For a long time, it was considered that, unlike the other vitamins, vitamin E had no specific functions; rather it was the major lipid-soluble, radical-trapping antioxidant in membranes. Many of its functions can be met by synthetic antioxidants; however, some of the effects of vitamin E deficiency in experimental animals, including testicular atrophy and necrotizing myopathy, do not respond to synthetic antioxidants. The antioxidant roles of vitamin E and the trace element selenium are closely related and, to a great extent, either can compensate for a deficiency of the other. The sulfur amino acids (methionine and cysteine) also have a vitamin E-sparing effect.

More recent studies have shown that vitamin E also has roles in cell signaling, by inhibition or inactivation of protein kinase C, and in modulation of gene expression, inhibition of cell proliferation, and platelet aggregation. These effects are specific for α-tocopherol and are independent of the antioxidant properties of the vitamin.

Deficiency of vitamin E is well established in experimental animals, resulting in reproductive failure, necrotizing myopathy, liver and kidney damage, and neurological abnormalities. In human beings, deficiency is less well de-fined, and it was only in 1983 that vitamin E was conclusively demonstrated to be essential. Deficiency is a problem only in premature infants with low birth weight and in patients with abnormalities of lipid absorption or congenital lack of β-lipoproteins – abetalipoproteinemia – or a genetic defect in the α-tocopherol transfer protein. In adults, lipid malabsorption only results in signs of vitamin E deficiency after many years.