Abstract
In recent years, the specific cellular effects of vitamin E that are the consequence of modulating signal transduction and gene expression have been described. The natural (alpha-, beta-, gamma-, and delta-tocopherol and alpha-, beta-, gamma-, and delta-tocotrienol) and synthetic vitamin E analogues affect the cellular behavior differentially, suggesting that they do not act on a single molecular target. Furthermore, these effects are often not explainable by a general antioxidant action and thus most likely reflect specific interactions of vitamin E with enzymes, structural proteins, lipids and transcription factors. At the cellular level, the different vitamin E analogues can modulate cell proliferation, apoptosis, platelet aggregation, monocyte adhesion and the differentiation of hippocampus neurons. At the enzyme level, the tocopherols inhibit protein kinase C (PKC), protein kinase B (PKB), tyrosine kinases, 5-lipoxygenase and phospholipase A2, and activate protein phosphatase 2A and diacylglycerol kinase. At the transcriptional level, the expression of a growing number of genes is modulated by the tocopherols. Further research is required to define which of these activities render tocopherol (and, in particular, alpha-tocopherol), an essential nutrient-a vitamin-in humans.
