The NRC (1994) requirement for vitamin E for poultry species varies from 5 to 25 IU per kg (2.3 to 11.4 IU per lb) of diet. Growing and laying chickens have the lowest requirement at 5 IU per kg (2.3 IU per lb) while breeding turkeys and Japanese quail have the highest requirement at 25 IU per kg (11.4 IU per lb). Vitamin E requirements are exceedingly difficult to determine because of the interrelationships with other dietary factors, therefore its requirement is dependent on dietary levels of polyunsaturated fatty acids (PUFA), antioxidants, sulfur amino acids and selenium. The requirement may be increased with increasing levels of PUFA, oxidizing agents, vitamin A, carotenoids and trace minerals and decreased with increasing levels of fat-soluble antioxidants, sulfur amino acids and selenium (McDowell et al., 1996; McDowell, 2000a).
The levels of PUFA found in unsaturated oils such as cod liver oil, corn oil, soybean oil, sunflower seed oil, linseed oil and blended commercial feed grade fat all increase the vitamin E requirements. This is especially true if these oils are allowed to undergo oxidative rancidity in the diet or are in the process of peroxidation when consumed by the animal. If they become completely rancid before ingestion, the only damage is the destruction of the vitamin E present in the oil and in the feed containing the rancidifying oil. But if they are undergoing active oxidative rancidity at the time of consumption, they apparently cause destruction of body stores of vitamin E as well (Scott et al., 1982).
As previously noted, vitamin E requirement depends very much on the level and kind of PUFA in the diet. For example, PUFA generate an additional vitamin E requirement in the order of 0.6, 0.9, 1.2, 1.5, and 1.8 mg of vitamin E (RRR-alpha-tocopherol-equivalents), respectively, for 1 g of dienoic, trienoic, tetraenoic, pentaenoic, and hexaenoic fatty acids (Bassler, 1991; Surai, 1999). In this respect, some vitamin E- containing oils have a positive vitamin E balance (sunflower and wheat germ oils), corn oil has zero balance, and fish oil and lard have negative vitamin E balance. Inclusion of such oils and fat into the diet increases the vitamin E requirement. Fish oil PUFA that contains arachidonic acid (20:4), docosapentaenoic acid (22:5) and docosahexaenoic acid (22:6) require much more vitamin E for stabilization than typical plant PUFA such as linoleic acid (18:2) and linolenic acid (18:3). The longer the carbon chain of a fatty acid and the more double bonds, the greater the vitamin E requirement.
Requirements of both vitamin E and selenium are greatly dependent on the dietary concentrations of each other. As noted earlier, they are mutually replaceable within certain limits. Chicks consuming a diet containing 100 mg per kg (45 mg per lb) vitamin E required 0.01 ppm selenium, while those receiving no added vitamin E required 0.05 ppm selenium (Thompson and Scott, 1969). Determination of vitamin E requirements is further complicated because the body has an ability to store both vitamin E and selenium. A number of studies to establish requirements for both nutrients have underestimated the requirements by failing to account for both body stores as well as experimental dietary concentrations.
There is a delicate balance between pro-oxidants and antioxidants in the organism, and dietary vitamin E supplementation is considered to be an effective means of antioxidant system enhancement in stress conditions. The risk of lipid peroxidation is related to both dietary and environmental factors, which can greatly vary (Surai, 1999). Dietary factors include balance of antioxidant nutrients, such as selenium, vitamin E, carotenoids, ascorbic acid and synthetic antioxidants, with pro-oxidant nutrients, such as PUFA, copper and iron. Environmental factors include atmospheric pollutants, toxins, infectious agents and other stressors of various types (Herdt and Stowe, 1991).
The amount of vitamin E needed to maintain adequate growth, egg production, and reproduction would not necessarily be enough to ensure optimal immune function as noted previously. For example, chicks hatched from hens supplemented with very high levels of vitamin E had significantly higher antibody titers at one and seven days of age than chicks from the control group (Haq et al., 1996). Vitamin E supplementation has been shown to increase resistance to infection in farm and laboratory animals (Tengerdy, 1989). Vitamin E increases immune response against infections by improving phagocytic cell function. Phagocytic macrophages in young poults were increased when vitamin E in the diet was at 120 IU per kg (54.5 IU per lb), while a higher level at 300 IU per kg (136.4 IU per lb) was shown to optimize humoral immunity when poults were challenged with sheep red blood cells. Up to 115 IU per kg (52.3 IU per lb) of vitamin E was required to minimize red blood cell destruction in poults that were challenged with sheep red blood cells (Soto-Salanova, 1997). Reduced mortality and increased humoral immune titers were reported when chicks infected with Escherichia coli were supplemented with 150 or 300 mg dl-alpha-tocopherol per kg (682 to 136.4 mg per lb) diet (Heinzerling et al., 1974). Supplementation of vitamin E may enhance the immune status of layers during heat stress and potentially during other stress periods such as transport, vaccination and molt.
