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(Journal of Nutrition. 2000;130:1649-1652.)
© 2000 The American Society for Nutritional Sciences


Article

Specific Cellular Responses to {alpha}-Tocopherol1 ,2

Angelo Azzi3, Isabel Breyer, Maria Feher, Mariella Pastori, Roberta Ricciarelli, Stefan Spycher, Mariagrazia Staffieri, Achim Stocker, Sabine Zimmer and Jean-Marc Zingg

Institute of Biochemistry and Molecular Biology, University of Bern, 3012 Bern, Switzerland

3To whom correspondence should be addressed.

In the last 10 years precise cellular functions of {alpha}-tocopherol, some of which are independent of its antioxidant/radical-scavenging ability, have been revealed. Absorption of {alpha}-tocopherol from the gut is a selective process. Other tocopherols are not absorbed or are absorbed to a lesser extent. At the post-translational level, {alpha}-tocopherol inhibits protein kinase C and 5-lipoxygenase and activates protein phosphatase 2A and diacylglycerol kinase. Some genes [platelet glycoprotein IV/thrombospondin receptor/class B scavenger receptor (CD36), {alpha}-tocopherol transfer protein ({alpha}-TTP), {alpha}-tropomyosin, connective tissue growth factor and collagenase] are affected by {alpha}-tocopherol at the transcriptional level. {alpha}-Tocopherol also inhibits cell proliferation, platelet aggregation, monocyte adhesion and the oxygen burst in neutrophils. Other antioxidants, such as ß-tocopherol and probucol, do not mimic these effects, suggesting a nonantioxidant, {alpha}-tocopherol–specific molecular mechanism.


KEY WORDS: • vitamin E • {alpha}-tocopherol • antioxidant • cell proliferation • protein kinase C • gene expression




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