Vitamin E is the generic descriptor of two families of compounds, the tocopherols and tocotrienols (see Figure 4). The different vitamers (α-vitaminers, β-vitaminers, γ-vitaminers, δ-vitaminers) have different biologic potency, where the most active is D-α tocopherol. As Murray et. al. (2009) mentioned, there is no precisely defined metabolic function in this vitamin. It acts as a lipid-soluble antioxidant in cell membranes, where many of its functions can be provided by synthetic antioxidants. It is also important to maintain the fluidity of cell membranes. Vitamin E is also said to have a poorly defined role in cell signaling.
Vitamin E, a hydrophobic and lipophilic character, associates with circulating blood lipoproteins, cellular membranes and fat/lipid deposits. It also acts as scavengers for free radicals, preventing the nonenzymatic peroxidation of unsaturated fatty acids especially in cell membranes. The α-Tocopherol is the most potent scavenger for reactive O2 species and on the other hand, γ-Tocopherol is the most potent scavenger for reactive nitrogen species. Vitamin E also has a role in cellular respiration where it stabilizes ubiquinone; and it also in the prevention of LDL oxidation to reduce the risk of cardiovascular disease.
According to Murray (2009), effects of Vitamin E deficiency in humans is unknown although existing experiments on animals recorded that resorption of fetuses and testicular atrophy happens due to Vitamin E deficiency. Patients with severe fat malabsorption, cystic fibrosis, and some forms of chronic liver disease suffere deficiency because they are unable to absorb vitamin or transport it exhibits nerve and muscle membrane damage. Premature infants observed with deficiency of this vitamin experience hemolytic anemia as a result of a fragile erythrocyte membrane as a result of peroxidation.
According to Murray (2009), effects of Vitamin E deficiency in humans is unknown although existing experiments on animals recorded that resorption of fetuses and testicular atrophy happens due to Vitamin E deficiency. Patients with severe fat malabsorption, cystic fibrosis, and some forms of chronic liver disease suffere deficiency because they are unable to absorb vitamin or transport it exhibits nerve and muscle membrane damage. Premature infants observed with deficiency of this vitamin experience hemolytic anemia as a result of a fragile erythrocyte membrane as a result of peroxidation.