According to the oxidative damage theory of aging , free radicals and other reactive oxygen species (ROS), developed throughout mitochondrial metabolism, may end up producing impaired molecules including carbonylated proteins, lipid peroxides, and oxidized DNA , the accumulation of which is supposedly the primary cause of cellular senescence, age-related telomere attrition and diseases. Accumulated ROS excess can be allegedly destroyed by the endogenous physiological antioxidative systems including the enzymes superoxide dismutase (SOD), glutathione reductase, catalase and glutathione peroxidase, which help to keep the balance between oxidative and antioxidative processes. In terms of chronic oxidative stress, however, the endogenous antioxidant systems happen to be insufficiently effective, and it has been believed that administration of certain exogenous antioxidants such as vitamins E and C, curcumin, melatonin, β-carotene, lipoic acid, coenzyme Q10, glutathione, polyphenols, phytoestrogens, as well as certain minerals including zinc, manganese and selenium, can be a factor in maintaining homeostasis. Vitamin E (CAS # 1406-18-4) comprises a group of several fat-soluble compounds including tocopherols and tocotrienols, of which α-tocopherol is the most potent antioxidant form of vitamin E. Due to their lipophilic features, they can be found in lipoproteins, cellular membranes, and fat deposits. Vitamin E is the key defender against free radicals effects. It is stored in the liver and fat cells and protects cellular components and especially cellular membranes from damage. Vegetable oils such as sunflower, soybean, and safflower oils are some of the best sources of vitamin E.