Food Sources of Vitamin K
wheat germ and wheat-germ oil afford the richest source of this factor, but it is so widely distributed in common foods that it is actually difficult to obtain a food mixture for experimental purposes that is deficient in vitamin E.
The vitamin E content of vegetable oils and fats has been reported to vary according to source of the plant, time of harvest, stability after harvest, refining procedure, and commercial hydrogenation procedures.
Animal foods are relatively poor sources of vitamin E although depot fat and liver contain moderate amounts. Some tocopherol is removed from oils in the purification process. When chlorine dioxide is used to bleach flour, tocopherol is lost. lists some common representative food sources of vitamin E.
There have been many misleading claims but very little experimental evidence that supplementation of the diet with pharmacologic doses of vitamin E cures or prevents human abnormalities, such as sterility, lack of virility, abnormal termination of pregnancy, heart disease, muscle weakness, cancer, ulcers, skin disorders, or burns. Although there is no medical justification for megavitamin therapy in large population groups with such disorders, there is increasing evidence that pharmacological doses of vitamin E may have some beneficial effects in a few specific conditions, including intermittent claudication and some hereditary enzyme deficiencies.The evidence for such medical uses of vitamin E has been discussed in recent reviews. Recently, megadoses of vitamin E have been shovm to increase the vitamin K requirement of young rats about tenfold and that its major metabolite, tocopheryl quinone, is a competitive inhibitor of vitamin K-dependent y-carboxylation.This anti-vitamin K activity and its reported inhibition of platelet aggregation has been suggested to explain the claims that vitamin E has beneficial effects in some patients with undesirable blood clotting.The effect of vitamin E on platelet aggregation could involve the production of thromboxane a potent initiator of platelet aggregation synthesized from arachidonic acid (and related to prostaglandins). The conversion of arachidonic acid to endoperoxides, thromboxane precursors, depends on hydroperoxide activation of cyclo-oxygenase. Vitamin E has been reduce the sharp rise in hydroperoxides usually associated with platelet aggregation.
Fortunately, vitamin E appears to be relatively nontoxic in comparison \vith vitamins A and D. However,just as the lack of a specific disease syndrome in vitamin E deficiency does not indicate that there is no need for vitamin E, the lack of symptoms from ingestion oflarge doses of vitamin E does not guarantee the absence of undesirable effects, especially from long term ingestion.
