Vitamin cyclooxygenase activity

VITAMIN E AND PLATELET AGGREGATION a-Tocopherol, a natural antioxidant, inhibits platelet aggregation and release. The effect of vitamin E is dne to a redaction in platelet cyclooxygenase activity and inhibition of lipid peroxide formation. It is believed that snpplementing the diet with vitamin E could play a role in the treatment of thromboembolic disease, especially if it is given in conjnnc-tion with an inhibitor of platelet aggregation. 

Beharka, A.A., Wu, D., Serafmi, M., and Meydani, S.N., Mechanism of vitamin E inhibition of cyclooxygenase activity in macrophages from old mice role of peroxynitrite. Free Radio. Biol. Med. 32,503,2002. 

This observation is now challenged by Chan, Allen and Hegarty (1980) who found that vitamin E deficiency caused a significant reduction in cyclooxygenase activity without changing the PGEa/PGFga ratio. 

Vitamin E appears to act as an immunosuppressant due to its ability to suppress both humoral and cellular immune responses. Tocopherol supplementation significantly enhances lymphocyte proliferation, interleukin-2 production, and delayed-type hypersensitivity skin response and decreases prostaglandin E2 production by inhibiting cyclooxygenase activity. There appears to be compelling evidence that intervention with dietary antioxidants, such as vitamin E, may help maintain the well-preserved... 

Many dietary supplements have antiplatelet activity, which may increase the risk of bleeding when used concurrently with anticoagulants. Feverfew inhibits cyclooxygenase and phospholipase A2 and may interact with anticoagulants and potentiate the antiplatelet effect of aspirin. Other supplements that possess antiplatelet activity include but are not limited to garlic, ginkgo, vitamin E, vitamin A, and selenium. 

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