University of Nebraska Cooperative Extension MP 70
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The Antioxidative and Immune Functions of Vitamin E

Uaichai Puthpongsiriporn
Sheila E. Scheideler¹

Antioxidative Functions

Vitamin E is known to be a lipid component of biological membranes and is considered a major chain-breaking antioxidant (Halliwell and Gutteridge, 1989) during heat stress. Vitamin E is found mainly in the hydrocarbon part of membrane lipid bilayer towards the membrane interface and in close proximity to oxidase enzymes which initiate the production of free radicals (Burton and Ingold, 1989). Vitamin E is capable of interacting with free radicals in both the aqueous phase and the membrane. Vitamin E protects cells and tissues from oxidative damage induced by free radicals. It does this primarily by scavenging free radicals, which can directly induce initiation (¹O₂, O_2-., HO·, etc) or propagation (lipid peroxyl radicals) of lipid peroxidation (Sies et al., 1993). Vitamin E suppresses the radical in reaction by donating its phenolic hydrogen to the oxygen radicals (Burton and Ingold, 1986). For example, lipid hydroperoxide is formed together with a vitamin E radical, when vitamin E reacts with the lipid peroxyl radical.

In the peroxidation of lipids, the lipid peroxyl radical acts as a chain carrier (1), where LH, LOO·, LOOH and L· are lipid, lipid peroxyl radical, lipid hydroperoxide and lipid radical, respectively. Vitamin E must scavenge this lipid peroxyl radical before it attacks the lipid molecule (2), where EH and E. are -tocopherol and -tocopheroxyl radical, respectively.

In organic homogeneous solutions, tocopherol scavenges the peroxyl radical about 10 times faster than lipid reacts with the radical (Burton and Ingold, 1986). Approximately 90 percent of the peroxyl radicals are scavenged by tocopherol before they attacking the lipid molecules. The tocopheroxyl radical can react with another lipid peroxyl radical to give an adduct which may be reduced to tocopherylquinone. It may also react with another vitamin E radical to give a dimer or trimer.

It has been believed supplementing vitamin E into diets containing high levels of polyunsaturated fatty acids may prevent feed oxidation and increase egg production. Scheideler and Froning (1996) reported hens fed various flaxseed diets with high level of vitamin E (50 IU/kg diet) significantly improved egg production compared to hens fed the same diets with low level of vitamin E (27 IU/kg diet).

Immune Functions

Vitamin E supplementation has been shown to increase infection resistance in farm and laboratory animals (Tengerdy, 1990). Vitamin E increases immune response against infections by improving phagocytic cell function. The antioxidation action of vitamin E plays an important role in protecting phagocytotic cells and surrounding tissues from oxidative reactions by free radicals produced by the respiratory burst of neutrophils and macrophages during phagocytosis (Baboir, 1984). Lipid peroxidation and free radical attack may alter the membrane fluidity, and resulting in changes in cell-to-cell and cell-to-substrate interaction and subsequent metabolism in lymphoid tissue (Reddy et al., 1986). In 1992, Hogan et al. reported that vitamin E both inhibits autoxidation of polyunsaturated fatty acids (PUFAs) in neutrophil membrane and enhances neutrophil function. Impaired neutrophil function associated with the oxidative burst of metabolism has been documented in vitamin E deficient animals (Hogan et al., 1990; Hogan et al., 1992).

Vitamin E may also enhance immune function by inhibiting the production of immunosuppressive prostaglandin. Some of the lymphocyte functions inhibited by free radicals formed during prostaglandin synthesis include mitogen responsiveness, cell-mediated cytotoxicity and lymphokine production (Romach et al., 1993). Vitamin E scavenges these free radicals and enhances immune function (Lawrence et al., 1985). In studies of granulocyte chemotaxis in relation to vitamin E supplementation, vitamin E has been found to attenuate the degree of rabbit granulocyte adherence to endothelial surface and enhances the rate of recovery of absolute granulocyte count (Lafuze et al., 1984).

Preliminary studies at the University of Nebraska (Scheideler, 1996; Scheideler and Froning, 1997) have indicated some benefit of vitamin E supplementation to laying hens during heat stress. Indepth studies are underway at the University of Nebraska to elucidate the beneficial effects of vitamin E on free radical (TBARS) production in laying hens, as well as effects on their immune function as measured by lymphocyte blastogenesis.

Issued in furtherance of Cooperative Extension work, Acts of May 8 and June 30, 1914, in cooperation with the U.S. Department of Agriculture. Elbert C. Dickey, Director of Cooperative Extension, University of Nebraska, Institute of Agriculture and Natural Resources.

University of Nebraska Cooperative Extension educational programs abide with the non-discrimination policies of the University of Nebraska-Lincoln and the United States Department of Agriculture.