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Department of Nutrition and Food Management, Linus Pauling Institute, Oregon State University, Corvallis, OR 97331-6512 and Division of Critical Care and Pulmonary Medicine, Department of Internal Medicine, University of California, Davis, School of Medicine, Sacramento, CA 95817
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
-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.
-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
-tocopherol has also been reported. More studies are
required to relate
-tocopherol intakes to optimal tissue responses
in humans.
KEY WORDS:
-tocopherol atherosclerosis cytokine adhesion molecule platelet aggregation nitric oxide superoxide