Vitamin E prevents cell membrane damage by inhibiting peroxidation of membrane phospholipids and disrupting free radical chain reactions induced by formation of lipid peroxides. Peroxidation is the process by which fatty acids get oxidized (rancid).
The oxidation of LDL cholesterol is considered to be a trigger for a number of cellular events which lead to the formation of atherosclerotic plaque. This includes the uptake of oxidized LDL- by monocytes which leads to foam cell formation, endothelial cell damage and stimulation of cytokine and growth factor release from cells in the artery wall. Vitamin E protects LDL cholesterol from oxidation, thereby limiting the initiation of plaque formation in the arteries.
The Daily Reference Intake of vitamin E for individuals over age fifty is 15 mg.
Vitamin E is found only in foods of plant origin and predominantly in plant oils.
One fourth a cup of sunflower seeds, contains 17.0 mg vitamin E, one tablespoon of sunflower oil contains 7.0 mg, two tablespoons of peanut butter contains 3.3 mg, and two tablespoons of wheat germ contains 2.6 mg of vitamin E.
Vitamin E is a fat-soluble vitamin; its bioavailability depends on fat intake for stimulation of bile acids required for micelle formation. As such, sliced red grapes with a dallop of sour cream (fat content) and a tablespoon of sunflower seeds is a healthful snack.
Vitamin E occurs in food as tocopherols or tocotrienols. Alpha-tocopherol has the highest bioactivity. Vitamin E occurs naturally as d-alpha-tocopherol. The synthetic version is the dl-isomer has 25% less bioactivity than the d-isomer. A vitamin supplement that lists "dl"-alpha-tocopherol in the ingredient is less expensive and less potent.
Vitamin E along with selenium, copper, and manganese are integral components of the cellular antioxidant defense system.
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