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«Available online at Scholars Research Library Annals of Biological Research, 2011, 2 (4) :244-251 ...»

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capacity, it prevents oxidation of unsaturated lipid materials within cells, thus protecting fats within the cell membrane from breaking down. It is the oxidation of vitamin E that prevents oxidation of other lipid materials to free radicals and peroxides within cells, thus protecting the cell membrane from damage [8]. If lipid hydroperoxides are allowed to form in the absence of adequate tocopherols, direct cellular tissue damage can result, in which peroxidation of lipids destroys structural integrity of the cell and causes metabolic derangements. Vitamin E reacts or functions as a chain-breaking antioxidant, thereby neutralizing free radicals and preventing oxidation of lipids within membranes. Free radicals may not only damage their cell of origin but migrate and damage adjacent cells in which more free radicals are produced in a chain reaction leading to tissue destruction [9]. At least one important function of vitamin E is to interrupt production of free radicals at the initial stage. Myodystrophic tissue is common in cases of vitamin E-Se deficiency with leakage of cellular compounds such as creatinine and various transaminases through affected membranes into plasma. The more active the cell, the greater the inflow of lipids for energy supply and the greater the risk of tissue damage if vitamin E is limiting. This antioxidant property also ensures erythrocyte stability and maintenance of capillary blood vessel integrity. Interruption of fat peroxidation by tocopherol explains the well-established observation that dietary tocopherol protect or spare body supplies of such oxidizable materials as vitamin A, vitamin C, and the carotenes. Certain deficiency signs of vitamin E can be prevented by diet supplementation with other antioxidants, thus lending support to the antioxidant role of tocopherols. Semen quality of boars was improved whit Se and vitamin E supplementation, whit vitamin E playing a role in maintaining sperm integrity in combination whit Se [10]. Chemicals antioxidants are stored only at very low levels, thus they are not as effective as tocopherol. It is clear that highly unsaturated fatty acids in the diet increase vitamin E requirements. When acting as an antioxidant, vitamin E supplies become depleted, thus furnishing an explanation for the often observed fact that the presence of dietary unsaturated fats augments or precipitates vitamin E deficiency.

Relationship to toxic elements or substance Both vitamin E and Se provide protection against toxicity whit three classes of heavy metals [18].

In one class, which includes metals like cadmium and mercury, Se is highly effective in altering toxicities, but vitamin E has little influence. In the second class, which includes silver and arsenic, vitamin is highly effective; Se is also effective but only at relatively high levels. The third class, which includes lead, is counteracted by vitamin E, but Se has little effect. Vitamin E can be effective against other toxic substance. For example, treatment with vitamin E gave protection to weanling pigs against monensin-induced skeletal muscle damage [12].

Requirements Whanger [21], after reviewing the literature, concluded that the minimum vitamin E requirement of normal animals and humans is approximately 30 ppm of diet. Vitamin E requirements are exceedingly difficult to determine because of the interrelationships with other dietary factors. The requirement may be increased with increasing levels of PUFA, oxidizing agents, vitamin A, carotenoids, gossypol, or trace minerals and decreased with increasing levels of fat-soluble antioxidants, sulfur amino acids, or Se [13].on otherwise adequate diets containing sufficient cysteine and methionine and containing a minimum of PUFA, vitamin E requirements appear to be low. This is evidence by difficult in producing deficiency signs on such diets under optimum environmental conditions. The levels of PUFA found in unsaturated oils such as cod liver oil, corn oil, soybean oil, sunflower seeds oil, and linseed oil increase vitamin E requirements. This is especially true 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 Scholars Research Library Hamed Amini Pour et al Annals of Biological Research, 2011: 2 (4):244-251 _____________________________________________________________________________

ingestion, the only damage is the destruction of the vitamdiffin 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 [20]. The vitamin E requirement for dogs is five times higher under conditions of high PUFA intake [15].

The amount of vitamin E required per gram of PUFA is dependent on experimental conditions, species differences, levels and kinds of PUFA, and test used [16]. A combination of stress of infection and presence of oxidized fats in swine diets was reported to exaggerate vitamin E needs still further [1]. These researchers reported that supplements of 100 IU of vitamin E per kilogram of diet and 0.1 ppm Se 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 concentration 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 αocopherol. Early cases of steatites 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. 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 Se produced normal piglets during the first reproductive cycle of the deficiency, and clinical deficiency signs occurred only after five such cycle [8]. 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. It has been concluded that in humans, a daily intake of 3 to 15 mg of tocopherol is required from natural diets [14]. However, the allowances will not be adequate in inviduals who, for a variety of reasons, do not absorbed fat efficiently or who have medical conditions that result in an abnormal vitamin E status in the blood and tissue. As in other species, the human requirement for vitamin E is related to dietary intake of PUFA. However, in normal diets in the united states, this relationship is probably of little significant, inasmuch as primary dietary sources of PUFA-vegetable oils, margarine, and shortening-are also rich sources of vitamin E. this situation is not true when foods consumed contain the longer-chained fatty acids.





Effects of deficiency White muscle disease (WMD), also known as nutritional muscular is caused by Se deficiency but is influenced by vitamin E status. White muscle disease occurs whit two clinical patterns; the first is a congenital type of muscular dystrophy in which young ruminants are stillborn or die within a few days of birth after sudden physical exertion, such as nursing or running. The second pattern develops after birth; it is observed most frequently in lambs within 3 to 6 weeks of birth but May occurs as late as 4 months after birth. The condition in calves is generally manifested at 1 to 4 months of age. Typically; WMD is characterized by generalized weakness, stiffness, and deterioration of muscles; affected animals have difficulty standing. Affected animals have difficulty standing and exhibit crossover walking and impaired suckling ability because the tongue musculature is affected [6]. Calves whit WMD has chalky white striations, degeneration, and necrosis in the skeletal muscles and heart. Often, death occurs suddenly from heart failure as a result of severe damage to the heart muscle. In calves whit milder cases, in which the chief clinical signs are stiffness and difficulty standing, dramatic, rapid improvement can result whit vitamin E-Se injection. An acute and chronic as well as peracute from of the disease can be distinguished in older calves, usually already in the finishing period. In particular, stress situation such as transport, regrouping, or abrupt changes in feed composition are generally considered precipitating factors. Sudden death without previous unmistakable signs of disease is the main facture of the peracute condition [11]. The cause is usually found in advanced degeneration of the myocardium, and motor disturbances such as an unsteady gait or stiff-calf disease; hard lumber, Scholars Research Library Hamed Amini Pour et al Annals of Biological Research, 2011: 2 (4):244-251 _____________________________________________________________________________

neck, and forelimb muscle; muscle tremor, and perspiration are encountered in the acute form. In Florida, the condition is most common in "buckling" calves that come off the truck or out of the processing chute white weakness of rear legs, buckling of fetlocks, and frequently a generalized shaking or quivering of muscles. Many calves become progressively worse until they are unable to rise and ay appear to be paralyzed. Many animals will be down or continue to buckle for extended periods, and death loos is high in severe cases. Calves whit excitable temperaments appear to be most affected. Postmortem examination of affected calves reveals pale chalky streaks in the muscles of the hamstring and back, and the heart, rib muscles, and diaphragm may also be affected [3]. In lambs, WMD takes a course similar to that found in calves. There are motor disturbances such as unsteady gait; stiffness in rear quarters, neck, and forelimb muscles;

and arched back. Muscle tremor and perspiration are encountered in the acute form. One necropsy, the disease is manifested as white striations in cardiac muscles and is characterized by bilateral lesions in skeletal muscles. A gradual swelling or the muscles, particularly in the lumbar and rear thigh regions, gives the erroneous impression of an especially muscular young animal. In addition to the peracute from encountered in calves, chronic cardiac muscle degeneration is also found in the lamb. Despite good initial development, affected lambs quickly lose weight after the third week of life and are unthrifty. They try to avoid any strain and usually stand apart from the herd. Cardiac arrhythmia and increased heart rate can result even after slight exercise. In the advance stage, animals eat little feed and rapidly waste away. Other conditions responsive in ESee are not restricted to young animals and relate to unthriftiness, occurring in lambs and hoggets at pasture [19]. Yearling sheep can also be affected by WMD. In sheep of 9 to 12 months of age, the disease is frequently observed following driving, whit the rapid onset of listlessness, stiffness, inability to stand, prostration, and in the most acute cases, death within 24 hours. Andrews and Hartedly [2] reported that the incidence of barren ewes was reduced from over 30 to 5% whit Se administrations. Farms in New Zealand have had lamb losses as high as 40 to 50%. Vitamin E was reduced losses by only 60%; Se by 96%. The immune response in sheep has been improved with supplemental vitamin E. vitamin E improved disease resistance in lambs challenged whit chlamydia. Myopathic lambs exhibited low lymphocyte responses when deficient in vitamin E and Se. The poor lymphocyte response of the lambs with nutritional myopathy was rapidly reversed by intramuscular administration of these nutrients, whit the prophylaxis most effective during the first 5 weeks of life. Most nutritional myophaty cases have involved young ruminants, whit effects less fully described for adult animals. However, degenerative myophaty in adult cattle has been reported, and a group of year ling Chianina heifers experienced absorption, stillbirth, and periparturient recumbency [21]. Adequate amounts of vitamin E in the diet are needed to prevent oxidative flavors in milk. However, the cost is high, whit efficiency of transfer into milk less than 2%.

Toxicity Compared with vitamin A and vitamin D, both acute and chronic studies whit animals have shown that vitamin E is relatively nontoxic but not entirely devoid of undesirable effects.

Hypervitaminosis E studies in rats, chicks, and humans indicate maximum tolerable levels in the range of 1000 to 2000 IU/kg of diet. Massive doses of vitamin E caused reduced packed-cell volumes in trout [4]. Administration of vitamin E to vitamin K-deficient rats, dogs, chicks, and humans exacerbated the coagulation defect associated with vitamin K deficiency [19]. In chickens, the effects of vitamin E toxicity are depressed growth rate, reduced hematocrit, reticulocytosis, increased prothrombin time, and reduced calcium and phosphorus in dry, fat-free bone ash. In humans, isolated and inconsistent reported have appeared on the adverse effects from high intakes of dl-α-tocopheryl acetate, but most adults appear to tolerate these doses.

Negative effects in human subjects consuming up to 1000 IU was vitamin E per day included Scholars Research Library Hamed Amini Pour et al Annals of Biological Research, 2011: 2 (4):244-251 _____________________________________________________________________________

headache, fatigue, nausea, muscular, weakness, and double vision. Large doses of α-tocopherol in anemic children suppress normal hematological response to parenteral iron administration.

REFERENCES

[1] Adams, C.R. 1973. National academy of science, Washington D.C.

[2] Andrews, E.D., and Hartely, W.J. 1968. N.Z. vet. J. 16.3.

[3] Bartov, I., and basker, D. 2005. Vet. Rec. 92.288.

[4] Beck. M.A. 2007. J. Nutr. 127.966s.

[5] Bell. J.G. and Cowey. C.B. 2008. Br. J. Nutr.53.

[6] Bostedt. H. 1999. Collegium Vet 51.45.

[7] Brownlee. N.R. and Huttner. J.J. 1977. Am. J. 25.265.

[8] Chew. B.P. 1995. J. Nutr 125.1804.

[9] Chow. C.K. 1979. Am. J. Clin. Nutr. 32.1066.

[10] Dove. C.R and Rebhom. W.C.2000. J. Anim. Sci. 68.2407.

[11] Drouhner. W. 1986. Ubers Terenabrung. 4.93.

[12] Gardner. H.W. 1999. Med. 7.65.

[13] Glienke. L.R. and Ewan. R.C. 1974. J. Anim. Sci. 39.975.

[14] Hoffmann la roche. 1994. Nutely, New Jersey.

[15] Lopez-Bote. C.J. and Rey. A.I. 1997. J. Nutr. 127.1176.

[16] Marin-Guzman. 1997. J. Anim. Sci. 75.2994.

[17] mcCay. P.B. and Gibson. D. D. 1981. Fed. Proc. 40.199.

[18] McDowll. L.R. and Williams. S. N. 2001. Ganiesville, Florida.

[19] Muth. O.H. 1955. J. Am. Vet. 126.355.

[20] NRC. 1987. Washington, D.C.

[21] Whanger. P.D. 1991. P. 230. AVI. Westport.

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