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The National Research Council (NRC) subcommittees have established vitamin A requirements for growth that approximate 2,200 IU per kg of diet dry matter (1,000 IU per lb) for both beef and dairy cattle (NRC, 1989, 1996) and 940 to 2,833 IU per kg (427 to 1,288 per lb) for sheep (NRC, 1985). Typical requirements are illustrated in Table 1. For beef breeding animals, dietary vitamin A requirements are 2,800 IU per kg (1,273 IU per lb) for pregnant heifers and cows, and 3,900 IU per kg (1,773 IU per lb) for lactating cows and breeding bulls (NRC, 1996). For dairy cattle, the requirements are 3,200 IU per kg (1,455 IU per lb) for cows and mature bulls, and 4,000 IU per kg (1,818 IU per lb) for dry, pregnant cows and the first three weeks of lactation (NRC, 1989). The NRC publication for dairy cattle lists the vitamin A requirement for a 1,320-lb (600 kg) mature cow as 46,000 IU per day regardless of the stage of reproductive cycle. No direct allowance is made for increments of milk production in the 1989 NRC publication. The dietary guidelines listed above would result in daily vitamin A intakes of approximately 70,400 IU for lactating cows consuming 48.4 lbs (22 kg) of dry matter daily and 40,000 IU/day for dry, pregnant cows consuming 22 lbs (10 kg) dry matter per day. The resulting increase of 30,400 IU/day vitamin A intake in lactating cows is equal to the vitamin A contained in approximately 60 lbs (27 kg) of milk, using average values for vitamin A content of cow's milk (Table 2).
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Practical factors influencing vitamin A requirements are listed in Table 3. Minimum requirements have been determined by various bioassay methods, including prevention of night blindness, maintenance of liver stores, maintenance of reproduction and maintenance of normal pressure in the cerebrospinal fluid (CSF). The minimum vitamin A requirement for normal growth may be lower than the requirements for higher rates of gain, resistance to various diseases, normal bone development and nervous system function in ruminants (Weichenthal et al., 1963). The vitamin A requirement of calves was increased by as much as sevenfold, depending on the criteria used to determine it (Lewis and Wilson, 1945). The vitamin A requirement values (IU per 100 kg body weight) were 2,640 for adequate weight gains, 5,280 for increased weight gains and 17,600 for optimum weight gains and vitamin A liver stores (1,200, 2,400 and 8,000 IU per 100 lbs body weight, respectively). The authors suggested that calves born with low vitamin A liver stores or calves deprived of adequate colostrum should receive a minimum of 16,500 IU per 100 kg (7,500 IU per 100 lbs) body weight. Three to five times this level may be necessary for adequate vitamin A liver stores in calves during the critical first few months of life. Many commercial calf milk replacers contain 20,000 IU vitamin A per pound of powder.
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Calf vitamin A requirements and fortification rates have been the subject of recent studies. Franklin et al. (1998) supplemented milk with 0, 15,000 or 30,000 IU per day of vitamin A as retinyl acetate and studied growth and immune system parameters through six weeks of age. Vitamin A administered by this route did not significantly elevate plasma retinol concentrations or affect growth performance or immune cell parameters, but it did lower plasma vitamin E concentrations. Given that normal milk contains approximately 10,000 IU of vitamin A activity per kg solids, and that calves were fed 4.54 kg of milk per day (12% solids), the total vitamin A intakes of calves in the study would have been 5,448, 20,448 and 35,448 IU per day. Hammell et al. (1998) reported greater weight gains in bull calves fed no supplemental vitamin A than in calves fed either 34,000 or 68,000 IU vitamin A per day, while weight gain of calves fed 1,700 IU vitamin A per day was not statistically different from either the controls or the higher vitamin A levels.
In contrast to these findings, Eicher et al. (1994) reported that feeding milk replacer fortified with 87,000 IU vitamin A per kg solids (39,474 IU/calf/day) did not depress plasma vitamin E concentrations and improved fecal scores of calves through 45 days of age, compared to feeding 7,000 IU per kg milk replacer solids. Vitamin E was fed at either 11.2 or 57 IU per kg solids. There was a positive interaction between vitamins A and E on bactericidal activity of neutrophils. The route of administration of vitamin A in these studies, added directly to milk versus manufactured into milk replacer, may be a factor in the contrasting outcomes.
Most recently, Swanson et al. (1999) reported findings indicating that current NRC vitamin A requirements for dairy calves may be too low to maintain liver stores during the first weeks of life. Calves were fed milk replacers containing 1,900, 3,800, 7,600, 15,200 or 44,000 IU vitamin A per kg solids (863, 1,727, 3,454, 6,908 or 20,000 IU/lb solids). Feeding rates of milk replacer (12% solids) were 10% of body weight during week 1 and 12% of body weight during weeks 2 to 4 of the experiment. Liver biopsies were performed at 4, 9, 15, 21 and 28 days of age and showed that hepatic vitamin A (retinol) stores were only maintained by the 7,600 IU level of vitamin A and continued to increase through the highest level of 44,000 IU per kg (20,000 IU per lb) of vitamin A supplementation. The current NRC vitamin A requirement for calves is 3,800 IU per kg solids in milk replacer. In this study, the vitamin A concentrations of both liver and serum were low, despite feeding of adequate colostrum at birth. Only at the highest level of supplementation (44,000 IU/kg) did liver and serum vitamin A reach levels generally accepted as being adequate (Figure 1).
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In grow-finish lambs, May et al. (1987) used cerebrospinal fluid (CSF) pressure and plasma and liver retinol concentrations to assess minimum vitamin A requirements. Lambs were first depleted of liver vitamin A stores and then for 16 weeks fed varying levels of vitamin A (2, 4, 8, 16, 32 or 64 µg per kg live weight per day). This equates to 6.7, 13.3, 26.6, 53.3, 106.6 or 213.1 IU per kg live weight. Under these experimental conditions, CSF pressure was maintained at normal levels by actual vitamin A intakes of 14 µg/kg live weight or greater. Plasma concentrations of 20 µg retinol/dl were adequate to maintain normal CSF pressure. The minimum vitamin A intake required to prevent elevated CSF pressure in this study is essentially equal to that published by the NRC (14.1 µg/kg liveweight).
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As discussed earlier in this section, different animal species convert beta-carotene to vitamin A with varying degrees of efficiency. The conversion rate of the rat has been used as the standard value, with 1 mg of beta-carotene equal to 1,667 IU of vitamin A, for 50% conversion efficiency. Of the species studied, only poultry are equal to the rat in vitamin A conversion efficiency.
For ruminants, 1 mg of beta-carotene in the diet is equivalent to approximately 400 IU of vitamin A (retinol) for beef cattle (NRC, 1996), dairy cattle (NRC, 1989) and goats (NRC, 1981), and 400 to 700 IU for sheep (NRC, 1985) (Table 4). There has been variation in experimental results (Bauernfeind, 1981).
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Factors that influence the rate at which carotenoids are converted to vitamin A include type of carotenoid, class and production level of animal, individual genetic differences in animals and level of carotene intake (NRC, 1996). Efficiency of conversion of beta-carotene to retinol decreases with increasing intake of either carotenes or vitamin A (van Vliet et al., 1996). For example, the conversion efficiency ratio varies from 4:1 (25%) to 16:1 (6.25%) in the dairy calf as intake of vitamin A equivalents increases from markedly deficient to excess levels (Bauernfeind, 1981; Dolge et al., 1956). Stress conditions, such as extremely hot weather, viral infections and impaired thyroid function, have also been suggested as causes for reduced carotene conversion to vitamin A. Vitamin A requirements are increased by stress conditions such as environmental stress and increased disease exposure. This may reflect increased activity of the adrenal gland, which is known to be dependent on vitamin A. In general the disease state results in decreased serum concentrations of vitamin A (Figure 2).
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Dietary factors can affect vitamin A metabolism and increase requirements. These factors include (a) deficiencies of protein, vitamin E, zinc, iodine or phosphorus; (b) elevated nitrate levels in feeds or water; (c) the presence of mycotoxins or ethanol in feed; and (d) the feeding of high concentrate rations or the feeding of significant quantities of polyunsaturated fatty acids (Chhabra and Afora, 1987; Gallup et al., 1953; Frye et al., 1991; Miller et al., 1969; Harris, 1975; Bauernfeind, 1981). Conversely, very low-fat diets impair absorption of vitamins A, D, E and K. There is considerable research and some controversy on the relationship of' nitrates to vitamin A nutrition. In a review of this subject by Rumsey (1975), it was concluded that although nitrates can be shown to have an adverse effect on vitamin A in vitro, this effect does not appear to be significant under most feeding conditions. Bauernfeind (1981) cites data showing that nitrite, the initial reduction product of nitrate, destroys vitamin A activity in stored forages, especially at pH below 5, which is typical of silages.
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