Biological functions and metabolic fate of vitamin E revisited

Information accumulated lately has confirmed the essentiality of vitamin E for humans and provided a better understanding of its biological function and metabolic fate. The discovery of alpha-tocopherol transfer protein, which preferentially binds to RRR-alpha-tocopherol, not only provides conclusive evidence of the essentiality of vitamin E for humans, but also sheds light on the superiority of RRR-alpha-tocopherol biologically over other isomers. The presence of tocopherol regeneration systems and multiple interdependent antioxidant systems is largely responsible for the lack of a widespread deficiency in humans and the difficulty to deplete vitamin E in the adult. The bulk of excess tocopherols consumed is excreted to feces unchanged or to urine with the side chain shortened but the chroman ring intact. The ability of dietary vitamin E to mediate mitochondrial superoxide generation affords a possible mode of action of vitamin E at the tissue levels. By decreasing the generation and/or the levels of reactive oxygen/nitrogen species, dietary vitamin E not only protects against oxidative damage, but also modulates the expression and/or activation of redox-sensitive biological response modifiers that regulate important cellular events.