The NRC (1998) requirement for vitamin E for growing swine varies from 11 to 16 IU per kg (5 to 7 IU per lb) of diet. Limited information is available on the vitamin E requirements for reproduction. The NRC (1998) has estimated 22 IU per kg (10 IU per lb) of diet is required for breeding and lactating swine. After conducting a survey of the Australian pig industry, Cargill et al. (1994) concluded that levels above 35 mg alpha-tocopherol per kg of diet are required to maintain adequate plasma tocopherol levels in sows and piglets at weaning. These authors also concluded that tocopherol levels in sow diets appear to have a larger influence on the alpha-tocopherol status of weanling piglets than do weanling pig diets. Thus, feeding diets adequate in alpha-tocopherol to sows during gestation and lactation to prevent problems for the piglets after weaning was strongly recommended. Mahan (1991) found that supplemental vitamin E levels less than 16 IU per kg of diet were inadequate for sows. If sows were not provided adequate dietary vitamin E, the author indicated that smaller litter size, sow agalactia and pig mortality during the first week after birth might be exacerbated. Increasing the sows' dietary vitamin E level was found to improve the alpha-tocopherol status of the nursing piglets throughout lactation in addition to proving beneficial during the postweaning period. Mahan concluded that even if some tissue tocopherol might be mobilized, the main source of vitamin E for reproducing sows, nursing pigs and weaned pigs should be the diet. In a subsequent study, Mahan (1994) indicated that vitamin E requirements of reproducing sows are higher than the 1988 NRC recommendations of 10 to 22 IU per kg of diet. In his 1994 report, Mahan indicated that litter size improved and the incidence of mastitis, metritis and agalactia was reduced when 44 or 66 IU dl-alpha-tocopherol acetate per kg of diet was provided during gestation and lactation. These higher dietary vitamin E levels resulted in a better vitamin E status of piglets at weaning compared to the piglets from the sows fed the lower dietary level. Grandhi et al. (1993) did not detect a significant response in growth rate, feed intake or feed efficiency when gilts were fed vitamin E at above 1988 NRC-recommended levels during prepubertal development. Grandhi et al. (1993) did suggest ,however, that gilts may require a higher supplementation of vitamin E during prepubertal development (50 or 100 mg per kg of diet) for improved estrus and a minimum of 50 IU per kg during prebreeding and gestation for improved ovulation rate.
The effect of vitamin E levels in sow diets on postweaning progeny and vitamin E deficiency lesions postweaning was studied by Mahan (1985). Sows were fed a corn-soybean meal diet with no supplemented selenium. Supplemental vitamin E was added at the rate of either 0, 44 or 220 IU per kg (0, 20 or 100 IU per lb) of diet. Results suggest that sows deplete tissue tocopherol from the first to second parity. Progeny from sows not supplemented with vitamin E had a higher incidence of cardiac muscle degeneration, liver necrosis and ceroid pigmentation of body fat than those of supplemented sows at four weeks postweaning. All pigs from unsupplemented sows in the second parity exhibited gut edema; no offspring of supplemented sows were affected in this manner. Also, sows from the second parity supplemented with 220 IU per kg (100 IU per lb) of diet had no vitamin E deficiency signs at necropsy.
Young et al. (1977) and Whitehair et al. (1983a) studied the effects of supplemental vitamin E and (or) selenium in diets containing high moisture corn and soybean meal. Young et al. (1977) found that supplementation of gilt diets with selenium or vitamin E led to increased levels of these nutrients in the gilts' serum and colostrum as well as in their offspring's serum. The vitamin E supplementation of the sows had the greatest effect on the piglets through the colostrum versus the placental transfer of vitamin E. In the Whitehair et al. (1983a) study, sows were fed high-moisture corn with or without 50 IU per kg (23 IU per lb) of supplemental vitamin E and 0.10 ppm selenium. Supplemented sows had a greater number of pigs born and weaned, as well as increased litter weight gains compared to unsupplemented sows. Also, 50% of the unsupplemented sows had clinical signs of mastitis-metritis-agalactia (MMA), whereas no vitamin E-supplemented sows were observed with clinical MMA.
Bertsch et al. (1975) investigated the effect of dietary vitamin E on the subsequent uptake of radioactive selenium by swine erythrocytes in vitro and also on reproductive performance. The authors concluded that dietary vitamin E partially alleviated the increased need for dietary selenium due to lactation stress. They also reported that hypogalactia was less pronounced in supplemented sows although the incidence of MMA and reproductive performance were not significantly influenced by dietary vitamin E (150 mg of dl-alpha tocopherol per day during gestation and lactation plus an additional 50 mg per pig nursing).
Sow colostrum and milk vitamin E concentrations are affected by dietary vitamin E. Mahan (1985) reported that, regardless of dietary vitamin E supplementation level, colostrum has a high alpha-tocopherol content that decreases rapidly as lactation proceeds. Pregnant gilts and sows supplied with adequate dietary vitamin E will produce healthy, normal baby pigs with limited amounts of vitamin E (Mahan, 1986). Nielsen et al. (1973) and Loudenslager et al. (1986) reported that swine colostrum has high concentrations of alpha-tocopherol compared to that of milk and this has been confirmed by others (e.g., Hidiroglou et al., 1993; Mahan, 1994); however, higher concentrations of beta- and gamma-tocopherol were present in milk than in colostrum. As sows age, vitamin E content of colostrum decreases (Mahan, 1985). Consequently, the amount of vitamin E activity available to the pig decreases, resulting in poor vitamin E tissue status in the weaning pig. Mahan (1985) has also indicated that vitamin E status in the breeding female can be compromised with continued reproduction. These observations, coupled with the fact that non-alpha-tocopherols in milk at or near weaning have low vitamin E biological activity (10% to 40%), result in young pigs consuming low quantities prior to weaning. Meyer et al. (1981) reported that plasma tocopherol concentrations decreased in pigs postweaning. These data suggest that weaned pigs are highly susceptible to vitamin E deficiency, which may increase mortality at weaning or shortly afterward until consumption of a well-fortified vitamin E diet is adequate. Carrion et al. (1994) evaluated the effect of injectable (600 IU of d-alpha-tocopherol injected I.M. at breeding and at day 110 of gestation) versus dietary (23 IU of d-alpha-tocopherol acetate per lb) of vitamin E on tocopherol status of sows and their progeny over three parities. The researchers found that both dietary and injectable tocopherol supplementation enhanced tocopherol status of sows (based on serum and milk tocopherol concentrations) and their offspring.
Additionally, reproductive performance was improved for sows consuming a diet of 15 IU per kg (7 IU per lb) of vitamin E and 0.1 ppm selenium when injectable vitamin E and selenium were administered (Chavez and Patten, 1986). Litter size, total litter weight at birth and litter size at weaning were significantly greater for supplemented animals. Additionally, the effect of vitamin E and selenium on reproductive performance was more pronounced in older sows with three or more parities than in gilts. Piatkowski et al. (1979) reported that 0.1 ppm of added selenium and 22 IU of added vitamin E per kg (10 IU per lb) of diet appear necessary to maintain tissue vitamin E levels. The Agricultural Research Council (ARC, 1981) has suggested a higher requirement than the NRC (1998) for growing pigs: 20 to 50 IU per kg (9 to 23 IU per lb) of diet. In order to obtain a certain safety margin for prevention of vitamin E and selenium deficiency syndromes, Jensen et al. (1988b) suggested growing swine receive 30 IU of supplemental vitamin E per kg (14 IU per lb) of diet.
Myer et al. (1992) found no effect on farrowing percentage or the number of pigs born alive when sows were injected with 500 to 600 IU vitamin E and 10 to 12 mg selenium prior to breeding. Anderson et al. (1997) investigated the effect of vitamin A and (or) beta-carotene injections just before and (or) shortly after breeding and of dietary supplementation of vitamin E on blood and tissue concentrations of alpha-tocopherol in gestating gilts. Although previous authors had presented evidence with chicks and laboratory rats that very high dietary vitamin A may interfere with vitamin E absorption and blood alpha-tocopherol concentrations, Anderson et al. (1997) did not find any detrimental effect of three 350,000-IU injections of vitamin A shortly before, at and shortly after breeding on vitamin E status of gilts during early gestation. Increases in alpha-tocopherol concentration in serum and tissues were noted following dietary vitamin E supplementation as expected. Anderson et al. (1995a) also found no consistent evidence that high levels of dietary vitamin A interfere with performance or serum and tissue concentrations of alpha-tocopherol in growing-finishing swine. Hoppe et al. (1992) reported the effects of dietary retinol on plasma and tissue alpha-tocopherol in pigs. While no effects on M. longissimus and backfat alpha-tocopherol levels were evident, alpha-tocopherol levels in heart and liver showed an inverse relationship with dietary retinol. Dietary retinol up to 10,000 IU per kg did not affect tocopherol concentrations except in cardiac muscle.
In boars, it was reported that vitamin E enhanced fertility even when supplementation was raised from 40 to 80 mg per kg feed (Westendorf and Richter, 1977). Not only was production improved, but semen volume and sperm concentration were increased. Marin-Guzman et al. (1997) reported that when diets low in selenium and vitamin E were fed, the percentage of abnormal sperm increased and sperm motility declined. Boars that were fed low-selenium diets had a higher percentage of abnormal sperm primarily due to abnormal tail morphology. In these experiments, Marin-Guzman and co-workers evaluated the effects of dietary selenium at 0 or 0.5 ppm and vitamin E at 0 or 220 IU per kg. They indicated that boars with a low selenium status had fewer sperm that reached and penetrated the zona pellucida, which could lower the fertilization rate. The authors stated that vitamin E had a less dramatic effect than did selenium. This led them to suggest that although both selenium and vitamin E have important roles in maintaining semen and sperm quality in boars, their effects are unique with vitamin E, perhaps acting through its antioxidant properties.
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. For example, Simesen et al. (1979) reported that oxidized herring meal increased the requirement for vitamin E while oxidized lard had very little effect on the requirement. The requirement may be increased with higher levels of PUFA oxidizing agents, vitamin A, carotenoids and trace minerals and decreased with increasing levels of fat-soluble antioxidants, sulfur amino acids or selenium. Gebert et al. (1999a) evaluated the requirements for vitamin E supplementation when dietary phytase was included in pig diets susceptible to lipid oxidation. They concluded that an extra dietary supplementation with alpha-tocopheryl acetate might be recommended when dietary phytase is included in order to avoid detrimental effects on fat digestibility. In a separate report, Gebert et al. (1999b) determined that the combined addition of vitamin E and phytase increased the cecal digestibility of dietary fat, oleic acid and linoleic acid.
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 needs still further (Teige et al., 1978a). These researchers reported that supplements of 100 IU of 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. Under the conditions of certain experiments, an effect of including dietary fat in gilt rations on alpha-tocopherol concentrations in their plasma or in colostrum or milk is not always observed (Hidiroglou et al., 1993, 1995). However, Wang et al. (1996) reported that vitamin E and lipid peroxidation were both affected by dietary vitamin E and dietary PUFA. In their study the requirement for vitamin E in young pigs increased as PUFA levels in the diet increased. Furthermore, the authors indicated that lipid peroxidation response of pigs was a suitable index for evaluating vitamin E requirements. The lipid peroxidation response was assessed by thiobarbituric acid-reactive substances in erythrocytes and ethane and pentane levels in exhaled gases.
Sauer et al. (1997) indicated that when milk replacer diets contain canola oil as the sole fat source, additional vitamin E supplementation is required. This finding did not appear to be related to PUFA concentration. The authors indicated that the factor or factors present in canola oil that increase vitamin E requirements for the young pigs remain to be determined. However, they referred to the fact that the higher phytosterol content in canola oil could interfere with vitamin E absorption or accelerate its rate of depletion in tissues.
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) reported that 15 IU of vitamin E per kg (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 of vitamin E per kg (91 IU per lb) of diet was required. For pigs, 150 IU of supplemental vitamin E per kg (68 IU per lb) of diet resulted in a higher activity lysozyme and a higher rate of yeast lysis (Riedel-Caspari et al., 1986).
Requirements of both vitamin E and selenium are greatly dependent on the dietary concentrations of each other. Hitchcock et al. (1978) investigated the effects of dietary vitamin E on utilization of selenium by swine. Hakkarainen et al. (1978b) determined that either selenium or vitamin E supplementation individually was inadequate but together in appropriate amounts did prevent the development of vitamin E-selenium deficiency. In reports by Van Vleet and Ruth (1977) and Van Vleet (1982), the efficacy of supplements in the prevention or control of selenium-vitamin E deficiency was evaluated. In 1982, Van Vleet suggested that approximately 0.2 mg of selenium per kg of feed and 30 IU of vitamin E per kg of feed be included in the diets of growing swine to prevent selenium-vitamin E deficiency. Bengtsson et al. (1978a) were able to prevent the occurrence of vitamin E and selenium-deficiency syndrome in pigs fed a selenium-deficient diet by supplementing with 45 mg of dl-alpha-tocopheryl acetate per kg of diet beyond that present in the basal diet. In a related study, Bengtsson et al. (1978b) reported that selenium supplementation in the diet of weaned pigs could not overcome the effects of vitamin E-deficient basal rations. Wastell et al. (1972) investigated the effects of supplemental vitamin E and (or) selenium on performance, deficiency symptoms and blood components of growing-finishing pigs fed diets low in vitamin E and selenium.
Regional dietary considerations arise as well. Ku et al (1972) noted significant regional differences in dietary selenium content after surveying dietary selenium and vitamin E concentrations in diets fed to growing swine in 13 different states. Piper et al. (1975) indicated that when cull pea rations are utilized, as is common in the Pacific Northwest regions of the United States, selenium-vitamin E deficiency can develop unless a minimum selenium requirement for growing pigs of 0.06 to 0.07 ppm is provided. Determination of vitamin E requirements is further complicated because the body has a fairly large ability to store both vitamin E and Se. Sows maintained on a diet deficient in vitamin E and selenium produced normal piglets during the first reproductive cycle of the deficiency and clinical deficiency signs occurred only after five such cycles (Glienke and Ewan, 1974). A number of studies to establish requirements for both nutrients have underestimated the requirements by failing to account for their augmentation from both body stores as well as experimental dietary concentrations. Regarding the relationship between selenium and vitamin E, Malm et al. (1976a) suggested that selenium may play a role in the transport of vitamin E across the placenta in swine. In this study, efficient placental transfer of vitamin E was observed even in dams, which had low serum concentrations of alpha-tocopherol.
A unique consideration arises for pigs fattened under certain organic farming systems. Kienzle et al. (1993) recently reported that a variety of deficiencies including vitamin E and selenium were observed in one such herd with resulting deaths.
