as soybean and corn oils), the intake of α-tocopherol equivalents is greater than the intake of α-tocopherol (2R-stereoisomeric forms) alone (see later section “Intake of Vitamin E” for suggested conversion factor).
Unlike most nutrients, a specific role for vitamin E in a required metabolic function has not been found. Vitamin E's major function appears to be as a non-specific chain-breaking antioxidant.
Vitamin E is a chain-breaking antioxidant that prevents the propagation of free-radical reactions (Burton and Ingold, 1986; Burton et al., 1983; Ingold et al., 1987; Kamal-Eldin and Appelqvist, 1996; Packer, 1994; Tappel, 1962). The vitamin is a peroxyl radical scavenger and especially protects polyunsaturated fatty acids (PUFAs) within membrane phospholipids and in plasma lipoproteins (Burton et al., 1983). Peroxyl radicals (abbreviated ROO•) react with vitamin E (abbreviated Vit E-OH) 1,000 times more rapidly than they do with PUFA (abbreviated RH) (Packer, 1994). The phenolic hydroxyl group of tocopherol reacts with an organic peroxyl radical to form the corresponding organic hydroperoxide and the tocopheroxyl radical (Vit E-O•) (Burton et al., 1985):
In the presence of vitamin E: ROO•+Vit E-OH → ROOH + Vit E-O•
In the absence of vitamin E: ROO•+RH → ROOH+R•R•+ O2 → ROO•
The tocopheroxyl radical can then undergo several possible fates. It can (1) be reduced by other antioxidants to tocopherol (see section on “ Antioxidant Interactions ”), (2) react with another tocopheroxyl radical to form non-reactive products such as tocopherol dimers, (3) undergo further oxidation to tocopheryl quinone (see section on “ Metabolism ”), and (4) act as a prooxidant and oxidize other lipids (see section on “ Antioxidant Interactions ”).
In addition to its direct antioxidant function, α-tocopherol reportedly has specific molecular functions, α-Tocopherol inhibits