#VitaminE #CellHealth

Vitamin E is one of the most important lipid-soluble elements in the cell defense system made by antioxidants. Diet is the exclusive source of Vitamin E in the body.

Protects cell membranes

• Vitamin E plays a crucial role in tightening the bilipid membrane and provides enhanced stability to the cell structure.
• Existing evidence has established that Vitamin E is needed to maintain the homeostasis of skeletal muscle structure.
• When Vitamin E is given as a supplementation, repair of plasma membrane ensues.

In vitro studies have depicted that when cultured cells are faced with an oxidative challenge, the cell membrane repair is impeded. However, the presence of Vitamin E allows for repair of the membrane phospholipids since it prevents lipid peroxidation. Hence, it prevents the formation of oxidized phospholipids and promotes membrane repair.

Regulates platelet aggregation and protein kinase C activation

• The enhanced presence of Vitamin E in the endothelial cells inhibits platelet aggregation and stimulates the release of prostacyclin from the endothelium.
• α-tocopherol (Vitamin E) plays a role in downregulation of the intracellular cell adhesion molecule and the vascular cell adhesion molecule, which reduces the adhesion of blood cell components to the endothelium.
• The upregulation of the arachidonic acid cascade is also facilitated by Vitamin E, which eventually leads to a potent vasodilator and inhibitor of platelet aggregation in humans.
• Another study hypothesizes that the inhibition of protein kinase C and increased activity of nitric oxide synthase caused by Vitamin E also inhibits platelet aggregation.

Naturally, α-tocopherol has RRR configuration which is 2 times more potent compared with other racemic α-tocopherols in inhibiting protein kinase C activity. The attenuating effect of α-tocopherol on the release of membrane-derived diacylglycerol,which facilitates protein kinase C translocation and thereby enhance its activity. Alpha-tocopherolalso raised the activity of protein phosphatase type 2A, which inhibits protein kinase C autophosphorylation and consequently its activity.

Resource: Rizvi S, et al. Sultan QaboosUniv Med J. 2014;14(2):e157-e165.