|Title||Does vitamin E decrease heart attack risk? summary and implications with respect to dietary recommendations.|
|Publication Type||Journal Article|
|Year of Publication||2001|
|Date Published||2001 Feb|
|Keywords||Animals, Antioxidants, Heart Diseases, Humans, Models, Animal, Nutrition Policy, Risk Factors, Vitamin E|
The hypothesis that oxidative stress has a role in atherosclerosis rests on a large body of experimental work carried out in animal models of heart disease. The situation is more complex in humans, in that the results from vitamin E supplementation trials have been conflicting. Nonetheless, there is emerging information that alpha-tocopherol may play a critical role in maintaining the function of key cellular components in the atherosclerotic process through its ability to inhibit the activity of protein kinase C, a key player in many signal transduction pathways. alpha-Tocopherol modulates pathways of platelet aggregation, endothelial cell nitric oxide production, monocyte/macrophage superoxide production and smooth muscle cell proliferation. Regulation of adhesion molecule expression and inflammatory cell cytokine production by alpha-tocopherol has also been reported. More studies are required to relate alpha-tocopherol intakes to optimal tissue responses in humans.
|Alternate Journal||J. Nutr.|