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 PUFA, antioxidants, sulfur amino acids, and selenium. The requirement may be increased with higher levels of PUFA, oxidizing agents, vitamin A, carotenoids, gossypol and trace minerals, and decreased with increasing levels of fat-soluble antioxidants, sulfur amino acids or selenium (McDowell, 2000; Dove and Ewan, 1990; Nockels, 1990).
The levels of PUFA found in unsaturated oils such as cod liver oil, corn oil, soybean oil, sunflower seed oil and linseed oil all increase 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). A combination of stress of infection and presence of oxidized fats in swine diets was reported to exaggerate vitamin E needs still further (Tiege et al., 1978). These researchers reported that supplements of 100 IU vitamin E per kg (45 IU per lb) of diet and 0.1 ppm selenium did not entirely prevent deficiency lesions in weanling pigs afflicted with dysentery and fed 3% cod liver oil.
Of all factors, the most important determinant of vitamin E requirements is the dietary concentrations of unsaturated fatty acids. A diet that contains high levels of fish oil may cause a threefold to fourfold increase in a cat's daily requirement for alpha-tocopherol. Early cases of pansteatitis ("yellow fat disease") occurred almost exclusively in cats that were fed a canned, commercial fish-based cat food, of which red tuna was the principal type of fish.
Since the PUFA content of membranes can be altered by dietary fats, it is not surprising that the dietary requirement for vitamin E is closely related to the dietary concentration of PUFA. When a large amount of polyunsaturated fat is fed after it has been stripped of tocopherols, as much as 100 mg alpha-tocopherol per kg (45.5 mg per lb) of diet may be insufficient to protect against lipofuscin formation (Hayes et al., 1969).
Harris and Embree (1963) have proposed a dietary alpha-tocopherol:PUFA ratio (mg/g) of 0.6:1 as a minimum to protect against PUFA peroxidation. This is a step in being more accurate for determining vitamin E requirements for pets; however, it should be realized that some PUFA require much more vitamin E to counteract detrimental effects than others. Fish oil PUFA that contain arachidonic acid (20:4), docosapentaenoic acid (22:5) and docosahexaenoic acid (22:6) require much more vitamin E for stabilization than do typical plant PUFA such as linoleic acid (18:2) and linolenic acid (18:3) (McDowell, 2000). The longer the carbon chain of a fatty acid and the more double bonds, the greater the vitamin E requirement. As an example, when 5% tuna oil (long carbon chain and greater unsaturation) was substituted for 5% of the lard (shorter carbon chain and less unsaturation), steatitis was severe in cats unsupplemented with vitamin E. The severity of steatitis was diminished by supplemental vitamin E, but was not entirely prevented by 34 IU per kg (15.5 IU per lb) of diet. When 136 IU per kg (61.8 IU per lb) of diet were provided, no lesions were seen (Gershoff and Norkin, 1962). By-product organs (e.g., liver) in the diet would also have more of the longer-chained, more unsaturated fatty acids.
Exact requirements for tocopherol in dogs and cats have not been established, but they are definitely a function of the peroxidizable PUFA consumed, and probably vary from as little as 5 mg per kg (2.3 mg per lb) of diet to as much as 100 mg per kg (45.5 mg per lb) when a high quantity of PUFA is fed. The requirement would range from approximately 0.25 to 5 IU per day for a cat and 1 to 20 IU per day for the average-sized dog.
The amount of vitamin E needed to maintain adequate growth and reproduction would not necessarily be enough to ensure optimal immune function as noted previously. For example, in the rat, Bendich et al. (1986) reports that 15 IU per kg vitamin E (7 IU per lb) of diet prevented muscle abnormalities and 50 IU per kg (23 IU per lb) of diet was necessary to prevent red blood cell breakdown, but for maximum lymphocyte stimulation 200 IU vitamin E per kg (91 IU per lb) of diet was required. For pigs, 150 IU per kg (68 IU per lb) of supplemental vitamin E resulted in a higher activity of lysozyme and a higher rate of yeast lysis (Riedel-Caspari et al., 1986).
Stress, exercise, infection and tissue trauma all increase vitamin E requirements (Nockels, 1991). Handling and bleeding heifers periodically in a 10-day period resulted in a large decrease in the vitamin E content of red blood cells and a 62% decrease in neutrophil vitamin E levels (Nockels, 1991). Vitamin E supplementation to stressed cattle reduces neutrophil vitamin E (Hogan et al., 1990) and increases immune response (Golub and Gershwin, 1985) in stressed calves. Nockels et al. (1996) noted that for most sampled tissues, stress did not affect alpha-tocopherol concentration, although other indicators confirmed a deficiency.
Requirements of both vitamin E and selenium are greatly dependent on the dietary concentrations of each other and they are mutually replaceable above certain limits. The relationship has been quantified to a certain degree for poultry. Chicks consuming a diet containing 100 IU per kg (45.5 IU 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 the 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 their augmentation from body stores as well as experimental dietary concentrations.
