Vitamin E

Vitamin E is used to refer to a group of fat-soluble compounds that include both tocopherols and tocotrienols. There are many different forms of vitamin E, of which tocopherol is the most common in the North American diet. Tocopherol can be found in corn oil, soybean oil, margarine and dressings. Tocopherol, the most biologically active form of vitamin E, is the second most common form of vitamin E in the North American diet. This variant of vitamin E can be found most abundantly in wheat germ oil, sunflower, and safflower oils. It is a fat-soluble antioxidant that stops the production of reactive oxygen species formed when fat undergoes oxidation.

Tocopherol

Tocopherol is an important lipid-soluble antioxidant. It performs its functions as antioxidant in what is known by the glutathion peroxidase pathway and that it protects cell membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction. This would remove the free radical intermediates and prevent the oxidation reaction from continuing. The oxidized α-tocopheroxyl radicals produced in this process may be recycled back to the active reduced form through reduction by other antioxidants, such as ascorbate, retinol or ubiquinol. However, the importance of the antioxidant properties of this molecule at the concentrations present in the body are not clear and it is possible that the reason why vitamin E is required in the diet is unrelated to its ability to act as an antioxidant. Other forms of vitamin E have their own unique properties; for example, gamma-tocopherol is a nucleophile that can react with electrophilic

mutagens.

Vitamin E has many biological functions. The antioxidant function is considered to be the most important function vitamin E is best known for. However, there are other functions that have also been recognized to be of importance. α-Tocopherol has a regulatory effect on enzymatic activities. For instance, protein kinase C (PKC), which plays a role in smooth muscle growth, can be inhibited by α-tocopherol. α-Tocopherol has a stimulatory effect on the dephosphorylation enzyme, protein phosphatase 2A, which in turn, cleaves phosphate groups from PKC leading to its deactivation, bringing the smooth muscle growth to a halt. Vitamin E also has an effect on gene expression. Macrophages rich in cholesterol are found in the atherogenetic tissue. Scavenger receptor CD36 is a class B scavenger receptor found to be up-regulated by oxidized low density lipoprotein (LDL) and binds it. Treatment with alpha tocopherol was found to down regulate the CD36 scavenger receptor gene expression as well as the scavenger receptor class A (SR-A). In addition to the effect it has been shown to have on SRA and CD36, α-tocopherol also has an effect on expression of the connective tissue growth factor (CTGF). CTGF gene, when expressed, is responsible for the repair of the wounds and regeneration of the extracellular tissue that is lost or damaged during atherosclerosis. Moreover, vitamin E also plays a role in neurological functions, and inhibition of platelet aggregation and it has even been suggested that the most important function of vitamin E is as a signaling molecule, and that it has no significant role in antioxidant metabolism.




So far, most studies about vitamin E have supplemented using only alpha-tocopherol, but doing so leads to reduced serum gamma- and delta-tocopherol concentrations. Moreover, a 2007 clinical study involving alpha-tocopherol concluded that supplementation did not reduce the risk of major cardiovascular events in middle aged and older men.

Tocotrienols

Compared with tocopherols, tocotrienols are sparsely studied. Less than 1% of PubMed papers on vitamin E relate to tocotrienols. Current research direction is starting to give more prominence to the tocotrienols, the lesser known but more potent antioxidants in the vitamin E family. Some studies have suggested that tocotrienols have specialized roles in protecting neurons from damage and cholesterol reduction by inhibiting the activity of HMG-CoA reductase; delta-tocotrienol blocks processing of sterol regulatory element‐binding proteins (SREBPs).
Oral consumption of tocotrienols is also thought to protect against stroke-associated brain damage in vivo. Until further research has been carried out on the other forms of vitamin E, conclusions relating to the other forms of vitamin E, based on trials studying only the efficacy of alpha-tocopherol, may be premature.

Health effects

The first use for vitamin E as a therapeutic agent was conducted in 1938 by Widenbauer. Widenbauer used wheat germ oil supplement on 17 premature new born infants suffering from growth failure. Eleven out of the original 17 patients recovered and were able to resume normal growth rates. Later on, in 1948, while conducting experiments on alloxan effects on rats, Gyorge and Rose noted that the rats receiving tocopherol supplements suffered from less hemolysis than those that did not receive tocopherol. In 1949, Gerloczy administered all-rac-α-tocopheryl acetate to prevent and cure edema. Methods of administration used were both oral, that showed positive response, and intramuscular, which did not show a response. This early investigative work on the benefits of vitamin E supplementation was the gateway to curing the vitamin E deficiency caused hemolytic anemia described during the 1960s. Since then, supplementation of infant formulas with vitamin E has eradicated this vitamin’s deficiency as a cause for hemolytic anemia. The consensus in the medical community is that there is no good evidence to support health benefits from vitamin E supplementation in the short term, nor is there good evidence to support adverse effects on health. While some argue that taking more than 400 IU of vitamin E per day for extended periods may increase the risk of death others have shown that taking up to 5,500 IU per day has no adverse effects on health.

http://en.wikipedia.org/wiki/Vitamin_E