Regular ArticleTocopherols and 6-Hydroxy-chroman-2-Carbonitrile Derivatives Inhibit Vascular Smooth Muscle Cell Proliferation by a Nonantioxidant Mechanism
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Vitamin E Nutrition in the Fetus and Newborn
2017, Fetal and Neonatal Physiology, 2-Volume SetVitamin E attenuates homocysteine and cholesterol induced damage in rat aorta
2013, Cardiovascular PathologyCitation Excerpt :As proliferation of vascular SMCs is essential for the formation of intimal hyperplasia, inhibition of proliferation of these cells could help to diminish the progression. Studies have shown that vitamin E specifically inhibits rat and human SMC proliferation at physiological concentration, and this occurs via inhibition of PKC activity, one of the important elements in signal transduction cascades [36–38]. Previous studies by our group have shown that, vitamin E prevents cholesterol-induced atherosclerotic lesions in rabbits via inhibition of PKC [13] and CD36 [14] activity.
Vitamin E Metabolism in the Fetus and Newborn Infant
2011, Fetal and Neonatal Physiology E-Book, Fourth EditionMolecular mechanism of α-tocopherol action
2007, Free Radical Biology and MedicineStudies in Vitamin E: Biochemistry and Molecular Biology of Tocopherol Quinones
2007, Vitamins and HormonesCitation Excerpt :A purported arylating property for an α‐T quinone tautomer that modifies specific cysteinyl groups in key enzymes has been suggested (Dowd and Zheng, 1995). However, tautomerization does not appear to be a general property of α‐TQ, which shows little cytotoxicity in most studies (Bolton et al., 1997; Boscoboinik et al., 1995; Van De Water and Pettus, 2002). An alternative explanation for the difference between α‐T and γ‐ or δ‐T, which we do not cover in this chapter, may involve a dramatically higher stability of the α‐T phenoxonium cation compared to its undermethylated congeners (Wilson et al., 2006).
Vitamin E Nutrition in the Fetus and Newborn
2003, Fetal and Neonatal Physiology: Third Edition