostralgenesis. Intake of polyunsaturated fatty acids increases the vitamin E requirement of nonruminants. As methods for protecting fats from biohydrogenation in the rumen improve, additional vitamin E may be required when pro- tected unsaturated fats are fed. Additional vitamin E may be useful during periods of immunosuppression (peripartum period). Large amounts of supplemental vitamin E (~1000 IU/day) can reduce oxidative flavors in milk (St.-Laurent et al., 19901. TOXICITY Vitamin E is one of the least toxic vitamins due in part to its relatively low absorption. Toxicity studies have not been conducted with ruminants but data from rats suggest an upper limit of approximately 75 IU/kg of body weight per day (National Research Council, 19871. Vitamin K Vitamin K is a generic term used to describe a group of quinone compounds exhibiting antihemorrhagic effects. The basic form of vitamin K is 2-methyl-1,4-naphthoqui- none. Isomers of vitamin K differ in the length and nature of the side chain (Frye et al., 19911. The three most com- mon isomers or vitamers of K are: phylloquinone (vitamin Kit, menaquinones (vitamin K2 ~ and menadione (vitamin Kay. The phylloquinones are commonly found in the chloro- plast of green plants and have side chains consisting of several isoprenoid units. Menaquinones are synthesized by bacteria flora and have isoprene side chains containing double bonds. Menadione (2-methyl-1,4-napthoquinone without a side chain) does not exist naturally. Menadione and its derivatives are the synthetic forms of vitamin K used in feed supplements (Combs, 19921. Cattle require vitamin K for the synthesis of at least a dozen proteins. Among these are four blood clotting fac- tars; prothrombin (factor II), and factors VII, IX and X. These vitamin K dependent protein factors are components of a complex system that functions to prevent hemorrhage by activation of thrombin and ultimately clot formation (Combs, 19921. Because large quantities of menaquinones are synthe- sized by ruminal bacteria and ruminant diets generally contain green forages and/or pasture plants high in phyllo- quinones, a deficiency of vitamin K rarely occurs. The only reported deficiencies have occurred when moldy sweet clover hay was fed (National Research Council, 19891. Dicoumarol is a fungal metabolite produced from sub- stances in sweet clover that inhibits the synthesis of clotting factors. Holstein calves were shown to develop dicoumarol toxicosis when fed sweet clover hay containing 18 mg/kg of dicoumarol for two weeks or longer (Yamini et al., 19951. Early signs of vitamin K deficiency include stiffness and/ or lameness and hematoma of tissues. Prolonged feeding of dicoumarol leads to uncontrolled bleeding. Dicoumarol

OCR for page 162
Vitamins 169 can pass placental barriers resulting in the fetus or newborn Folic Acid animals being affected (Frye et al., 19911. Vitamin K3 was found to be ineffective in preventing the anticoagulant effects of dicoumarol (Casper et al., 1989~. Toxicity data for either naturally occurring or synthetic forms of vitamin K are extremely limited. For humans and laboratory animals the presumed upper safe level for oral ingestion of menadione (K3) is 1,000 times the dietary requirement (National Research Council, 1987), but toxic- ity data for cattle are not available. WATER-SOLUBLE VITAMINS Ruminal microorganisms synthesize most water-soluble vitamins (biotin, folic acid, niacin, pantothenic acid, pyri- doxine, riboflavin, thiamin, and vitamin B12) and common foodstuffs generally contain high concentrations of most of those vitamins. Vitamin C is synthesized by ruminant animals. True deficiencies of these vitamins are rare in animals with a functional rumen. To date, a limited amount of research has been conducted on most water-soluble vitamins (niacin is the exception) for adult cattle; however, research in this area has increased during the past few years. Adequate data to quantify bioavailability, ruminal synthesis, and requirements for most water-soluble vita- mins are not available. Deficiency diseases for most B vitamins can be induced when preruminant calves are fed synthetic diets but are rare when calves are fed milk. Milk replacers should be supplemented with B vitamins as described in Chapter 10. B -VITA M I N S Biotin Biotin acts as a cofactor for many enzymes involved in carboxylation reactions. Ruminal bacteria normally synthe- size biotin and concentrations of the vitamin may exceed 9 ~g/L of strained ruminal fluid (Briggs et al., 1964~. Biotin is not extensively metabolized in the rumen and increased intake of dietary biotin results in elevated concentrations of biotin in serum and milk (Frigg et al., 1993; Midla et al., 1998~. Unpublished epidemiologic data suggest a negative relationship between serum concentrations of bio- tin and the incidence of clinical lameness in dairy cattle. In controlled long-term field studies, feeding approxi- mately 20 mg/day of supplemental biotin statistically improved measures of hoof health (Bergsten et al., 1999; Fitzgerald et al., 2000; Midla et al., 1998~. However, insuff~- cient data are available at this time to quantify the require- ment for biotin of dairy cattle. Folic acid containing coenzymes are involved in move- ment of one-carbon units in biochemical pathways. Methi- onine also serves as a methyl donor; therefore, folic acid mav snare methionine. Folic acid is necessary for the syn- thesis of nucleic acids. Growth rate and hematologic responses have been used to access adequacy in animal studies. Microbial degradation of supplemental folic acid can be extensive (Zinn, 1987~. Consequently, parenteral administration of folic acid is usually used to examine responses to supplemental folic acid. Weekly intramuscular injections of 40 mg folic acid from 45 days after mating until 6 weeks after parturition did not alter blood parameters or influence calf birth weight, therefore, dietary folic acid and microbial synthesis of this vitamin appear to supply sufficient amounts to prevent deficiency symptoms in adult dairy cattle (Girard et al., 1995~. Young calves that do not have a completely devel- oped ruminal microflora may be most susceptible to folic acid deficiency. Calves given weekly intramuscular injec- tions of 40 mg of folic acid from 10 days of age until 16 weeks of age increased average daily gain by 8 percent during the 5 weeks following weaning (approximately 7 to 12 weeks of age; Dumoulin et al., 19911. Treatment also increased serum folates, blood hemoglobin, and packed cell volume suggesting that folic acid may be deficient in young calves. Parenteral supplementation of 160 mg of folic acid each week from 45 days of gestation until 6 weeks postpartum tended to increase milk and milk protein production during mid to late lactation of primi- and multiparous cows. After calving, milk protein percentage was increased in multipa- rous cows only during the first 6 weeks of lactation (Girard et al., 1995~. Milk production during days 1 to 200 of lactation was increased linearly for multiparous cows but not for primiparous cows when O. 2, or 4 mg folate/kg BW were fed (Girard and Matte, 19981. Blood folates were increased indicating that some dietary folic acid escaped ruminal degradation. Deficiency symptoms for folate have not been observed in lactating dairy cattle. The increased milk production observed when supplemental folate was fed may be a direct response to the vitamin or may be an indirect response caused by sparing methionine. Insuffi- cient data are currently available to quantify the folic acid requirement of cattle. Inositol Inositol is an important nutrient in the metabolism and transport of lipids, and is a constituent of phospholipids, and has lipotropic activity. Myo-inositol is found in feeds as a component otphytic acid (Gerloffet al., 19841. Because physic acid can be degraded in the rumen, deficiencies of

OCR for page 162
170 Nutrient Requirements of Dairy Cattle inositol are not likely to occur. However, during periods of hepatic lipidosis or fatty liver syndrome where feed intakes may be low, supplementation of inositol has been investigated as an aid to help minimize triglyceride accu- mulation in the liver. Gerloff et al. (1984) in a field study involving 80 multiparious cows reported that the lipid con- tent of liver was not decreased by feeding 17 grams of nonphytate myo-inositol for one month pre- and postpar- tum. Similarly, Grummer et al. (1987) indicated that nei- ther milk production nor milk fat percentage were increased with abomasal infusion of 37 grams of myo- inositol. Dietary requirements for inositol have not been demon- strated in dairy animals with normal rumen activity. Bacte- rial synthesis in the rumen and/or the amounts in feeds apparently supply adequate amounts to meet metabolic requirements. The previous edition of Nutrient Require- ments of Dairy Cattle, (National Research Council, 1989) cited research from 1940 and 1950 showing deficiencies in calves after several weeks when fed purified or semi- purif~ed diets. Because dairy products are generally good sources of these vitamins (Combs, 1992) and milk replacers are fortified with additional amounts (Tomkins and [aster, 1991), deficiencies are unlikely to occur under typical calf . . . raising practices. Niacin Niacin is a generic name for pyridine 3-carboxylic acids and their derivatives that demonstrate activity similar to the amide form (i.e., nicotinamide). Niacin functions as a coenzyme for the pyridine nucleotide electron carriers NAD(H) and NADP(H). Consequently, niacin plays a criti- cal role in mitochondrial respiration and the metabolism of carbohydrates, lipids, and amino acids. Net synthesis of niacin in the rumen is likely because supply of niacin to the intestine exceeds intake when unsupplemented diets are fed to cattle (Zinn et al., 19871. Rate of niacin synthesis may be inversely related to level of supplementation (Abdouli and Schaefer, 1986b). During supplementation, the amount of niacin reaching the intes- tine may be less than that fed, indicating niacin degradation or absorption from the rumen (Zinn et al., 19871. Niacin absorption from the rumen appears to be low, particularly for nicotinic acid (Erickson et al., 19911. Feeding supple- mental niacin increases concentrations in ruminal and duo- denal fluid, which suggests that some supplemental niacin reaches the small intestine (Zinn et al., 1987; Campbell et. al., 19941. Estimates are that 17 to 30 percent of supple- mental niacin reaches the small intestine (Harmeyer and Kollenkirchen, 1989; Campbell et al., 19941. Nicotinamide is rapidly converted to nicotinic acid in the reticulorumen (Harmeyer and Kollenkirchen, 1989; Campbell et al., 19941. Niacin may increase microbial protein synthesis (Shields et al., 1983; Riddell et al., 198O, 19811; however, several studies indicate no effects (Hannah and Stern, 1985; Abdouli and Schaefer, 1986a; Doreau and Ottou, 19961. Differences between these studies, all of which utilized in vitro systems, may reflect the amount and availability of niacin in the unsupplemented diet, the niacin status of the microbes, or both. When niacin was fed in combination with other B-vitamins to feedlot calves (Zinn et al., 1987), or nicotinic acid or nicotinamide was fed to lactating cows (Doreau and Ottou, 1996), there were no treatment effects on microbial flow to the intestine. Niacin is requiredin the diet of preweaned calves. Calves fed synthetic milk that was deficient in niacin developed scours within 48 hours (Hopperand;[ohnson, 19551. Imme- diate improvement was observed on the day following oral (6 mg/head/day) or intramuscular (10 mg/head/day) nico- tinic acid administration. Niacin supplementation did not improve growth rates of heifers that began on trial at approximately 110 or 370 kg (Riddell et al., 19811. A total of 30 treatment comparisons from peer reviewed literature (Fronk et al., 1980; Kung et al., 1980; Riddell et al., 1981; Dufva et al., 1983; [aster et al., 1983a,b; Homer et al., 1986, 1988; Muller et al., 1986; Skaar et al., 1989; Driver et al., 1990; Erickson et al., l99O, 1992; Martinez et al., 1991; Lanham et al., 1992; Zimmerman et al., 1992; Bernard et al., 1995; Ottou et al., 1995; Madison-Anderson et al., 1997; Minor et al., 1998) were summarized to exam- ine niacin effects on lactation; a significant increase or decrease was declared if P <0.05. One comparison indi- cated a significant increase in milk production and 29 com- parisons indicated no significant change in milk production. For the fourteen comparisons in which niacin administra- tion began prepartum or prior to two weeks postpartum, none indicated a positive response. The absence of a response in many trials may be the consequence of inade- quate replication. The only positive milk yield response was from one of the two field trials that have utilized large animal numbers (Muller et al., 19861. The numbers of significant positive, neutral, or significant negative responses were 3, 26, and 1 for milk fat percentage and 5, SO, and 2 for milk protein percentage. A similar summary by Erdman (1992) indicated that average milk yield response was 0.3 kg/day; 0.4 kg/day if studies were restricted to those in which niacin supplemen- tation began prepartum. A summary of 23 to 30 treatment comparisons by Drackley (1992) indicated that average milk production was increased by 0.62 kg/day and milk fat and protein were increased by 0.033 and 0.002 percentage units when supplemental niacin was fed. Summaries by Erdman (1992) or Drackley (1992) indicated that milk production was decreased 1.1 or 0.42 kg/day when niacin was added to diets that contained supplemental fat. How- ever, there have been no significant (P <0.05) interactions

OCR for page 162
Vitamins 171 between fat and niacin for milk yield in the eight studies that have tested for interactions (Homer et al., 1986; Skaar et al., 1989; Driver et al., 1990; Martinez et al., 1991; Erickson et al., 1992; Lanham et al., 1992; Ottou et al., 1995; Madison-Anderson et al., 19971. Niacin is antilipolytic and has been examined closely as a feed additive to prevent or treat fatty liver and ketosis. Early studies indicated that small (12 g/day until negative milk acetone test; Fronk and Schultz, 1979) or large (160 grams over 8 hours; Waterman et al., 1972) pharmacologic doses of niacin reduced blood ketones in ketotic cows. In these studies, there were no ketotic cows assigned to a control (no niacin) treatment. Consequently, niacin effects were confounded with time. A slug dose of 12 or 120 grams of niacin decreased plasma concentrations of nonesterif~ed fatty acids but not beta-hydroxybutyrate ([aster et al., 1983a). A summary of 14 treatment comparisons in which niacin was fed (Fronk et al., 1980; Dufva et al., 1983; [aster et al., 1983a; Skaar et al., 1989; Driver et al., 1990; Erickson et al., 1990; Martinez et al., 1991; Erickson et al., 1992; Zimmerman et al., 1992; Bernard et al., 1995; Chilliard and Ottou, 1995; Ottou et al., 1995; Minor et al., 1998) indicated plasma nonesterif~ed fatty acids were significantly reduced once, increased twice, and not altered 11 times. If restricted to studies in which niacin was fed prepartum or within two weeks postpartum, plasma nonesterif~ed fatty acids were significantly reduced once, increased twice, and not altered 8 times. In 10 comparisons (9 of which niacin treatment began prepartum or prior to two weeks postpar- tum) plasma ketones were significantly reduced 4 times and not affected 6 times. However, three of the four com- parisons in which significant reductions were observed were from a single experiment and corresponded to con- trasts between three different doses of niacin to a control treatment (Dufva et al., 19831. Initiating the feeding of niacin prepartum did not reduce the amount of fat in liver of cows at 1 to 2 days or 28 to 35 days postpartum (Skaar et al., 1989; Minor et al., 19981. Niacin requirements for dairy cattle are not known. Sup- plemental niacin may be required by calves fed milk replacer (Hopper and Johnson, 1955) but not by post weaned "rowing heifers (Riddell et al., 19811. Data summa- rized from more than 25 trials does not support routine use of niacin to enhance lactation performance of dairy cattle. Data also do not support the routine use of niacin to minimize the risk of lipid-related metabolic disorders such as ketosis and fatty liver. Pantothenic Acid Pantothenic acid is a constituent of coenzyme A and is therefore essential for several fundamental reactions in metabolism including fatty acid oxidation, amino acid catabolism and acetylcholine synthesis (Smith and Song, 19961. No dietary requirement for pantothenic acid has been established as synthesis of pantothenic acid by rumi- nal microorganisms appears to be 20 to 30 times more than dietary amounts. Net microbial synthesis of panto- thenic acid in the rumen of steer calves has been estimated to be 2.2 mg/kg of digestible organic matter consumed per day and degradation of dietary pantothenic acid in the rumen is estimated to be 78 percent (Zinn et al., 19871. Supplementation of pantothenic acid at five to 10 times theoretic requirements did not improve performance of feedlot cattle (Cole et al., 1982; Zinn et al., 19871. Def~- ciency symptoms are very diverse and nonspecific. In non- ruminants, some generally reported symptoms include: dis- orders of the nervous, gastrointestinal, and immune sys- tems, reduced growth rate, decreased food intake, skin lesions and changes in hair coat, alterations in lipid and carbohydrate metabolism and death (Smith and Song, 19961. Riboflavin (B2) Riboflavin is a constituent of several enzyme systems associated with intermediary metabolism. No dietary requirement for ruminants has been established. Tissue requirements are apparently met through microbial syn- thesis of the vitamin in the rumen as destruction of dietary riboflavin in the rumen is nearly 100 percent (Zinn et al., 19871. Miller et al. (1986) reported ruminal synthesis of riboflavin to be 148 percent of intake with apparent absorp- tion from the small intestine averaging 23 percent. Synthe- sis of riboflavin in the rumen and flow to the small intestine was unaffected by concentrate content of the diet fed to steers. Zinn et al. (1987) estimated the flow of riboflavin from the rumen at 15.2 mg/kg of digestible organic matter consumed per day and a net absorption from the small intestine of 25 percent. Thiamin (Big Thiamin is a water-soluble vitamin, which in pure form is white in color, and has a sulfurous odor. It functions as an important coenzyme in several energy metabolism pathways and has a role, although not well defined, in nerve and brain function (Combs, 19921. Sources of thia- min include grains, grain by-products, soybean meal, and brewers yeast. Amounts of thiamin synthesized daily in the rumen (28 to 72 ma) have been reported to equal or exceed dietary intake (Breves et al., 19811. A dietary requirement for thiamin has not been estab- lished for healthy animals with a functional rumen. The combination of thiamin in feeds and synthesis of thiamin in the rumen meet or exceed metabolic requirements even with an estimated 48 percent destruction of dietary thiamin in the rumen (Zinn et al., 19871. Thiamin is generally

OCR for page 162
172 Nutrient Requirements of Dairy Cattle nontoxic as the upper safe feeding level for most nonrumi- nants is 1,000 times the requirement (National Research Council, 19871. An upper safe feeding level has not been established for ruminants. Deficiencies of thiamin have been found when thiamin- ases associated with either feeds or produced from altered ruminal fermentation destroy thiamin or produce an anti- metabolite of thiamin, which blocks thiamin dependent reactions. Bracken ferns and some raw fish products have been found to contain thiaminases. Feeding diets high in sulfate (Gould et al., 1991) or those which cause a sudden drop in ruminal pH (Zinn et al., 1987) can result in a thiamin deficiency. Because thiamin is intricately involved in several of the energy producing Krebs cycle reactions and because of the importance of glucose as an energy supply for the brain, any deficiency of thiamin results in a central nervous system disorder. Polioencephalomalacia (PEM), is the most common thiamin deficiency disorder. Symptoms of PEM include a profuse, but transient diar- rhea, listlessness, circling movements, opisthotonus (head drawn back over neck), and muscle tremors. If treated promptly by parenteral injection of thiamin (2.2 mg/kg of body weight), the condition can be reversed (National Research Council, 19961. Vitamin Be Vitamin Be is a cofactor for two major enzymes; methyl- malonyl coenzyme A mutase necessary for conversion of propionate to succinate, and tetrahydrofolate methyl trans- ferase which catalyzes transfer of methyl groups from 5- methyltetrahydrofolate to homocysteine to form methio- nine and tetrahydrofolate. Vitamin B12 is not found in the tissues of plants. Microbes are the only natural source of vitamin Be. Ruminal microbes can produce all of the vita- min Be required by the cow provided adequate available cobalt is in the diet (see section on cobalt, Chapter 61. Vitamin Be deficiency has been demonstrated in calves when fed diets devoid of animal protein (Lassiter et al., 1953) demonstrating that vitamin B12 is a required nutrient in dairy cattle. Based on this work, it was suggested that the vitamin Be requirement for dairy cattle was between 0.34 and 0.68 ~g/kg of live weight. Vitamin Be deficiency is the principle manifestation of cobalt deficiency (See section on cobalt). Significant quantities of vitamin Be are synthesized in the rumen. Vitamin Bl2 activity in the rumen tends to be greater in animals either grazing or fed high forage diets compared with animals fed high concentrate diets (Sutton and Elliot, 1972; Walker and Elliot, 19721. Data from beef cattle (Zinn et al., 1987) suggest more than adequate syn- thesis of vitamin Be to meet expected requirements for lactating dairy cows (Erdman, 1992), although exact requirements have not been established. In the mature ruminant, vitamin Be is of interest because of its roles in propionate metabolism (gluconeogenesis) and in methionine synthesis. It was suggested that inade- quate Be may be related to the low-milk fat syndrome in cows fed high grain diets (Frobish and Davis, 19771. Studies using both supplemental (Elliot et al., 1979) and injected (Croom et al., 1981) vitamin Be failed to show any response in fat test from cows fed high grain diets. There is no evidence that lactating dairy cows fed adequate amounts of cobalt will respond to dietary or intramuscular injections of vitamin Be Vitamin Be also is required as part of the enzyme com- plex methionine synthase in which methionine is synthe- sized from S-adenosylhomocysteine and 5-methyl tetrahy- drofolate. Methionine is used as a methyl donor for synthe- sis of choline, carnitine, and others compounds; therefore, a deficiency of vitamin Be is likely to affect methionine and methyl donor metabolism. Methyl donor requirements are not defined in ruminants and again it is unlikely that vitamin Be deficiency is of practical significance except during cobalt deficiency. B-Vitamins General In general, B-vitamin requirements can be met through synthesis by ruminal microorganisms and escape of dietary sources from the rumen. Table 7-1 illustrates potential requirements extrapolated from swine requirements and average vitamin concentrations found in milk. Based on these estimated requirements and limited research on B- vitamins of Miller et al. (1986) and Zinn et al. (1987) only folio acid and pantothenic acid appear to be limiting based on ruminal synthesis and escape of these vitamins occurring naturally in feeds. In contrast, some studies have demon- strated production and/or health benefits to dairy cows when diets have been supplemented with B-vitamins, most notably niacin, biotin, and folio acid. At the present time, almost no research is available on requirements of B com- plex vitamins for gestation, health, and milk production of high producing dairy cows. VITAMIN C Vitamin C or ascorbic acid is synthesized from L-gulonic acid within the cells of ruminants. Calves cannot synthesize ascorbic acid until approximately 3 weeks of age (Cummins and Brunner, 19911. Therefore, vitamin C is not considered an essential nutrient for healthy cattle that are older than about 3 weeks. Some studies, however, have reported ben- ef~cial responses when supplemental vitamin C is adminis- tered to cattle, particularly calves. Ascorbic acid functions as awater-soluble cellular antioxidant. Specifically, ascorbic acid is thought to be involved in regulation of steroid syn- thesis and the concentration of ascorbic acid is high in

OCR for page 162
Vitamins 173 TABLE 7-1 Estimated Absorption of Selected B-vitamins From the Small Intestine Compared with Estimated Requirements for Tissue and Milk Synthesis of a 650-kg Cow Producing 35 kg of 4 Percent Fat-Corrected Milk/Day Dally Estimated Requirement Rumlnal Rumlnal Tissuea MilLb Total Synthesist Escaped from Vitamin (mg/day) (mg/day) (mg/day) (mg/day) diet (%) Biotin 5 1 6 14 100 Folic acid 33 2 35 7 3 Niacin 256 33 289 1804 6 Pantothenic acid 304 121 425 38 22 Riboflavin 95 61 156 261 1 Thiamin 26 15 41 143 52 Be 26 22 48 96 100 Be 0.4 0.2 0.6 70 10 aBased on lactating sow (175 kg) requirements (NRC, 1998) adjusted to 650 kg lactating cow weight. bAdapted from Jenness (1985) and adjusted to 35 kg milk production. Readapted from Miller et al. (1986)C and Zinn et al. (1987)d and adjusted to digestible organic matter intake of 17.2 kg/day (total DM intake 22.9 kg/day). steroid secreting cells. Plasma concentrations of ascorbic acid were lower in calves (Cummins and Brunner, 1991) and growing steers (Hidiroglou et al., 1977) reared under stressful (i.e., slatted floors, cold stress) conditions than animals housed in better environments. That effect may be mediated by cortisol. Oral supplementation of 1 or 2 grams of vitamin C/day to preruminant calves elevated plasma concentrations of ascorbic acid compared with no supplemental vitamin C (Hidiroglou et al., 19951. The 2 grams supplementation rate tended to increase plasma con- centrations of ascorbic acid above the 1 gram rate but the difference was not statistically consistent during the 35 day experiment. Data are lacking on the effect of oral supplementation of vitamin C with cattle. Most orally ingested ascorbic acid is destroyed in the rumen, but newer formulations of vitamin C may provide some protection from ruminal metabolism. With sheep, oral supplementa- tion of 4 g/day of various forms of vitamin C for 28 days significantly increased plasma ascorbic acid concentrations (Hidiroglou et al., 19971. No growth response has been reported when calves were supplemented with vitamin C. Because of its antioxidant function, most research has concentrated on the effects of vitamin C on immune function. Immunoglobulin titers in calves were generally not affected by vitamin C supplemen- tation (Cummins and Brunner, 1989; Hidiroglou et al., 19951. Steers injected subcutaneously with 20 mg of ascorbic acid/kg of BW had improved neutrophil function compared with uninjected controls (Roth and Kaeberle, 19851. In the same study, an injection of 40 mg of ascorbic acid/kg of BW counteracted the negative effects on neutro- phil function induced by dexamethasone. Current data do not support routine supplementation of vitamin C to calves or adult cattle. CHOLINE Choline is not a vitamin in a traditional sense because it is not a part of an enzyme system, and is required in gram rather than milligram amounts as for true vitamins. Johnson et al. (1951) produced a choline deficiency in week-old dairy calves using synthetic milk replacer diets containing 15 percent casein. Choline requirements esti- mated from that experiment were 260 mg/L of milk replacer (1733 mg/kg DM). Current estimates of require- ments for the calf are 1000 mg/kg dry matter (DM) (Chap- ter 101. The predominant sign of choline deficiency in most animals is fatty liver. In calves, reported deficiency signs included muscular weakness, fatty infiltration of the liver, and renal hemorrhage; similar to those observed in other species. Both naturally occurring choline in feeds, predominantly found in phospholipids (lecithin) and dietary choline from supplements such as choline chloride have been shown to be extensively degraded in the rumen (Neil et al., 1979; Sharma and Erdman, 1988a,b, 1989b). Microbial degrada- tion of choline in the rumen results in the production of acetaldehyde and trimethylamine. Methyl group carbon from trimethylamine is subsequently degraded to methane (Neil et al., 19781. Supplementation of dietary choline in an unprotected form is useless because of extensive ruminal degradation (Erdman, 19921. Because of extensive degradation of dietary choline, methyl group requirements for synthesis of methyl-con- taining metabolites in the dairy cow are presumably pro- duced via methylation pathways involving methionine and the enzyme, S-adenosylmethionine methyl transferase. Sources of methyl groups for ruminants would include dietary methionine, betaine resulting from degradation of choline, and de nova synthesized methyl groups produced through 5-methyl tetrahydrofolate. Approximately one- third of the methionine methyl groups were transferred to choline in studies with lactating dairy goats (Emmanuel and Kennelly, 19841. Intravenous infusion of choline and carnitine reduced the irreversible loss of methionine by 18 to 25 percent in sheep suggesting that methionine could be spared with the addition of methyl-group-containing metabolites (Lobley et al., 19961.

OCR for page 162
174 Nutrient Requirements of Dairy Cattle Choline content of whole milk varies substantially (43 to 285 mg/L; Hartman and Hayden, 1974) with about 25 mg/L in the form of phospholipids. More recently, Deu- chler et al. (1998) found that the concentration of choline in milk ranged from 70 to 90 mg/L with an average secre- tion rate of choline into milk of between 2 to 3 g/day. Secretion of choline into milk was increased by either post~uminal infusion of choline chloride (Aliev and Bur- kova,1987; Deuchler et al., 1998) or by dietary supplemen- tation of ~umen-protected choline. This suggests that secre- tion of choline into milk could be used as a qualitative indicator of post~uminal choline supply. Choline requirements for lactating daily cows have not been established. As a ruminant animal, the daily cow has evolved under circumstances where intestinally absorbed choline is almost nonexistent because of extensive Nominal degradation of dietary choline. Experiments where choline has been supplemented either by feeding in a ~umen- protected form or by post~uminal infusion of choline chlo- ride have produced variable results. Milk production increased O to 3 kg/day in experiments where 15 to as much as 90 grams of choline chloride were infused post~uminally (Glummer et al., 1987; Erdman and Sharma, 1991; Sharma and Erdman, 1989a). In an experiment where methyl trans- fer from methionine was inhibited but choline was pro- vided, 4 percent FCM production was increased by 3.4 kg/day suggesting the importance of methionine in methyl group metabolism in the dairy cow (Sharma and Erd- man, 1988b). Lactational responses to choline are likely to be affected by methionine supply. Daily cows that are fed diets that supply adequate amounts of intestinally absorbed methio- nine are less likely to respond to supplemental choline than when methionine is limiting. Because of the relationship between fatty liver and ketosis, it has been speculated that choline could play a role in ketosis treatment and prevention, but there is no direct evidence to date to sup- port this theory (Erdman, 19921. The establishment of a choline requirement, either for the lactating daily cow, or for the transition cow in the late dry period and in early lactation, will require more extensive feeding experiments than were available at the time of this publication. R E F E R E N C E S Abdouli, H., and D. M. Schaefer. 1986a. Impact of niacin and length of incubation on protein synthesis, soluble to total protein ratio and fermentative activity of ruminal microorganisms. J. Anim. Sci. 62:244-253. Abdouli, H., and D. M. Schaefer. 1986b. Effects of two dietary niacin concentrations on ruminal fluid free niacin concentration, and of sup- plemental niacin and source of inoculum on in vitro microbial growth, fermentative activity and nicotinamide adenine dinucleotide pool size. J. Anim. Sci. 62:254-262. Alderson, N. E., Jr., G. E. Mitchell, C. O. Little, R. E. Warner, and R. E. Tucker. 1971. Preintestinal disappearance of vitamin E in ruminants. J. Nutr. 101:655-660. Aliev, A. A., and L. M. Burkova. 1987. Effect of choline chloride on the metabolism of nitrogen and choline in the stomach and intestines of lactating cows. Skh. Biol. 4:80-85. Astrup, H. N., and J. J. Nedkvitne. 1987. Effects of vitamin D supplement on cows and sheep. Norw.. J. Agric. Sci. 1:87-95. Baldi, A., V. Bontempo, F. Cheli, S. Carli, C. S. Rossi, and V. Dell'Orto. 1997. Relative bioavailability of vitamin E in dairy cows following intraruminal administration of three different preparations of DL-~- tocopheryl acetate. Vet. Res. 28: 1-8. Barton, B. A., N. A. Jorgensen, and H. F. DeLuca. 1987. Impact of prepartum dietary phosphorus intake on calcium homeostasis at parturi- tion. J. Dairy Sci. 70:1186-1191. Batra, T. R., M. Hidiroglou, and M. W. Smith. 1992. Effect of vitamin E on incidence of mastitis in dairy cattle. Can. J. Anim. Sci. 72:287-297. Bendich, A.1993. Physiological role of antioxidants in the immune system. J. Dairy Sci. 76:2789-2794. Bergsten, C., P. R. Greenough, J. M. Gay, R. C. Dobson, and C. C. Gay. 1999. A controlled field trial of the effects of biotin supplementation on milk production and hoof lesions. J. Dairy Sci. 82 (Suppl. 1):34 (Abstr.). Bernard, J. K., J. D. Quigley, H. H. Dowlen, and K. C. Lamar. 1995. Supplemental niacin and heat-treated whole soybeans for Jersey cows during early lactation. J. Dairy Sci. 78:2016-2023. Blaxter, K. L., P. S. Watts, and W. A. Woods. 1952. The nutrition of the young Ayrshire calf. 8. Muscular dystrophy in the growing calf. Br. J. Nutr. 6:125-169. Blomhoff, R., M. H. Green, J. B. Green, T. Berg, and K. Norum, R. 1991. Vitamin A metabolism: newperspectives on absorption, transport, and storage. Physiological Reviews 71:951-990. Breves, G., M. Brandt, H. Hoeller, and K. Rohr. 1981. Flow of thiamin to the duodenum in dairy cows fed different rations. J. Agric. Sci. Cambridge 96:587-591. Briggs, M. H., T. W. Heard, A. Whitcroft, and M. L. Hogg. 1964. Studies on urea-fed cattle. 2. Rumen levels of B vitamins and related coen- zymes. Life Sci. 3:11-14. Bruhn, J. C., and J. C. Oliver. 1978. Effect of storage on tocopherol and carotene concentrations in alfalfa hay. J. Anim. Sci. 61:980-982. Campbell, J. M., M. R. Murphy, R. A. Christensen, and T. R. Overton. 1994. Kinetics of niacin supplements in lactating cows. J. Dairy Sci. 77:566-575. Casper, H. H., A. D. Alstad, D. B. Tacke, L. J. Johnson, and W. E. Lloyd. 1989. Evaluation of vitamin K3 feed additive for the prevention of sweet clover disease. J. Vet. Diagn. Invest. 1:116-119. Chew, B. P. 1987. Vitamin A and Q-carotene in host defense. J. Dairy Sci. 70:2732-2743. Chew, B. P. 1993. Role of carotenoids in the immune response. J. Dairy Sci. 76:2804-2811. Chilliard, Y., and J. F. Ottou. 1995. Duodenal infusion of oil in midlacta- tion cows. 7. Interaction with niacin on responses to glucose, insulin, and Q-agonist challenges. J. Dairy Sci. 78:2452-2463. Coelho, M. B. 1991. Vitamin stability in premixes and feeds: a practical approach. Pp. 56-71. BASE Tech. Symp. Bloomington, MN. Cohen-Fernandez, S., P. Budowski, I. Ascarelli, H. Neumark, and A. Bondi. 1976. Low utilization of carotene by sheep. Int. J. Vit. Nutr. Res. 46:446-453. Cole, N. A., J. B. McLaren, and D. P. Hutcheson. 1982. Influence of preweaning and B-vitamin supplementation of the feedlot receiving diet on calves subjected to marketing and transit stress. J. Anim. Sci. 54:911-917. Combs, Jr., G. F. 1992. The Vitamins: Fundamental Aspects in Nutrition and Health. Academic Press Inc.

OCR for page 162
Vitamins 175 Croom, W. J., A. H. Rakes, A. C. Linnerud, G. A. Ducharme, and J. M. Elliot. 1981. Vitamin B12 administration for milk fat synthesis in lactating dairy cows fed a low fiber diet. J. Dairy Sci. 64:1555-1560. Cummins, K. A., and C. J. Brunner. 1989. Dietary ascorbic acid and immune response in dairy calves. J. Dairy Sci. 72:129-134. Cummins, K. A., and C. J. Brunner. 1991. Effect of calf housing on plasma ascorbate and endocrine and immune function. J. Dairy Sci. 74:1582-1588. Daynes, R. A., B. A. Araneo, J. Hennebold, E. Enioutina, and H. H. Mu. 1995. Steroids as regulators of the mammalian immune response. J. Invest. Dermatol. 105:14S-19S. DeLuca, H. F. 1979. The vitamin D system in the regulation of calcium and phosphorus metabolism. Nutr. Rev. 37:161-193. Deuchler, K. N., L. S. Piperova, and R. A. Erdman. 1998. Milk choline excretion as an indirect indicator of post-ruminal choline supply. J. Dairy Sci. 81:238-242. Doreau, M., and J. F. Otto. 1996. Influence of niacin supplementation on in viva digestibility and ruminal digestion in dairy cows. J. Dairy Sci. 79:2247-2254. Drackley, J. K. 1992. Niacin and carnitine in the nutrition of dairy cows. Page 8 in Proc Pacific Northwest Nutr. Conf. Tech. Symp., October 2O, Lonza Inc. ea., Spokane, WA. Driver, L. S., R. R. Grummer, and L. H. Schultz. 1990. Effects of feeding heat-treated soybeans and niacin to high producing cows in early lacta- tion. J. Dairy Sci. 73:463-469. Dufva, G. S., E. E. Bartley, A. D. Dayton, and D. O. Riddell. 1983. Effect of niacin supplementation on milk production and ketosis of dairy cattle. J. Dairy Sci. 66:2329-2336. Dumoulin, P. G., C. L. Girard, J. J. Matte, and G. J. St-Laurent. 1991. Effects of a parenteral supplement of folio acid and its interaction with level of feed intake of young dairy heifers. J. Anim. Sci. 69:1657-1666. Eaton, H. D., J. E. Rousseau, Jr., R. C. Hall, Jr., H. I. Prier, 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. Elliot, J.M., E. P. Barton, and J. A. Williams. 1979. Milk fat as related to vitamin B12 status. J. Dairy Sci. 62:642-645. Emmanual, B., and J. J. Kennelly. 1984. Kinetics of methionine and choline and their incorporation into plasma lipids and milk components in lactating goats. J. Dairy Sci. 67:1912-1919. Erdman, R. A. 1992. Vitamins. Pp. 297-308 in Large Dairy Herd Manage- ment. H. H. Van Horn and C. J. Wilcox, eds. American Dairy Science Association, Champaign, IL. Erdman, R. A., and B. K. Sharma. 1991. Effect of dietary rumen-protected choline in lactating dairy cows. J. Dairy Sci. 74:1641-1647. Erickson, P. S., M. R. Murphy, and J. H. Clark. 1992. Supplementation of dairy cow diets with calcium salts of long-chain fatty acids and nicotinic acid in early lactation. J. Dairy Sci. 75:1078-1089. Erickson, P. S., A. M. Trusk, and M. R. Murphy. 1990. Effects of niacin source on epinephrine stimulation of plasma nonesterif~ed fatty acid and glucose concentrations, on diet digestibility and on rumen protozoa! numbers in lactating dairy cows. J. Nutr. 120:1648-1653. Erickson, P. S., M. R. Murphy, C. S. McSweeney, and A. M. Trusk. 1991. Niacin absorption from the rumen. J. Dairy Sci. 74:3492-3495. Fitzgerald, T., B. W. Norton, R. Elliott, H. Podlich, and O. L. Svendsen. 2000. The influence of long-term supplementation with biotin on the prevention of lameness in pasture fed dairy cows. J. Dairy Sci. 83:338-344. Frigg, M., O. C. Straub, and D. Hartmann. 1993. The bioavailability of biotin in cattle. Internat. J. Vit. Nutr. Res. 63:122-128. Frobish, R. A., and C.L. Davis. 1977. Theory involving propionate and vitamin B12 in the low-fat milk syndrome. J. Dairy Sci. 60:268-276. Fronk, T. J., and L. H. Schultz. 1979. Oral nicotinic acid as a treatment for ketosis. J. Dairy Sci. 62:1804-1807. Fronk, T. J., L. H. Schultz, and A. R. Hardie. 1980. Effect of dry period overconditioning on subsequent metabolic disorders and performance of dairy cows. J. Dairy Sci. 63:1080-1090. Frye, T. M., S. N. Williams, and T. W. Graham. 1991. Vitamin def~ciencies in cattle. Veterinary Clinics of North America: Food Animal Practice. 7:217- 275. Gardner, R.M., T. A. Reinhardt, and R.L. Horst. 1988. The biological assessment of vitamin D3 metabolites produced by rumen bacteria. J. Ster. Biochem. 29:185-189. Gerloff, B. J., T. H. Herdt, R. S. Emery, and W. W. Wells. 1984. Inositol as a lipotropic agent in dairy cattle diets. J. Anim. Sci. 59:806-812. Girard, C. L., and J. J. Matte. 1998. Dietary supplements of folic acid during lactation: effects on performance of dairy cows. J. Dairy Sci. 81:1412-1419. Girard, C. L., J. J. Matte, and G. F. Tremblay. 1995. Gestation and lactation of dairy cows: A role for folic acid? J. Dairy Sci. 78:404-411. Goff, J. P., T. A. Reinhardt, G. W. Engstrom, and R. L. Horst. 1992. Effect of dietary calcium or phosphorus restriction and 1,25-dihyroxyvi- tamin D administration on rat intestinal 24-hydroxylase. Endocrinol- ogy 131:101-104. 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. Gray, R. W., and J. L. Napoli. 1983. Dietary phosphate deprivation increases 1,25-dihydroxyvitamin D3 synthesis in rat kidney in vitro. J. Biol. Chem. 258:1152-1155. Grummer, R. R., L. E. Armentano, and M. S. Marcus. 1987. Lactation response to short-term abomasal infusion of choline, inositol, and soy lecithin. J. Dairy Sci. 70:2518-2524. Hannah, S. M., and M. D. Stern. 1985. Effect of supplemental niacin or niacinamide and soybean source on ruminal bacterial fermentation in continuous culture. J. Anim. Sci. 61: 1252-1263. Hartman and Dryden. 1974. The vitamins in milk and milk products. In: Fundamentals of Dairy Chemistry, 2n~ ed. B. H. Webb, A. H. Johnson, and J. A. Alford (Editors) AVI Publishing Co. Westport, CT. Harmeyer, J., and U. Kollenkirchen.1989. Thiamin and niacin in ruminant tissues. Nutr. Res. Rev. 2:201-225. Harrison, J. H., D. D. Hancock, and H. R. Conrad. 1984. Vitamin E and selenium for reproduction of the dairy cow. J. Dairy Sci. 67:123-132. Hibbs, J. W., and H. R. Conrad. 1983. The relation of calcium and phosphorus intake on digestion and the effects of vitamin D feeding on the utilization of calcium and phosphorus by lactating dairy cows. Rep. No. 1150. Ohio State University. Hidiroglou, M., T. R. Batra, and X. Zhoa. 1997. Comparison of vitamin C bioavailability after multiple or single oral dosing of different formula- tions in sheep. Reprod. Nutr. Dev. 37:443-448. Hidiroglou, M., M. Ivan, and J. R. Lessard. 1977. Effect of ration and inside versus outside housing on plasma levels of ascorbic acid, lactic acid, glucose, and cholesterol in Hereford steers wintered under practi- cal conditions. Can. J. Anim. Sci. 57:519-529. Hidiroglou, N., L. R. McDowell, and O. Balbuena. 1989. Plasma tocoph- erol in sheep and cattle after ingesting free or acetylated tocopherol. J. Dairy Sci. 72:1793-1799. 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. Hidiroglou, M., T. R. Batra, M. Ivan, and F. Markham. 1995. Effects of supplemental vitamins E and C on the immune response of calves. J. Dairy Sci. 78:1578-1583. Hogan, J. S., K. L. Smith, W. P. Weiss, D. A. Todhunter, and W. L. Shockey. 1990. Relationships among vitamin E, selenium, and bovine blood neutrophils. J. Dairy Sci. 73:2372-2378.

OCR for page 162
176 Nutrient Requirements of Dairy Cattle Hogan, J. S., W. P. Weiss, and K. L. Smith. 1993. Role of vitamin E and selenium in host defense against mastitis. J. Dairy Sci. 76:2795-2803. Hogan, J. S., W. P. Weiss, D. A. Todhunter, K. L. Smith, and P. S. Schoenberg. 1992. Bovine neutrophil responses to parenteral vitamin E. J. Dairy Sci. 75:399-405. 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. Homer, J. L., C. E. Coppock, G. T. Schelling, J. M. Labore, and D. H. Nave. 1986. Influence of niacin and whole cottonseed on intake, milk yield and composition, and systematic responses of dairy cows. J. Dairy Sci. 69:3087-3093. Homer, J. L., L. M. Windle, C. E. Coppock, J. M. Labore, J. K. Lanhan, and D. H. Nave. 1988. Effects of whole cottonseed, niacin, and niacina- mide on in vitro rumen fermentation and on lactating Holstein cows. J. Dairy Sci. 71:3334-3344. Horst, R. L., and E. T. Littledike. 1982. Comparison of plasma concentra- tions of vitamin D and its metabolites in young and aged domestic animals. Comp. Biochem. Physiol. [B] 73:485-489. Horst, R. L., J. P. Goff, and T. A. Reinhardt. 1994. Calcium and vitamin D metabolism in the dairy cow. J. Dairy Sci. 77:1936-1951. Hurley, W. L., and R. M. Doane. 1989. Recent developments in the roles of vitamins and minerals in reproduction. J. Dairy Sci.72:784-804. Jaster, E. H., D. F. Bell, and T. A. McPherron. 1983a. Nicotinic acid and serum metabolite concentrations of lactating dairy cows fed supple- mental niacin. J. Dairy Sci. 66:1039-1045. Jaster, E. H., G. F. Hartnell, and M. F. Hutjens. 1983b. Feeding supple- mental niacin for milk production in six dairy herds. J. Dairy Sci. 66:1046-1051. Jennes, R. 1985. Biochemical and nutritional aspects of milk and colos- trum. In: Lactation. P.164, B. L. Larson, ea., Iowa State Press, Ames IA. Johnson, B. C., H. H. Mitchell, and A. Pinkos. 1951. Choline def~ciency in the calf. J. Nutr. 43:37-48. Jukola, E., J. Hakkarainen, H. Saloniemi, and S. Sankari. 1996. Effect of selenium fertilization on selenium in feedstuffs and selenium, vitamin E, and B-carotene concentrations in blood of cattle. J. Dairy Sci. 79:831-837. Kung Jr., L., K. Gubert, and J. T. Huber. 1980. Supplemental niacin for lactating cows fed diets of natural protein or nonprotein nitrogen. J. Dairy Sci. 63:2020-2025. Lanham, J. K., C. E. Coppock, K. N. Brooks, D. L. Wilks, and J. L. Homer. 1992. Effects of whole cottonseed or niacin or both on casein synthesis by lactating Holstein cows. J. Dairy Sci. 75:184-192. Lassiter, C. A., G. M. Ward, C. F. Huffman, C. W. Duncan, and H. D. Welester. 1953. Crystalline vitamin B~2 requirements of the young dairy calf. J. Dairy Sci. 36:997-1004. Leedle, R. A., J. A. Leedle, and M. D. Butine. 1993. Vitamin E is not degraded by ruminal microorganisms: assessment with ruminal contents from a steer fed a high-concentrate diet. J. Anim. Sci. 71:3442-3450. Littledike, E. T., and R. L. Horst. 1980. Problems with vitamin D injec- tions for prevention of milk fever: toxicity of large doses and increased incidence of small doses. J. Dairy Sci. 63(Supp. 1):89. Lobley, G. E., A. Connell, and D. Revell. 1996. The importance of transmethylation reaction to methionine metabolism in sheep: Effects of supplementation with creatine and choline. Brit. J. Nutr. 75:47-56. Madison-Anderson, R. J., D. J. Schingoethe, M. J. Brouk, R. J. Baer, and M. R. Lentsch. 1997. Response of lactating cows to supplemental unsaturated fat and niacin. J. Dairy Sci. 80:1329-1338. Martin, F. H., D. E. Ullrey, H. W. Newland, and E. R. Miller. 1968. Vitamin A activity of carotenes in corn silage fed to lambs. J. Nutr. 96:269-274. Martinez, N., E. J. DePeters, and D. L. Bath. 1991. Supplemental niacin and fat effects on milk composition of lactating Holstein cows. J. Dairy Sci. 74:202-210. McDermott, C. M., D. C. Beitz, E. T. Littledike, and R. L. Horst. 1985. Effects of dietary vitamin D3 on concentrations of vitamin D and its metabolites in blood plasma and milk of dairy cows. J. Dairy Sci. 68:1959-1967. Michal, J. J., L. R. Heirman, T. S. Wong, B. P. Chew, M. Frigg, and L. Volker. 1994. Modulatory effects of dietary Q-carotene on blood and mammary leukocyte function in periparturient dairy cows. J. Dairy Sci. 77:1408-1421. Midla, L. T., K. H. Hoblet, W. P. Weiss, and M. L. Moeschberger. 1998. Supplemental dietary biotin for prevention of lesions associated with aseptic clinical laminitis (Pododermatitis aseptica diffuse) in primipa- rous Holsteins. Am. J. Vet. Res. 59:733-738. Miller, B. L., J. C. Meiske, and R. D. Goodrich. 1986. Effects of grain and concentrate level on B-vitamin production and absorption in steers. J. Anim. Sci. 62:473-483. Miller, J. K., E. Brzezinska-Slebodzinska, and F. C. Madsen. 1993. Oxida- tive stress, antioxidants, and animal function. J. Dairy Sci. 76:2812-2823. Minor, D. J., S. L. Trower, B. D. Strang, R. D. Shaver, and R. R. Grummer. 1998. Effects of nonf~ber carbohydrate and niacin on periparturient metabolic status and lactation of dairy cows. J. Dairy Sci. 81:189-200. Muller, L. D., A. J. Heinrichs, J. B. Cooper, and Y. H. Atkin. 1986. Supplemental niacin for lactating cows during summer feeding. J. Dairy Sci. 69:1416-1420. National Research Council. 1996. Nutrient Requirements of Beef Cattle, Seventh Revised Ed. Washington, D.C.: National Academy Press. National Research Council. 1987. Vitamin Tolerance of Domestic Ani- mals. Washington, D.C.: National Academy Press. National Research Council.1989. Nutrient Requirements of Dairy Cattle. 6th rev. ed. Washington, D.C.: National Academy Press. National Research Council. 1998. Nutrient requirements of Swine. 10 revised edition. National Academy Press, Washington, DC. Neil, A. R., D. W. Grime, and R. M. C. Dawson. 1978. Conversion of choline methyl groups through trimethyl amine into methane in the rumen. Biochemical J. 170:529-535. Neil, A. R., D. W. Grime, A. M. Snoswell, A. J. Northrop, D. B. Lindsay, and R. M. C. Dawson. 1979. The low availability of dietary choline for the nutrition of the sheep. Biochem. J. 180:559-565. Oldham, E. R., R. J. Eberhart, and L. D. Muller. 1991. Effects of supple- mental vitamin A and B-carotene during the dry period and early lactation on udder health. J. Dairy Sci. 74:3775-3781. Ottou, J. F., M. Doreau, and Y. Chilliard. 1995. Duodenal infusion of rapeseed oil in midlactation cows. 6. Interaction with niacin on dairy performance and nutritional value. J. Dairy Sci. 78:1345-1352. Park, Y. W., M. J. Anderson, J. L. Walters, and A. W. Mahoney. 1983. Effects of processing methods and agronomic variables on carotene contents in forages and predicting carotene in alfalfa hay with near- infrared-reflectance spectroscopy. J. Dairy Sci. 66:235-245. Politis, I., M. Hidiroglou, T. R. Batra, J. A. Gilmore, R. C. Gorewit, and H. Scherf. 1995. Effects of vitamin E on immune function of dairy cows. Am. J. Vet. Res. 56:179-184. Politis, I., N. Hidiroglou, J. H. White, J. A. Gilmore, S. N. Williams, H. Scherf, and M. Frigg. 1996. Effects of vitamin E on mammary and blood leukocyte function, with emphasis on chemotaxis, in peripartur- ient dairy cows. Am. J. Vet. Res. 57:468-471. Potanski, A. A., R. E. Tucker, G. E. Mitchell Jr., and G. T. Schelling. 1974. Pre-intestinal losses of carotene in sheep fed high-starch or high- cellulose diets. Int. J. Vit. Nutr. Res. 44: Reinhardt, T. A., and R. L. Horst. 1989. Self-induction of 1,25-dihydroxy- vitamin D3 metabolism limits receptor occupancy and target tissue responsiveness. J. Biol. Chem. 264:15917-15921. Reinhardt, T. A., and F. G. Hustmyer. 1987. Role of vitamin D in the immune system. J. Dairy Sci. 70:952-962.

OCR for page 162
Vitamins 177 Riddell, D. O., E. E. Bartley, and A. D. Dayton. 1980. Effect of nicotinic acid on rumen fermentation in vitro and in viva. 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. Rode, L. M., T. A. McAllister, and K. J. Cheng. 1990. Microbial degrada- tion of vitamin A in rumen fluid from steers fed concentrate, hay or straw diets. Can. J. Anim. Sci. 70:227-233. Ronning, M. E., R. Berousek, J. R. Griffiths, and W. D. Gallop. 1959. Carotene requirement of dairy cattle. Pp. 30. Okla. Agric. Exp. Tech. Bull. No. T-76 Stillwater, OK. Ross, C., and M. E. Ternus. 1993. Vitamin A as a hormone: recent advances in understanding the actions of retinal, retinoic acid and beta carotene. J. Am. Diet. Assoc. 93:1285-1290. Roth, J. A., and M. L. Kaeberle. 1985. In viva effect of ascorbic acid on neutrophil function in healthy and dexamethasone-treated cattle. Am. J. Vet. Res. 46:2434-2436. Rousseau Jr., J. E., H. D. Eaton, C. F. Helmbolt, E. L. Hunghers, S. A. Robrish, G. Beall, and L. A. Moore. 1954. Relative value of carotene and vitamin A from a dry carrier fed at minimum levels to Holstein calves. J. Dairy Sci. 37:889-899. Sharma, B. K., and R. A. Erdman.1988a. Abomasal infusion of choline and methionine with or without 2-amino-2-methyl-1-propanol for lactating dairy cows. J. Dairy Sci. 71:2406-11. Sharma, B. K., and R. A. Erdman. 1988b. Effect of high levels of dietary choline supplementation on duodenal choline flow and production responses of dairy cows. J. Dairy Sci. 71: 2670-76. Sharma, B. K., and R. A. Erdman. 1989a. Effects of dietary added and abomasally infused choline on milk production responses of lactating dairy cows. J. Nutr. 119:248-254. Sharma, B. K., and R. A. Erdman. 1989b. In vitro degradation of choline from selected foodstuffs and choline supplements. J. Dairy Sci. 72:2771-2776. Shields, D. R., D. M. Schaefer, and T. W. Perry. 1983. Influence of niacin supplementation and nitrogen source on rumen microbial fer- mentation. J. Anim. Sci. 57:1576-1583. Skaar, T. C., R. R. Grummer, M. R. Dentine, and R. H. Stauffacher. 1989. Seasonal effects of prepartum and postpartum fat and niacin feeding on lactation performance and lipid metabolism. J. Dairy Sci. 72:2028-2038. Smith, C. M. and W. O. Song. 1996. Comparative nutrition of pantothenic acid. Nutr. Biochem. 7:312-321. Smith, K. L., J. H. Harrison, D. D. Hancock, D. A. Todhunter, and H. R. Conrad. 1984. Effect of vitamin E and selenium supplementation on incidence of clinical mastitis and duration of clinical symptoms. J. Dairy Sci. 67:1293-1300. 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. St.-Laurent, A. M., M. Hidiroglou, M. Snoddon, and J. W. Nicholson. 1990. Effect of a-tocopherol supplementation to dairy cows on milk and plasma a-tocopherol concentrations and on spontaneous oxidized flavor in milk. Can. J. Anim. Sci. 70:561-570. Sutton, A. L., and J. M. Elliot. 1972. Effect of ratio of roughage to concentrate and level of feed intake on ovine ruminal vitamin Be production. J. Nutr. 102:1341-1346. 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. 57:541-548. Tanaka, Y., and H. F. DeLuca. 1973. The control of 25-hydroxyvitamin D metabolism by inorganic phosphorus. Arch. Biochem. Biophys. 154:566-574. Thafvelin, B., and H. E. Oksanen. 1966. Vitamin E and linolenic acid content of hays as related to different drying conditions. J. Dairy Sci. 49:282-286. Thomas, J. W., and L. A. Moore. 1951. Factors affecting the antirachitic activity of alfalfa and its ability to prevent rickets in young calves. J. Dairy Sci. 34:916-928. Tomkins, T., and E. H. Jaster. 1991. Preruminant calf nutrition. Vet. Clinics of North Am.: Food Anim. Pract. 7:557-576. Tramontano, W. A., D. Ganci, M. Pennino, and E. S. Dierenfeld. 1993. Distribution of a-tocopherol in early foliage samples in several forage crops. Phytochem. 34:389-390. Van Saun, R. J., T. H. Herdt, and H. D. Stowe. 1989. Maternal and fetal vitamin E concentrations and selenium-vitamin E interrelationships in dairy cattle. J. Nutr. 119: 1156-1164. Vinet, C., H. R. Conrad, T. A. Reinhardt, and R. L. Horst. 1985. Minimal requirements for vitamin D in lactating cows. Fed. Proc. 28:549 (Abstr.). Walker, C. K., and J. M. Elliot. 1972. Lactational trends in vitamin Bl2 status on conventional and restricted roughage rations. J. Dairy Sci.55:474-482. Ward, G., R. C. Dobson, and J. R. Dunham. 1972. Influences of calcium and phosphorus intakes, vitamin D supplement, and lactation on cal- cium and phosphorus balances. J. Dairy Sci. 55:768-776. Ward, G., G. B. Marion, C. W. Campbell, and J. R. Dunham. 1971. Influences of calcium intake and vitamin D supplementation on repro- ductive performance of dairy cows. J. Dairy Sci. 54:204-206. Warner, R. L., G. E. Mitchell, Jr., C. O. Little, and N. E. Alderson. 1970. Pre-intestinal disappearance of vitamin A in steers fed different levels of corn. International J. Vitamin Research 40:585-588. Waterman, R., J. W. Schwalm, and L. H. Schultz. 1972. Nicotinic acid treatment of bovine ketosis I. Effects on circulatory metabolites and interrelationships. J. Dairy Sci. 55:1447-1453. Weiss, W. P., J. S. Hogan, and K. L. Smith. 1994. Use of a-tocopherol concentrations in blood components to assess vitamin E status of dairy cows. Agri-Practice 15 (7):5-8. Weiss, W. P., J. S. Hogan, D. A. Todhunter, and K. L. Smith. 1997. Effect of vitamin E supplementation in diets with a low concentration of selenium on mammary gland health of dairy cows. J. Dairy Sci. 80:1728-1737. Weiss, W. P., K. L. Smith, J. S. Hogan, and T. E. Steiner. 1995. Effect of forage to concentrate ratio on disappearance of vitamins A and E during in vitro ruminal fermentation. J. Dairy Sci. 78:1837-1842. Wichtel, J. J., A. L. Craigie, K. G. Thompson, and N. B. Williamson. 1996. Effect of selenium and a-tocopherol supplementation on postpartum reproductive function of dairy heifers at pasture. Theriogenology 46:491-502. Wing, J. M. 1969. Effect of source and season on apparent digestibility of carotene in forage by cattle. J. Dairy Sci. 52:479-483. Yamini, B., R. H. Poppenga, W. E. Braselton, Jr. and L. J. Judge. 1995. Dicoumarol (moldy sweet clover) toxicosis in a group of Holstein calves. J. Vet. Diagn. Invest. 7:420-422. Zimmerman, C. A., A. H. Rakes, T. E. Daniel, and B. A. Hopkins. 1992. Influence of dietary protein and supplemental niacin on lactational performance of cows fed normal and low fiber diets. J. Dairy Sci. 75:1965-1978. Zinn, R. A., F. N. Owen, R. L. Stuart, J. R. Dunbar, and B. B. Norman. 1987. B-Vitamin supplementation of diets for feedlot calves. J. Anim. Sci.65:267-277.