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:
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.
FREE RADICALS AND WATER-SOLUBLE AND FAT-SOLUBLE ANTIOXIDANTS:
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
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-).
THE RELATIONSHIP OF VITAMIN E AND SELENIUM:
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.
ABSORPTION AND DISTRIBUTION OF VITAMIN E:
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.
DIETARY LEVELS IN FEEDSTUFFS:
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
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.
CLINICAL STUDIES OF VITAMIN E ACTIVITY:
- 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.