Metabolic functions of vitamin E
The main function of vitamin E is as a radical-trapping antioxidant in cell membranes and plasma lipoproteins. It is especially important in limiting radical damage resulting from oxidation of PUFAs, by reacting with the lipid peroxide radicals before they can establish a chain reaction. The tocopheroxyl radical formed from vitamin E is relatively unreactive and persists long enough to undergo reaction to yield non-radical products. Commonly, the vitamin E radical in a membrane or lipoprotein is reduced back to tocopherol by reaction with vitamin C in plasma. The resultant monodehydroascorbate radical then undergoes enzymic or non-enzymic reaction to yield ascorbate and dehydroascorbate, neither of which is a radical.
The stability of the tocopheroxyl radical means that it can penetrate further into cells, or deeper into plasma lipoproteins, and potentially propagate a chain reaction. Therefore, although it is regarded as an antioxidant, vitamin E may, like other antioxidants, also have pro-oxidant actions at high concentrations.
This may explain why, although epi-demiological studies have shown a clear association between high blood concentrations of vitamin E and lower incidence of atherosclerosis, the results of inter-vention trials have generally been disappointing. In many trials there has been increased all-cause mortal-ity among those taking vitamin E and other antioxi-dant supplements.
The tocotrienols have lower vitamin activity than tocopherols, and indeed it is conventional to consider only γ-tocotrienol as a significant part of vitamin E intake. However, because of their unsaturated side-chain, the tocotrienols also have a hypocholesterol-emic action not shared by the tocopherols. They act to reduce the activity of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA) reductase, the rate-limiting enzyme in the pathway for synthesis of cholesterol, by repressing synthesis of the enzyme.