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Scholars Research Library

Annals of Biological Research, 2011, 2 (4) :244-251


ISSN 0976-1233


Effects of vitamin E on ruminant animal

Hamed Amini Pour1*, Naser Maheri Sis2, Saeid Najafyar Razlighi1, Mohammad SalamatAzar1,

MohammadHasan Babazadeh1, Mohammad Taher Maddah1, Navid Reazei1, Mojtaba Namvari1

Department of Animal Science, Islamic Azad University Sarab Branch, Sarab, Iran Department of Animal Science, Islamic Azad University Shabestar Branch, Shabestar, Iran ______________________________________________________________________________

ABSTRACT Vitamin E is used to refer to a group of fat-soluble compounds that include both tocopherols and tocotrienols. There are many different forms of vitamin E, of which γ-tocopherol is the most common in the North American diet. γ-Tocopherol can be found in corn oil, soybean oil, margarine and dressings. α-Tocopherol, the most biologically active form of vitamin E, is the second most common form of vitamin E in the North American diet. This variant of vitamin E can be found most abundantly in wheat germ oil, sunflower, and safflower oils. It is a fat-soluble antioxidant that stops the production of reactive oxygen species formed when fat undergoes oxidation. The first use for vitamin E as a therapeutic agent was conducted in 1938 by Widen Bauer. Widen Bauer used wheat germ oil supplement on 17 premature new born infants suffering from growth failure. Eleven out of the original 17 patients recovered and were able to resume normal growth rates. Later on, in 1948, while conducting experiments on alloxan effects on rats, Chow (9) noted that the rats receiving tocopherol supplements suffered from less hemolysis than those that did not receive tocopherol. In 1949, administered all-rac-α-tocopheryl acetate to prevent and cure edema. It can be the Focal segmental glomerulosclerosis cure. Methods of administration used were both oral, that showed positive response, and intramuscular, which did not show a response. This early investigative work on the benefits of vitamin E supplementation was the gateway to curing the vitamin E deficiency caused hemolytic anemia described during the 1960s. Since then, supplementation of infant formulas with vitamin E has eradicated this vitamin’s deficiency as a cause for hemolytic anemia. The consensus in the medical community is that there is no good evidence to support health benefits from vitamin E supplementation in the short term, nor is there good evidence to support adverse effectson health. While some argue that taking more than 400 IU of vitamin E per day for extended periods may increase the risk of death others have shown that taking up to 5,500 IU per day has no adverse were effects on health.


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Vitamin E is recognized as an essential nutrient for all species of animals, including humans.

However, opinions differ among research workers as well as practical livestock producers regarding conditions under which vitamin E supplementation is required and at what levels it should be fed. For years, vitamin E in human nutrition was described as "a vitamin looking for a disease". Some vitamin E-deficiency conditions that accrued in animals were not seen in humans;

however, a number of medical claims for physiological benefits from the vitamin have been made. In more recent years, vitamin E has been shown to be important against free-radical injury;

enhancing the immune response; and paying a role in prevention of cancer, heart disease, contracts, Parkinson s disease, and a number of other disease condition.

Structure Vitamin E activity in food derives from a series of compounds of plant origin, the tocopherols and tocotrienols. Eight forms of vitamin E are found in nature: four tocopherols (α, β, γ, and δ) and four tocotrienols (α, β, γ, and δ). All have a 6-chromanol ring structure and a side chain.

The structures of α-tocopherol and the commercially available α-tocopheryl acetate are presented in Fig. 4.1, while different active forms of vitamin E are shown in Fig.

4.2.Differences among α, β, γ, and δ are due to the placement of methyl groups on the ring.

The difference between tocopherols and tocotrienols is due to unsaturation of the side chain in the latter.

The dl-α-tocopheryl acetate (also called all -rac-α-tocopheryl acetate) is accepted as the International Standard(1mg= 1international unit). Syntheticfree tocopherol, dl-α-tocopherol, has a potency of 1.1 IU/mg. Activity of naturally occurring α-tocopherol, d-α-tocopherol (also called RRR-tocopherol, see below), is 1.49 IU/mg, and of its acetate, 1.36 IU/mg. The dlα-tocopheryl acetate is made by the extraction of natural tocopherols from vegetable oil.

Extracted t o c o p h e r o l s u n d e r g o distillation to obtain t h e alpha form, and are then acetylated to produce t h e acetate ester. Α Tocopherol,the most active compound, is fully methylated, with methyl groups at positions 5, 7,and 8(2 R, 4´R, 8´R-α-tocopherol, abbreviated RRR).

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Scholars Research Library Hamed Amini Pour et al Annals of Biological Research, 2011: 2 (4):244-251 _____________________________________________________________________________

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Metabolism Vitamin E absorption is related to fat digestion and is facilitated by bile and pancreatic lipase [5].

The primary site of absorption appears to be the medial small intestine. Wether presented as free alcohol or as esters, most vitamin E is absorbed as the alcohol. Esters are largely hydrolyzed in the gut wall, and the free alcohol enters the intestinal lacteals and is transported via lymph to the general circulation. Medium-chain triglycerides particularly enhance absorption, whereas polyunsaturated fatty acids (PUFAs) are inhibitory. Balance studies indicate that much less vitamin E is absorbed, or at least retained, in the body than vitamin A. Vitamin E recovered in feces from a test dose was found to range from 65 to 85% in the human, rabbit, and hen, although in chicks, it was reported at about 25%. It is not known how much fecal vitamin E represents unabsorbed tocopherol and how much may come via secretion in the bile. As the intake increases, the percentage of tocopherol absorbed decreases, suggesting a saturation process. The tocopherol form, which is the naturally occurring one, is subject to destruction in the digestive tract to some extent, whereas the acetate ester is not. Much of the acetate is readily split off in the intestinal wall, and the alcohol is reformed and absorbed, thereby permitting the vitamin to inject into the body evidently, is converted there to the alcohol form. Vitamin E in plasma is attached mainly to lipoprotein in the globulin faction withincells and occurs mainly in mitochondria and microsomes. The vitamin is taken up by the liver and is released in combination whit low-density lipoprotein (LDL) cholesterol. Rates and amounts of absorption of the various tocopherol and tocotrienols are in the same general order of magnitude as their biological potencies. αTocopherol is absorbed best, whit γ-tocopherol absorption 85% that of α-forms but whit a more rapid excretion. One can generally assume that most of the vitamin E activity within plasma and other animal tissues is α-tocopherol [17]. In humans, whose natural diet contains a high percentage of non-alpha forms, blood serum tocopherols identified consisted of about 87% α-, 11% γ, and 2% β-tocopherol [14].

Storage and excretion Vitamin E is sorted throughout all body tissues; major deposits are in adipose tissue, liver Scholars Research Library Hamed Amini Pour et al Annals of Biological Research, 2011: 2 (4):244-251 _____________________________________________________________________________

contains only a small fraction of total body stores, in contrast to vitamin A, for which about 95% of the body reserves are in the liver. The extent of storage is shown by the fact that fameless born of mothers whose diets contained a liberal supply frequently have enough in their bodies at birth to carry them through a firs pregnancy. Rats reared on natural foods rich in the vitamin and then placed on a deficient diet may produce three or four litters before exhausting their reserves [11].

However, Gardner [12] reports that unlike vitamin A, lower body stores of vitamin E are available for periods of low dietary intake. Tocopherol entering the circulatory system becomes distributed throughout the body, whit most of it localizing in the fatty tissues. Subcellular fractions from different tissues vary considerably in their tocopherol content; the highest levels are found in membranous organelles, such as microsomes and mitochondria, which contain highly active redox systems [1]. Small amounts of vitamin E will persist tenaciously in the body for a long time. However, stores are exhausted rapidly by PUFAs in the tissue; the rate of disappearance is proportional to the intake of PUSAs. A major excretion route of absorbed vitamin E is bile, in which tocopherol appears mostly in the free from. Usually less than 1% of orally ingested vitamin E is excreted in the Urine.

Functions Vitamin E has been shown to be essential for integrity and optimum function of the reproductive, muscular, circulatory, nervous, and immune system [2]. It is well established that some functions of vitamin E, however, can be fulfilled in part or entirely by traces of Se or by certain synthetic antioxidants. Even the sulfur-bearing amino acids, cystine and methionine, affect certain vitamin E functions. Much evidence points to undiscovered metabolic roles for vitamin E that may be paralleled biologically by roles of Se and possible other substances. The most widely accepted functions of vitamin E are discussed in this section.

Vitamin E as a biological antioxidant Vitamin E has a number of different but related functions. One of the most important functions is its role as an intercellular and intracellular antioxidant. Vitamin E is part of the body s intracellular defense against the adverse effects of reactive oxygen and free radicals that initiate oxidation of unsaturated phospholipids [18] and critical sulfhydryl groups [4]. Vitamin E functions as a quenching agent for free radical molecules whit single, highly reactive electrons in their outer shells. Free radicals attract a hydrogen atom, along whit its electron, away from the chain structure of a PUFAs, satisfying the electron needs of the original free radical is formed that joins whit molecular oxygen to from a peroxyl radical that steals a hydrogen-electron unit from yet another PUFA. This reaction can continue in a chain, resulting in the destruction of thousands of PUFA molecules [17]. Free radicals can be extremely damaging to biological systems [1]. Free radicals, including hydroxy, hypochlorite, peroxy, alkoxy, superoxide, hydrogen peroxide, and single oxygen, are generatedby autoxidation or radiation, or from activities of some oxidases, dehydrogenases, and peroxidases. Highly reactive oxygen species, such as superoxide anion radical (O2), are continuously produced in the course of normal aerobic cellular metabolism. Hydroxyl radical (HO), hydrogen peroxide (H2O2), and singlet cellular metabolism. Also, phagocytic granulocytes undergo respiratory burst to produce oxygen radicals to destroy the intracellular pathogens. However, these oxidative products can, in turn, damage healthy cells if they are not eliminated. Antioxidants serve to stabilize these highly reactive free radicals, thereby maintaining the structural and functional integrity of cells [5]. Therefore, antioxidants are very important to the immune defense and health of humans and animals. The antioxidant function of vitamin E is closely related to and synergistic whit the role of Se.

Selenium has been shown to act in aqueous cell media by destroying hydrogen peroxide and hydroperoxides via the enzyme glutathione peroxidase (GHSpx) of which it is a co-factor. In this Scholars Research Library Hamed Amini Pour et al Annals of Biological Research, 2011: 2 (4):244-251 _____________________________________________________________________________

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