Vitamin E is the most effective chain-breaking lipid-soluble antioxidant in biological membranes, where it contributes to membrane stability and protects critical cellular structures against damage from free radicals and reactive products of lipid oxidation (Burton and Ingold, 1981). There are suggestions however that it has a variety of other effects, for example on immune function, platelet and vascular functions, prevention of oxidative damage to DNA and DNA repair and modulation of signal transduction pathways (Morrissey and Sheehy, 1999).
Immune function in the elderly is often the focus of vitamin-supplementation studies but, while some workers, e.g. Meydani et al (1997), were able to demon strate improvements in both cellular and humoral responses from vitamin E supplements, others who used less vitamin E (67 mg aTE/d) were unable to do so (de Waart et al, 1997). Meydani and colleagues suggested that a consumption of at least 147mg a-TE/d (ie 5-10 times a normal dietary intake) was needed to benefit the immune response. Dose may play a critical role in the effects of vitamin E on immune function and high doses may enhance the immune system of the aged by suppression of prostaglandin E2 (PGE2) production and/or decreasing free radical formation. An increase in oxidant stress associated with an inadequacy of vitamin E will stimulate nuclear factor kB (NFkB) formation, stimulating inflammation and the formation of PGE2 (Grimble, 1997). At low concentrations PGE2 is believed to be necessary for certain aspects of cellular immunity. However, at higher concentrations, it suppresses several indices of cellular and humoral immunity such as antibody formation, delayed-type hypersen-sitivity (DTH) skin tests, lymphocyte proliferation and cytokine production (Meydani and Beharka, 2001). Tocopherols decrease the release of arachidonic acid from membrane phospholipids, resulting in a decreased production of PGE2, hence mega-doses of vitamin E may stimulate immune function reducing the risk of free radical formation and reducing the substrate for PGE2 formation, but such doses can have adverse effects. Mega-dose amounts of vitamin E have been reported to antagonise the pro-coagulant effects of vitamin K and this can have serious consequences in elderly people on warfarin therapy (Corrigan and Marcus, 1974).
In addition to the protection provided by vitamin E against LDL oxidation, several studies have consistently reported that platelet aggregation is reduced by vitamin E supplements but amounts used to demonstrate these effects are generally in excess of 250mg a-TE/d (Morrissey and Sheehy, 1999). However, a reduction in reactive oxygen species (ROS) that is promoted by vitamin E can protect against vascular cell dysfunction, preventing adhesion molecule expression and recruitment of monocytes and the production and release of nitric oxide (Baeuerle and Henkel, 1994; Goldring et al, 1995). a-Tocopherol has also been shown specifically to inhibit the proliferation of smooth muscle cells through modulation of protein kinase C and not a mechanism related to its antioxidant properties (Azzi et al, 2001).
Despite the use of high doses of vitamin E, large changes in the vitamin content of blood and liver and extended periods of study in animals and humans (smokers and non-smokers), vitamin E does not appear to have affected repair products of oxidative DNA damage, sister-chromatid exchanges in peripheral lymphocytes or DNA adducts in lymphocytes (Morrissey and Sheehy, 1999).
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