Vitamin E (alpha-tocopherol) contributes to the normal maintenance of biomembranes, the vascular and nervous systems, and provides antioxidant protection for vitamin A. The level of vitamin E in the plasma or serum after a 12- to 14-hour fast reflects the individual's reserve status.
The current understanding of the specific actions of vitamin E is very incomplete. The tocopherols (vitamin E and related fat-soluble compounds) function as antioxidants and free-radical scavengers, protecting the integrity of unsaturated lipids in the biomembranes of all cells and preserving retinol (vitamin A) from oxidative destruction. Vitamin E is known to promote the formation of prostacyclin in endothelial cells and to inhibit the formation of thromboxanes in thrombocytes, thereby minimizing the aggregation of thrombocytes at the surface of the endothelium. Those influences on thrombocyte aggregation may be of significance in relation to risks for coronary atherosclerosis and thrombosis.
Deficiency of vitamin E in children leads to reversible motor and sensory neuropathies; this problem has also been suspected in adults. Premature infants who require an oxygen-enriched atmosphere are at increased risk for bronchopulmonary dysplasia and retrolental fibroplasia; supplementation with vitamin E has been shown to lessen the severity of, and may even prevent, those problems.
Deficiencies of vitamin E may arise from poor nutrition or from intestinal malabsorption. At-risk persons, especially children, include those with bowel disease, pancreatic disease, chronic cholestasis, celiac disease, cystic fibrosis, and intestinal lymphangiectasia. Infantile cholangiopathies that may lead to malabsorption of vitamin E include intrahepatic and extrahepatic biliary atresia, paucity of intrahepatic bile ducts, arteriohepatic dysplasia, and rubella-related embryopathy. In addition, low blood levels of vitamin E may be associated with abetalipoproteinemia, presumably due to a lack of the ability to form very low-density lipoproteins and chylomicrons in the intestinal absorptive cells of affected persons.
Vitamin E toxicity has not been established clearly. Chronically excessive ingestion has been implicated as a cause of thrombophlebitis, although this has not been definitively verified.