Abstract
The natural vitamin E (RRR-α-tocopherol) exists in most biological membranes and functions as a chain-breaking antioxidant during lipid peroxidation1. Beyond its antioxidative property, vitamin E has been shown to inhibit the proliferation of smooth muscle cells by modulating protein kinase C2. The regulatory role of vitamin E in the production of certain lipid mediators has also been demonstrated. For instance, vitamin E was found to enhance the transacylation of alkylglycerophosphocholine3, alter the level of phosphatidic acid and diacylglycerol4, and potentiate prostacyclin synthesis in endothelial cells5. In addition, vitamin E was shown to inhibit thromboxane6 and leukotriene7 formation in platelets and neutrophils, respectively.
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Tran, K. et al. (1997). Vitamin E (α-Tocopherol) Enhances Arachidonic Acid Release in Rat Heart Myoblastic Cells Through the Activation of Cytosolic Phospholipase A2 . In: Honn, K.V., Marnett, L.J., Nigam, S., Jones, R.L., Wong, P.YK. (eds) Eicosanoids and other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury 3. Advances in Experimental Medicine and Biology, vol 407. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1813-0_19
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DOI: https://doi.org/10.1007/978-1-4899-1813-0_19
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