Vitamin E: A Powerful Natural Protector

by Barbara S. Veritas

Vitamin E is essential to good reproductive performance. The standard tests for potency of forms of vitamin E (tocopherols) measure the number of rats giving birth to at least one live offspring, or the amount of vitamin E required to prevent resorption during gestation. The term "tocopherol" derives from the Greek words "tokos" (childbirth) and "pherein" (to bear). The alpha tocopherol form possesses the most activity. Compared to d-alpha tocopherol, the so-called "mixed tocopherols" possess substantially less vitamin activity: d-beta tocopherol; 15% to 40%, d-gamma; 1% to 20%, and d-delta; 1%. The World Health Organization and others have established that 1 mg. of dl-alpha tocopheryl acetate equals 1 IU vitamin E. The relative activities of the various forms are:

1 milligram equals:
d-alpha tocopherol 1.49 IU
d-alpha tocopheryl acetate 1.36 IU
d-alpha tocopheryl acid succinate 1.21 IU
dl-alpha tocopherol 1.10 IU
dl-alpha tocopheryl acetate 1.00 IU
dl-alpha tocopheryl succinate .89 IU

Because of its outstanding stability and resistance to oxidation outside the body, dl-alpha tocopheryl acetate is the preferred form for animal supplementation and is widely used in capsule supplements for people.


Normal compounds produce their chemical bonds by sharing pairs of electrons, one from each atom. Free radicals pick up another electron from normal compounds (typically, oxygen), thus producing a stable product by pairing their unpaired electron. But in doing so they alter the "donor" compound and create another radical, since the process is still short one electron. In this way, free radicals alter tissue proteins and lipids (fats), causing cell damage and death. Free radical induced reactions tend to continue to produce unstable forms that go on to do further damage and release more radicals. The antioxidants convert free radicals to relatively stable compounds and stop or prevent the chain reaction of free radical damage. The most damaging free radical molecules are the superoxide anion (020), the hydroxyl radical (HO0) and the peroxide radical (OH-). Hydrogen peroxide (H2O2) while not a true radical, is unstable and is likely to be converted to the hydroxy radical, which is the most potent oxidizing agent known. So it, too, must be converted by antioxidants to water.

Superoxide, hydroxyl, peroxide radicals and hydrogen peroxide are detoxified by the enzymes superoxide dismutase, catalase and glutathione peroxidase in the water-based areas of the cell. Vitamin E is fat soluble and is found mainly in the cell membranes and fatty structures of most cells. In adipose (body fat) tissue, vitamin E is found in large quantities. Vitamin E detoxifies peroxides, thus preventing generation of the even more toxic hydroxyl and superoxide radicals and singlet oxygen (O-).


Production of glutathione peroxidase for free radical scavenging depends upon the availability of selenium. The uptake of selenium here requires cysteine, either delivered directly in the diet or produced from methionine. The resulting form, selenocysteine, is the active antioxidant portion of glutathione peroxidase. Because glutathione peroxidase in the water-based areas of the cell can stop free radical reactions that would otherwise go on to attack lipid-based areas (e.g., the cell membrane), it tends to "spare" vitamin E by reducing its workload. Likewise, since vitamin E conversion of free radicals prevents leaks or complete breakdowns of cell membranes, it spares glutathione peroxidase from having to convert free radicals that would otherwise invade the cell. This co-operation is the basis for the so-called sparing effects of vitamin E and selenium.


Vitamin E is absorbed in a mixture with other dietary fats (mostly triglycerides) through the wall of the duodenum (beginning of the small intestine). Because of this mechanism, absorption of vitamin E is enhanced when dietary fats are present. As dl-alpha tocopheryl acetate passes through the intestinal lining, it is almost completely hydrolyzed to form alpha tocopherol.

Absorption of vitamin E is limited. In rats and humans only 20% to 30% of orally administered vitamin E is absorbed. The efficiency of vitamin E absorption decreases with higher feeding levels. (Other fat soluble vitamins (A, D and K) have absorption efficiencies of 50% to 80%) Vitamin E absorption is poor in low fat diets. Absorption is also adversely affected by high levels of polyunsaturates or high levels of other fat soluble vitamins, particularly vitamin A. However, high levels of vitamin E do not appear to affect vitamin A absorption, although they may create a somewhat higher need for vitamin A.

As much as 90% of the vitamin E in the body is stored in adipose (body fat) tissue, with the balance occurring primarily in the liver and skeletal muscles. The rate at which vitamin E is depleted varies tremendously with the type of tissue. In studies with rats, the turnover of alpha-tocopherol was 7 to 10 days in the lungs and liver, but 76 days in the spinal cord. In guinea pigs, adipose levels of vitamin E declined only slightly over a 4 month period of dietary vitamin E deprivation. However, the animals showed clear signs of vitamin E deficiency, indicating that vitamin E stored in fat cells is essentially not available to the rest of the body, which depends on vitamin E supplied in the diet.


The richest food sources of vitamin E are vegetable oils, whole cereals, eggs, liver, legumes and most green plants. Green forages, especially alfalfa, are very good sources. The leaves of grasses contain 20 to 50 times the vitamin E found in the stems. Thus, vitamin E activity can decrease 70% to 90% from early growth to maturity in grasses, while in legumes the vitamin E activity decreases 34% to 65% from the early leafy to the post-flowering stages. Stability of all natural tocopherols is poor, and substantial losses occur when feeds are dried, processed and stored. Vitamin E is highly sensitive to heat, oxygen, moisture, oxidizing fats (especially polyunsaturates) and trace minerals. Oxidation of vitamin E is increased by grinding, pelleting, extruding or mixing minerals or fats in feeds. Losses from cutting, drying and baling hay range from 30% to 80%. From 54% to 73% of vitamin E activity is lost in alfalfa hay stored at 33E C for 12 weeks. The heaviest losses of vitamin E occur in high-moisture feeds.

In the following chart we see that the vitamin E content of common feedstuffs is often inadequate to meet the horse's needs. In a diet comprised of 11 kg (24.2 pounds) of feed, two-thirds of which is alfalfa hay and 1/3 of which is a 50/50 oats/corn mix, the total daily alpha-tocopherol content would be only 401 mg., or 597 IU vitamin E:

Alfalfa hay, total diet = .67 x 11 kg. = 7.37 kg.

Per kg. Feed: Alfalfa hay - 31 to 73 mg. alpha-tocopherol = 52 mg. avg x 7.37 = 3.83

Oats, total diet = .165 x 11 kg. = 1.815 kg.

Per kg. Feed: Oats - 4 to 8 mg. alpha-tocopherol = 6 mg. avg x 1.815 = 11 mg.

Corn, total diet = .165 x 11 kg. = 1.815 kg.

Per kg. Feed: Corn - 4 mg. alpha-tocopherol = 4 mg. x 1.815 = 7 mg.

Estimated total alpha-tocopherol content = 383 + 11 + 7 = 401 mg. daily

Using the standardized equivalent ratios, we can multiply by 1.49 to convert this figure for alpha-tocopherol to the equivalent amount of dl-alpha-tocopheryl acetate: 401 x 1.49 = 597 IU dl-alpha tocopheryl acetate. Obviously, as the grain content of the diet increases and the hay or forage proportion decreases, vitamin E content will drop off sharply.


  • Two groups of high altitude mountain climbers were evaluated for physical performance and indications of lipid peroxide activity. One group was supplemented with 400 IU vitamin E daily, while the other group received no additional vitamin E. After 4 weeks of chronic hypoxia (oxygen deprivation), the supplemented climbers experienced no significant decrease in anaerobic threshold. Pentane breath exhalation, considered a reliable indicator of lipid peroxidation, did not change significantly. However, the control group demonstrated a significant decrease in anaerobic threshold and their pentane exhalation increased 104%. Simon-Schnass I, et al., Influence of vitamin E on physical performance. Internal J Vit Nutr Res 1988;68:49-54.
  • Supplementation of 1000 IU vitamin E daily for 10 days resulted in a significant decrease in pentane breath exhalation in normal adults. Van Gossum A, et al., Decrease in lipid peroxidation measured by breath pentane output in normals after oral supplementation with vitamin E. Clin Nutr 1988;7:53-57.
  • In a study of 30 osteoarthritis patients, subjects were randomly selected to receive either 600 mg. tocopherol daily or a placebo. In ten days, 52% of the tocopherol group and only 4% of the placebo group reported a good analgesic effect. Machtey I, Ouaknine L., Tocopherol in osteoarthritis: A controlled pilot study. J Am Geriatric Society 1978;7:328.
  • Chronic venous insufficiency in humans usually results from deep vein thrombosis. Free radical generation may increase due to an incomplete ischemic (reduced blood delivery) state, leading to tissue necrosis and skin ulceration. Twenty patients with chronic venous stasis ulceration received debridement and split-thickness skin grafts and were divided into two equal groups. Group I received 400 IU vitamin E daily, while group II did not. After 18 months, 9 of 10 individuals in group I had stable grafts. All of the subjects in group II had unstable grafts. Researchers concluded that vitamin E limited lipid peroxidation and prevented recurrent skin ulceration. Ramasastry SS et al., Biochemical evidence of lipoperoxidation in venous stasis ulcer. Vitamin E: Biochemistry and Health Implications 1989; 570:506-508.