Biomedical Hypertexts Glossary

Vitamin E

Vitamin E is a the principle membrane-associated antioxidant molecule in mammals. It plays a major role in preventing oxidative damage to membrane lipids by scavenging free radicals.


Vitamin E is not a single molecule, but a family of 8 related molecules called tocopherols and tocotrienols. Moreover, each of the different tocopherols exists in eight stereoisomers. However, having described this molecular complexity, it turns out that dietary vitamin E is predominantly alpha and gamma-tocopherol. The structure of alpha-tocopherol is depicted below; note the long hydrocarbon chain similar to the tail of a fatty acid.

Absorption and Transport

Vitamin E is hydrophobic and is absorbed similarly to other dietary lipids. After solubilization by bile acids, it is absorbed into small intestinal epithelial cells, incorporated into chylomicrons, and transported into blood via lymphatics.

Once in the circulation, vitamin E is liberated from chylomicrons and much is taken up by the liver, where it is repackaged into very low density lipoproteins and secreted again into blood. Ultimately, vitamin E is transported in blood bound to a variety of lipoproteins, from which it is taken up by tissues throughout the body. Vitamin E is stored within the fat droplets of adipose tissue cells.

Physiologic Effects of Vitamin E

The claim to fame of vitamin E is as an antioxidant. In other words, it is a scavenger of free radicals such as reactive oxygen species (e.g. superoxide, hydrogen peroxide). Free radicals are generated by numerous processes within cells and have the ability to damage cell membranes, proteins and nucleic acids. Vitamin E is at the forefront of defense systems to prevent oxidative damage, and due to its lipid solubility, is particularly important in protecting cell membranes.

Mechanistically, when vitamin E absorbs a free radical, it is converted into a radical itself. The resulting tocopheroxyl radical is then reduced back to tocopherol by glutathione, vitamin C or other molecules.

Sources of Vitamin E

Vitamin E is particularly abundant in vegetable oils and derivative foods such as margarine and shortening. Leafy green vegetables are also rich in vitamin E. Animal products, including red meat and fish, are very poor sources of vitamin E.

Vitamin E Deficiency and Toxicity

Cellular vitamin E deficiency leads to an increase in peroxidation of membrane lipids. This often results in abnormalities in membrane transport, a decrease in mitochondrial energy production. An increased mutation rate due to oxidation of DNA is also commonly observed in deficient cells.

In animals, vitamin E deficiency has been associated with a number of problems:

  • Impaired fertility in both sexes. This is observed particularly in rodents, and resulted in vitamin E sometimes being called the "fertility vitamin".
  • Muscle disease. Vitamin E deficiency is a well known cause of nutritional myopathy (white muscle disease) in a variety of animals. This disorder is most commonly seen in pigs, cattle and sheep, and is characterized by cardiac and skeletal muscle necrosis and calcification, sometimes observed shortly after birth. In many cases, there is a clear interaction between vitamin E and selenium deficiency in the pathogenesis of this syndrome.
  • Degeneration of central nervous system and peripheral nerves. This is a primary manifestation of vitamin E deficiency in humans, where it is seen predominantly and most severely in children.
  • Accelerated destruction of red blood cells.

Due to the widespread occurance of vitamin E, deficiecy is relatively rare. In humans in is most commonly associated with lipid malabsorption syndromes, which can occur with genetic or acquired diseases affecting the intestine, pancreas or liver.

Recognition of the antioxidant properties of vitamin E have led to a rather huge interest in its use to reducing the risk of many degenerative diseases, including cancer, atherosclerosis, chronic inflammation and cataracts. At this time it seems fair to state that, other than consuming a balanced diet that would be expected to provide adequate vitamin E, there is little indication that vitamin E supplementation will provide substantive protection from such diseases.

The risk of overconsuming vitamin E appears to be low, but the effects of prolonged, high dose supplementation is not known.

References and Reviews

  • Blatt DH. Leonard SW, Traber MG: Vitamin E kinetics and the function of tocopherol regulatory proteins. Nutrition. 17:799-805, 2001.
  • Brigelius-Flohe R, Kelly FJ, Salonen JT, etc: The European perspective on vitamin E: current knowledge and future research. Am J Clin Nutrition 76:703-716, 2002.
  • Herrera E, Barbas C: Vitamin E: action, metabolism and perspectives. J Physiol Biochem 57:43-56, 2001.
  • Traber MG, Arai H: Molecular mechanisms of vitamin E transport. Annu Rev Nutr 19:343-355, 1999.
  • Van Metre DC, Callan RJ: Selenium and vitamin E. Vet Clinics North Am - Food Animal Practice 17:373-402, 2001.

Index of: Vitamins

Last updated on May 17, 2003
Author: R. Bowen
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