title: Does vitamin E decrease heart attack risk? summary and implications with respect to dietary recommendations.
abstract: 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.
authors.affiliation: Department of Nutrition and Food Management, Linus Pauling Institute, Oregon State University, Corvallis, OR 97331-6512, USA.
authors.forename: M G
authors.initials: MG
authors.lastname: Traber
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D006331:Heart Diseases / Q000188:drug therapy* / Q000517:prevention & control; D006801:Humans; D023421:Models, Animal; D018673:Nutrition Policy; D012307:Risk Factors; D014810:Vitamin E / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D014810:Vitamin E