New technology has further improved vitamin A stability by a cross-linking process, such as the reaction between gelatin and sugar, that makes the beadlet insoluble in water, giving it a more resistant coating that can sustain higher pressure, friction, temperature and humidity (Frye, 1994).
Several factors can influence the loss of vitamin A from feedstuffs during storage. The trace minerals in feeds and supplements, particularly copper, are detrimental to vitamin A stability. Dash and Mitchell (1976) reported the vitamin A content of 1,293 commercial feeds over a three-year period. The loss of vitamin A was over 50% in one year's time. Vitamin A loss in commercial feeds was evident even if the commercial feeds contained stabilized vitamin A supplements. There is evidence that yellow corn may lose carotene rapidly during storage. For instance, a hybrid corn high in carotene lost one-half of its carotene in eight months' storage at 25���C (77���F) and about three-quarters in three years. Less carotene was lost during storage at 7���C (45���F) (Quackenbush, 1963). Adams and Zimmerman (1984) showed that samples of moldy corn averaged 98% less carotene than sound corn. Because of vitamin A variability in feeds and losses during processing and storage, most animal nutritionists tend to ignore vitamin A activity in feedstuffs and rely exclusively on dietary fortification to arrive at vitamin allowances for poultry.
The stability of vitamin A in feeds and premixes has been improved tremendously in recent years by chemical stabilization as an ester, by the use of antioxidants and by physical protection using coatings (Shields et al., 1982). Nevertheless, vitamin A supplements should not be stored for prolonged periods prior to feedings.
Chen (1990) measured the stability of the three commercial cross-linked vitamin A beadlets on the market in trace mineral premixes and feeds. After three months' storage at high temperature and humidity, vitamin A retention varied from 30% to 80%, depending on the antioxidant present in the beadlet. In a 30% concentrate pelleted at 93��C (199��F), after three months' storage at high temperature and humidity, retention varied from 57% to 62%. The improvements in vitamin A stability through extrusion, in the last decade, increased by 35%, mainly because of the use of cross-linking processes (Frye, 1994).
Vitamin A and carotene destruction also occurs from processing feeds with steam and pressure. Pelleting effects of vitamin A in feed are determined by die thickness and hole size, which produce frictional heat and a shearing effect that can break supplemental vitamin A beadlets and expose the vitamin. In addition, steam application exposes feed to heat and moisture. Running fines back through the pellet mill exposes vitamin A to the same factors a second time. Between 5% and 40% of vitamin A present at mixing may be destroyed during pelleting of poultry feed.
Diseases and mycotoxins increase the need for supplemental vitamin A. It should be noted that diseases (i.e., enteric diseases such as malabsorption syndrome, coccidiosis and diarrhea, and mycotoxins) can interfere with the absorption and utilization of vitamin A. The effect of mycotoxins in the feed should also be considered since aflatoxin is known to interfere with protein synthesis (Doerr, 1987). Thus, it can be seen how mycotoxins might interfere with retinol-binding protein (RBP) synthesis and the transport of vitamin A. Aflatoxin can also cause poor pigmentation in birds by interfering with the absorption, transport and deposition of carotenoids (Tyczkowski and Hamilton, 1987).
Maximal immune responses in poultry may be achieved at higher dietary intakes of vitamin A and carotene than those needed for other functions (Sklan et al., 1994, 1995; Haq et al., 1996; Friedman and Sklan, 1997). Sklan et al. (1995) reported that vitamin A intakes between 2 and 6 ��g per g improve lymphocyte proliferation in poults as well as antibody titers to Newcastle disease virus. Cockerels fed beta-carotene and canthaxanthin were reported to produce significantly higher antibody titers in response to Newcastle disease virus vaccination than control birds (McWhinney et al., 1989). Tengerdy et al. (1990) reported that beta-carotene in combination with vitamin E provided increased protection against Escherichia coli infection in chickens.
The loss of carotenoids in poultry infected with coccidiosis was until recently believed to be the consequence of intestinal mucosal hyperplasia leading to malabsorption (Allen, 1988). Recent evidence indicates that the carotenoid losses are instead the result of oxidation resulting from the birds' cell-mediated immune response to the coccidial challenge (Allen, 1997). Oxidative bursts from the cell-mediated immune response have been documented to cause losses in vitamin E (Allen et al., 1996) and are presumed to have the same effect on vitamin A. To illustrate, Augustine and Ruff (1983) reported a 48% loss of plasma retinol levels in poults infected by Eimeria meleagrimitis.
Components of plants in the diets of poultry can impact the availability and metabolism of vitamin A. Saponins have been shown to interfere with vitamin A absorption (Jenkins and Atwal, 1994). Dietary exposure to pyrrolizidine alkaloids apparently impairs the mobilization of vitamin A stored in the liver (Huan et al., 1992).
Short-term administration of vitamin A in drinking water or by injection is recommended to support any specific measures used in treatment of diseased and convalescent animals. This is particularly true for poultry in which vitamin A stores may have been depleted due to fever or in animals suffering from intestinal disorders when vitamin A absorption is seriously impaired.
The decision for vitamin A supplementation should be based mainly on whether or not a deficiency could be a practical problem. As with most nutrients, a borderline deficiency is much more likely to occur than is a severe deficiency. Likewise, a marginal deficiency adversely affecting performance by a few percentage points is not easily detected (McDowell, 2000b). Based on the positive results that may be derived and taking into account that vitamin A supplementation is inexpensive and no toxicity problems have been reported when given at recommended levels, it seems beneficial to supplement vitamin A at all times for poultry and to increase the levels of supplementation fortification substantially for poultry that are subjected to disease or stress.
Increased levels of vitamin A are also important under intensive housing conditions where there are increased requirements in early life or under conditions of stress. The practice has been found particularly valuable under the following circumstances: for day-old chicks before transport and for laying hens when, for reasons unknown, laying performance suddenly drops (Hoffmann-La Roche, 1967). In laying hens, Squires and Naber (1993b) noted optimized egg production when hens were fed a vitamin A level of 8,000 IU per kg (3,636 IU per lb). However, hatchability of fertile eggs was optimized with a vitamin A level of 16,000 IU per kg (7,273 IU per lb).
