This review deals with the expectations of
vitamin E ability of preventing or curing, as a potent
antioxidant, alleged oxidative stress based ailments including
cardiovascular disease,
cancer,
neurodegenerative diseases,
cataracts,
macular degeneration and more. The results obtained with clinical intervention studies have highly restricted the range of effectiveness of this
vitamin. At the same time, new non-
antioxidant mechanisms have been proposed. The new functions of
vitamin E have been shown to affect cell signal transduction and gene expression, both in vitro and in vivo. Phosphorylation of
vitamin E, which takes place in vivo, results in a molecule provided with functions that are in part stronger and in part different from those of the non-phosphorylate compound. The in vivo documented functions of
vitamin E preventing the
vitamin E deficiency ataxia (AVED), slowing down the progression of non-alcoholic steato-
hepatitis (NASH), decreasing
inflammation and potentiating the immune response are apparently based on these new molecular mechanisms. It should be stressed however that
vitamin E, when present at higher concentrations in the body, should exert
antioxidant properties to the extent that its
chromanol ring is unprotected or un-esterified.