Vitamin E is a fat-soluble vitamin, absorbed in the upper small intestine and transported in the blood via low-density lipoprotein (LDL) particles. Vitamin E is fundamental in the metabolism of virtually all cells. It is essentially nontoxic and is known greatly for its antioxidant effects within the body.
Vitamin E falls into 2 classes: tocols and tocotrienols. The tocols have saturated side chains while the tocotrienols have unsaturated side chains. Each class is comprised of 4 vitamers that differ in the number of methyl groups on the chroman ring. Vitamers in both classes are designated as a, b, g, or d. Of the tocotrienols, only the a vitamer has any significant activity; a-tocotrienol has an activity similar to b-tocopherols.
a-tocopherol is the most active vitamer is provides 75% of the total vitamin E activity in the US food supply. Although g-tocopherol (soybean and corn oil) has 1/10 of the biological activity of a-tocopherol, it makes a significant contribution in foods. The level of vitamin E in a food source is correlated with the level of fat in the diet.
*Example of varying amounts of the vitamers in oils:
Vitamin E is known for its role as an antioxidant within the body. It is thought to have a basic functional importance in maintaining membrane integrity. Being an antioxidant reagent, vitamin E wanders around the body reducing the number for free radicals present within, thus limiting their potential damaging effects. Vitamin E accomplishes this by decreasing the oxidation of unsaturated fatty acids in the phospholipid of cell membranes (protects against lipid peroxidation). Vitamin E also maintains the intracellular membrane integrity, by donation of an electron to the free radical. Vitamin E itself then becomes a free radical and forms a fairly stable free radical. It can later become oxidized further to the quinone and/or hydroquinone and be lost in the bile and urine.
Autoxidation and antioxidation reactions involving vitamin E
1. Initiation (formation of a free radical) LH L
2. Reaction of radical with oxygen L + O2 LO2 (peroxy radical)
3. Propagation LO2 + LH (FA) L + ROOH
4. Antioxidant reaction LO2 + E (tocopherol) E + LOOH (hydroperoxide)
*Vitamin E provides one hydrogen particle to the free radical and becomes a free radical itself
5. Regeneration-both vitamin C and reduced glutathione (GSH) can regenerate active vitamin E
6. vitamin E + vitamin C vitamin E + vitamin C vitamin C + NADPH+ + H+ vitamin C + NADP
*Ascorbic acids gives 2 hydrogen molecules to desactivate vitamin E
vitamin E + 2GSH vitamin E + GSSG (reduced glutathione)(oxidized glutathione)
GSSG + NADPH+ + H+ 2GSH + NADP
**Glutathione is dependent on selenium
A vitamin E deficiency can result from either a lack of the vitamin in the diet or impaired absorption of it. Symptoms of a deficiency include red blood cell breakage and anemia, weakness, difficulty walking, leg cramps, and general degeneration. The prevention of lipid oxidation, specifically the peroxidation of unsaturated fatty acids and cholesterol, in cell membranes and in other sites of fat accumulation probably accounts for most of the symptoms associated with vitamin E deficiency in animals and humans. For instance, if you increase unsaturated fatty acids (double bonds) you are going to increase your requirement for vitamin E to avoid oxidation of these fatty acids.
Also, vitamin E interacts with vitamin C and selenium. As shown previous vitamin C interacts with the tocopheroxyl radical and regenerates the reduced tocopherol. Vitamin E can also protect again many symptoms of selenium deficiency and vice versa. Vitamin E and selenium are able to regenerate the other. This is due to the ability of both tocopherol and selenium-dependent glutathione peroxidase to decrease the production of lipid products. Overall the antioxidants rely on one another and work together to help regenerate and compensate for one another.