Vitamin E , a potent vitamin antioxidant, quenches the self-perpetuating cycle of lipid peroxidation: that is, the oxidation of lipids to produce a peroxide. In this process, free radicals are generated which abstract electrons from cell membrane lipids causing cell damage.
Apparently, vitamin E can protect against cardiovascular diseases (CVDs) using four different ways. In vitro studies show that vitamin E prevents the abnormal proliferation of vascular smooth muscle cells (VSMC). Aberrant proliferation of these cells arguably leads to plaque formation in the arteries. It also protects against free radical damage, which has been implicated in aging, cancer, and atherosclerosis. α -Tocopherol inhibits phosphokinase C (PKC) – a family of enzymes which regulates immune responses and cell growth. Because of its roles in regulating cell growth, inhibition of VSMC proliferation represents a physiological mechanism whereby diseased states such as atherosclerosis can be prevented. Also, contributing to the development of atherosclerosis are macrophage/monocytes class of white blood cells (WBCs). These white blood WBCs transition into foam cells which are formed when fat is deposited in the blood vessel walls. Consequently, they appear foamy – an essential first step towards the formation atherosclerotic plaques. Both in vivo as well as in vitro studies have shown that vitamin E inhibits foam cell formation and thus plaque formation.
Intercellular adhesion molecule-1 (ICAM-1), activates the binding of WBCs to the cells lining the blood vessels (endothelial cells) via ICAM-1. More than this, ICAM-1 enables the recruitment of inflammatory WBCs. They bind to the inner lining of the blood vessels (endothelium) resulting in plaque formation. Significantly, WBC recruitment in vivo is inhibited by α-tocopherol, consequently reducing plaque formation.
Whereas ICAM-1 is primarily involved in atherosclerosis, vascular cell adhesion molecule 1 (VCAM-1) is contributes to both atherosclerosis and arthritis. VCAM-1 also regulates adhesion of WBCs to the lining of blood vessels. However, the event plays a role in the development of both atherosclerosis and rheumatoid arthritis. Activation of endothelial cells by VCAM-1 is responsible for free radical generation, namely the release of reactive oxygen species (ROS), which is quenched by vitamin E. This process reduces the oxidative burden of having an overload of free radicals. The high concentration of free radicals adversely affects the cell factor NF-κB which in turn is linked inflammatory and autoimmune diseases like arthritis. Vitamin E mitigates this adverse effect by eliminating the buildup of free radicals. It also prevents monocyte invasion into endothelial cell walls thereby reducing plaques in the arteries.
