Vitamin E has a regulatory effect on gene expression. It has been shown to control proliferation of smooth muscle cells, which are involved in the development of atherosclerosis. Vitamin E, which is fat soluble, is present in lipids, most significantly in the lipids of cell membranes and in circulating low-density lipoproteins. When free radicals react with PUFAs, chain reactions generate free radicals in profusion. Vitamin E is more appropriately described as an antioxidant than a vitamin.
Most vitamins function as cofactors for enzymatic reactions.
Vitamin E does not function as a cofactor. Requirements for and utilization of vitamin E vary according to an individual's oxidative stress status. Concentrations of free radicals, other oxidants and the polyunsaturated fatty acid content of body tissues are major determinants of oxidative stress status. Also, deficiency of vitamin E does not produce a disease with rapidly developing symptoms such as scurvy, beriberi, pellagra, rickets or xerophthalmia. In humans, vitamin E produces overt deficiency symptoms in cases involving fat malabsorption syndromes, premature infants and patients on total parenteral nutrition.