Lipid al., 1999) that lipid peroxidation in LDL

Lipidperoxyl radical present in the plasma membrane interact with ?-tocopherolwhereby a lipid peroxide and the ?-tocopheroxyl radical result.

Ascorbic acid,by donating electrons to the ?-tocopheroxyl radical reduces it back to?-tocopherol. This property makes ascorbic acid, the primary plasma and cellantioxidant. Recycling of ?-tocopherol by ascorbate helps to protect membranelipids from peroxidation. The antioxidant capacity of ?-tocopherol is alsoevident in low density lipoproteins. The tocopherol mediated radicalpropagation is observed at a low rate of radical flux and it is suppressed byreductants such as ascorbic acid and ubiquinols (Gotoh et al., 1996; Steinberg1997; Esterbauer et al., 1997).B) Limit the progression ofAtherosclerosisLowlevels of ?-tocopherol have been associated with increased risk of coronaryartery disease and increased intake has shown to be protective ( Gey, 1998;Eiccholzer et al.

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, 1992). Datasupport a pathogenic role for oxidized LDL in atherosclerosis and a number ofstudies show that ?-tocopherol reduces the susceptibility of LDL to oxidation(Esterbauer et al., 1997).C) Protection from CancerInintervention studies, vitamin E treated patients had fewer incidents ofprostate and colorectal cancers compared to the group not receiving vitamin E.Protection by ?-tocopherol seems to occur also for certain types of breastcancer (Hartman et al., 1988; Gann et al., 1999; Albanes et al.,1995).

Tocopherols and tocotrienols can also induce the apoptosis in humanbreast cancer cells (Yu et al., 1999).D) Inhibition of Inflammation?-Tocopheroladdition to polymorphonuclear cells results in the inhibition of O2-generation (Kanno et al., 1995;Cachia et al., 1998; kanno et al., 1996).

Vitamin E has been shownto protect well against polymorphonuclear leukocyte dependent adhesion toendothelial cells (Yoshida, 1999).  E) Immune ResponseVitaminE, in amounts greater than currently recommended, enhances certain clinicallyrelevant invivo indexes of T-cell-mediated function in healthy elderly persons (Meydani et al., 1995; Meydaniet al., 1997; Meydani et al.

, 1998).F) Pro-oxidant effect of ?-tocopherolIthas been found (Bowry et al., 1992;Upston et al.

, 1999) that lipidperoxidation in LDL induced by a steady flux of aqueous peroxyl radicalsdeclines as vitamin E is consumed, (ii) is faster in the presence of vitamin Ethan following its complete consumption, (iii) is substantially accelerated byenrichment of the vitamin in LDL, either in vitro or by diet, and (iv) isvirtually independent of the applied radical flux. It was thus proposed thatthe vitamin E radical (i.e. ?- tocopheroxyl radical) propagates peroxidationwithin lipoprotein particles unless it becomes reduced by vitamin C (orubiquinol-10). The importance of pro-oxidation reactions of ?-tocopherol invivo, under physiological conditions however appears to be questionable.G) Vitamin E and neurodegenerativediseasesVitaminE is essential for neurological function. This fact, together with a growingbody of evidence indicating that neurodegenerative processes are associatedwith oxidative stress, lead to the convincing idea that several neurologicaldisorders may be prevented and/or cured by the antioxidant properties ofvitamin E.

( Ricciarelli et al., 2007).


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