To offset losses of vitamin E activity in feedstuffs, diets should be adequately fortified using dl-alpha-tocopheryl acetate, the most stable source of vitamin E activity available for feed use. Methods of providing supplemental vitamin E are: (1) as part of a concentrate or liquid supplement, (2) in drinking water preparations and (3) as an injectable product.
Commercially, the acetate esters of vitamin E are available in purified form or in various dilutions and include: (1) a highly concentrated oily form, for further processing; (2) emulsions incorporated in powders for use in dry premixes or water-dispersible preparations; and (3) adsorbates or absorbates of the oily tocopheryl acetate on selected carriers, in free-flowing, "dry" powder, meal or granules.
Injectable vitamin E preparations are also available which contain free d- or dl-alpha-tocopherol. Liquid emulsions of appropriate types are used in drinking water and liquid feeds, in regular feed and for injection. In this form, alpha-tocopherol is more efficiently absorbed from intramuscular injection sites than from a water-miscible preparation containing alpha-tocopheryl acetate or either form dissolved in an oily base (Machlin, 1984). Weaver et al. (1991) indicated that when dl-alpha-tocopheryl acetate was solubilized in 2% benzyl alcohol in sesame oil, the injection did not elicit a response, suggesting it was unavailable. Van Heugten et al. (1997) indicated that supplementation of drinking water with selenium and vitamin E can substantially increase intake and may improve the selenium and vitamin E status of weanling pigs. Products containing vitamin E and selenium are often given intramuscularly to animals exhibiting clinical signs of muscular degeneration. Response to treatment of this condition is extremely variable depending on degree of muscular degeneration. However, intramuscular injection of alpha-tocopherol and selenium to swine usually provides a rapid means of alleviating deficiencies of these nutrients (Mahan et al., 1973). Van Vleet et al. (1975) indicated that for treatment in herds diagnosed recently with selenium-vitamin E deficiencies or in order to ensure that pigs likely to develop the disease are protected, injection of selenium-vitamin E should provide a safe and effective alternative. In their report, the efficacy and safety of injections of different doses of selenium-vitamin E in newborn pigs were evaluated. Van Vleet (1975) concluded that the injection procedure was safe for the animals treated and for people who ultimately consume the meat products after an adequate withdrawal period. Van Vleet et al. (1973) also indicated the parenteral treatment of baby pigs with selenium-vitamin E injections and subsequent inclusion of moderate amounts of vitamin E in starter and grower rations led to a progressive decline in herd mortality and complete control of death losses from selenium-vitamin E deficiency. Mahan and Moxon (1980) reported that a single injection of vitamin E and selenium would apparently benefit herds experiencing vitamin E-selenium deficiency if given shortly prior to weaning.
The need for supplementation of vitamin E is dependent on the requirement of individual species, conditions of production, and the amount of available vitamin E in feed sources. The primary factors that influence the need for vitamin E supplementation in swine include: (1) vitamin E and (or) selenium-deficient concentrates; (2) diets that contain predominantly non-alpha-tocopherols and thereby are less biologically active; (3) diets that include ingredients that increase vitamin E requirements (i.e., unsaturated fats, waters high in nitrates); (4) harvesting, drying or storage conditions of feeds that result in destruction of vitamin E and (or) selenium; (5) accelerated rates of gain, production and feed efficiency that increase metabolic demands for vitamin E; (6) intensified production that also indirectly increases vitamin E needs of animals by elevating stress, which often increases susceptibility to various diseases; and (7) inclusion of high concentrations of trace elements (i.e., copper and iron) that accelerate the oxidative destruction of alpha-tocopherol.
Vitamin E-selenium deficiencies are found in specific world regions and are characterized by low concentrations of vitamin E and selenium in feedstuffs. One example of regional selenium-vitamin E deficiencies linked to low dietary tocopherol is that which occurs in the Pacific Northwest when cull pea diets are fed to swine (McDowell et al., 1974; Piper et al., 1975; McDowell et al., 1977). Moir and Masters (1979) described the outbreaks of hepatosis dietetica and mulberry heart disease in Western Australia and found that the extensive use of lupine seed as a protein source in pig rations may have contributed to an increase in the incidence of hepatosis dietetica since lupine seed is relatively low in selenium concentrations. Sharp et al. (1972b) indicated that in the case of diets containing high-moisture corn, the deficiency may be due to a shortage of vitamin E, while if diets contain Torula yeast, deficiencies may be due to selenium inadequacies. Regions that rely on concentrate importations from areas deficient in selenium and (or) vitamin E (i.e., midwestern United States) likewise must provide these nutrients to swine. Adverse conditions, such as poor weather (drought and early frost), molds and insect infestation, will reduce the vitamin E value of feedstuffs. Aflatoxins may exacerbate vitamin E deficiency in pigs (Harvey et al., 1995). The vitamin E activity in blighted corn was 59% lower than that in sound corn, and the vitamin E activity in lightweight corn averaged 21% below that in sound corn (Adams et al., 1975). Feed spoilage will also promote vitamin E-selenium deficiencies; therefore, to prevent loss of vitamin E in diets, the producer should use fresh feed at all times because the vitamin is rapidly destroyed under hot, humid conditions. Losses during storage increase as the duration and temperature of storage increase.
Many attempts have been made to control lipid oxidation in meats through the use of antioxidants. One such approach is through dietary supplementation of vitamin E, which functions as a lipid-soluble antioxidant in cell membranes (Linder, 1985), thus protecting phospholipids and even cholesterol against oxidation. Increased dietary levels of vitamin E result in higher tissue tocopherol concentrations and greater stability of these tissues toward lipid oxidation. Buckley and Connolly (1980) reduced the rate of rancidity development in frozen pork by including vitamin E in the feed (80 mg per day per animal) for seven days before slaughter of the pigs. Likewise, meat from turkeys raised on vitamin E-supplemented diets was more stable to rancidity development than meat from birds receiving control diets (Bartov et al., 1983; Uebersax et al., 1978). More recently, Faustman et al. (1989) demonstrated the improvement of pigment and lipid stability in Holstein steer beef by dietary supplementation with vitamin E. These investigators concluded that the benefit of supplementing Holstein steers with vitamin E is due to the incorporation of the antioxidant into the cell membranes where it has its physiological antioxidant effect. Exogenous addition of alpha-tocopherol to meat products during processing does not ensure that the antioxidant is properly positioned to perform its antioxidant role (Faustman et al., 1989).
Results of numerous studies have shown that feeding swine high supplemental vitamin E levels prior to slaughter increased the shelf life and delayed rancidity development and discoloration, thus preventing off-odors and off-flavors of pork (Hvidsten and Astrup, 1973; Marusich, 1978; Buckley and Connolly, 1980; Astrup and Langebrekke, 1985; Gray et al., 1989). Supplemental vitamin E was transferred from the diet to the fat of the pigs, increasing stability of the fat towards oxygen. Favorable effects of vitamin E supplementation on pork stability could result from 50 IU per kg (23 IU per lb) of diet fed continuously or 100 to 200 IU per kg (46 to 90 IU per lb) for one month prior to slaughter (Hvidsten and Astrup, 1973). These high supplemental vitamin E levels provided allowances greater than those needed for adequate growth, feed conversion or reproduction. Supplemental vitamin E extended the shelf life of fresh and frozen whole carcasses, as well as further processed meat products.
Gray et al. (1989) reported that lipid peroxidation of uncooked pork is initiated in membrane-bound lipids. Long-term supplementation (10 weeks) of 200 mg alpha-tocopherol per kg (91 mg per lb) of diet increased the stability of membrane lipids towards metmyoglobin/hydrogen peroxide initial peroxidation. Additionally, these researchers reported that pork chops stored at 4°C in the dark and under fluorescent lights from pigs fed alpha-tocopherol supplemented diets were more stable than those from control pigs. These authors concluded that incorporation of antioxidants such as alpha-tocopherol into the membrane lipids will influence stability of meat products, particularly during refrigerated and frozen storage of uncooked meat products. Pork chop drip loss was reduced by 39% and 34% after six and 10 days storage at 4°C under fluorescent lights, respectively (Gray, 1990). Numerous authors (Smith et al., 1997; Jensen et al., 1998; Van Heugten, 1999) have recently reviewed the role of vitamin E in pork quality.
