Dr. Amani A. Alrasheedi
Associated Professor
Nutrition and food Science
King Abdul Aziz University

• Vitamin E acts as a lipid-soluble antioxidant in cell membranes, but many of its functions can be replaced by synthetic antioxidants.
• There is epidemiological evidence that high intakes of vitamin E are associated with lower incidence of cardiovascular disease .
• Vitamin E supplements have been associated with increased all-cause mortality.

• Vegetable oils (canola, olive, sunflower, safflower, cottonseed) are rich sources of vitamin E,
• A significant amounts are also found in nuts and seeds. Whole grains, mayonnaise margarine.
• Most green leafy vegetables,
• and a variety of fish.

– Tocotrienols hydrolyzed; synthetic ester forms digested absorbed primarily in jejunum by nonsaturable, passive diffusion
– Chylomicrons for transport
– Liver recirculates some in VLDL
– Stored mostly in adipose tissues
 2009 Cengage-Wadsworth

• Vitamin E is susceptible to destruction during food preparation , processing and storage .
• Tocopherols can be oxidized with lengthy exposure to air .
• In addition, exposure of the vitamin to light and hea t also can lead to increased destruction.

• Vitamin E exists in eight different forms vitamers , each one contains a phenolic functional group on a chromanol ring and attached phytyl side chain (hydrophobic).
• Vitamin E is the generic descriptor for two families of compounds, the tocopherols and the tocotrienols.
• The different vitamers have different biological potency.
• The most active is α-tocopherol, and it is usual to express vitamin E intake in terms of mg α-tocopherol equivalents.
• The other vitamers have negligible vitamin activity.

• Tocopherols and tocotrienols are absorbed unchanged from the small intestine , in micelles with other dietary lipids , and incorporated into chylomicrons .
• The major route of excretion is in the bile , largely as glucuronides and other conjugates.

• There are of
for tissue uptake
.
• 1- Lipoprotein lipase releases the vitamin by hydrolyzing the triacylglycerols in chylomicrons and VLDLs.
• 2- Uptake of low-density lipoprotein (LDL)bound vitamin E by means of LDL receptors.

• There is no single storage organ for vitamin E: Adipose tissue > 90%.
• The vitamin storage increase with its dosage. vitamin E release from adipose tissues is slow even during period of low vitamin E intake.
• Other organs: have smallest amount ( liver, lung, heart, muscle, adrenal glands, spleen and brain ).
• Vitamin E concentration remains constant.
• Liver and plasma vitamin store provide a readily available source.

• The principal function of vitamin E is the maintenance of membrane integrity , including possible physical stability, in body cells .
• The mechanism by which vitamin E protects the membranes from destruction is through its ability to prevent oxidation (peroxidation) of unsaturated fatty acids contained in the phospholipids of the membranes.

• The main function of vitamin E is as a radical trapping antioxidant in cell membranes and plasma lipoproteins . It is especially important in limiting radical damage resulting from oxidation of PUFAs, by reacting with the lipid peroxide radicals before they can establish a chain reaction.

• Vitamin E thought to improve plasma membrane structure.
• Increased intake of vitamin E enhances immune response.
• Helps protect against prostate cancer and
Alzheimer’s disease.

• Positive relations:
• Interrelationship exists between vitamin E and selenium.
• Some of vitamin C functions are complement vitamin E, and vitamin C can regenerate vitamin E following its oxidation.
• Foods high in polyunsaturated fatty acids also tend to be relatively good sources of vitamin
E.

• Negative relations
• Vitamin E inhibits β- carotene absorption and its conversion to retinol in the intestinal.
• Vitamin E may impair vitamin K absorption.

Recommended Dietary Allowance and
Estimated average Requirement
19+ years male and female
RDA 15 (mg/day)  -tocopherol
EAR 12 (mg/day)  -tocopherol
Pregnancy
RDA 15 (mg/day)  -tocopherol
EAR 12 (mg/day)  -tocopherol
Lactation
RDA 19 (mg/day)  -tocopherol
EAR 16 (mg/day)  -tocopherol
 2009 Cengage-Wadsworth

• In experimental animals vitamin E deficiency results in a number of different conditions.
● Deficient female animals suffer the death and reabsorption of the fetuses. This provided the basis of the original biological assay of vitamin E.
● In male animals deficiency results in testicular atrophy and degeneration of the germinal epithelium of the seminiferous tubules.

• Both skeletal and cardiac muscle are affected in deficient animals. This necrotizing myopathy is sometimes called nutritional muscular dystrophy –an unfortunate term, since there is no evidence that human muscular dystrophy is related to vitamin E deficiency.
● The integrity of blood vessel walls is affected, with leakage of blood plasma into subcutaneous tissues and accumulation under the skin of a green fluid: exudative diathesis.
● The nervous system is affected, with the development of central nervous system necrosis and axonal dystrophy. This is exacerbated by feeding diets rich in PUFAs.

• Dietary deficiency of vitamin E in human beings is unknown, although patients with severe fat malabsorption, cystic fibrosis, some forms of chronic liver disease or (very rare) congenital lack of plasma β- lipoprotein suffer deficiency because they are unable to absorb the vitamin or transport it around the body

• Premature infants are at risk of vitamin E deficiency, since they are often born with inadequate reserves of the vitamin. The red blood cell membranes of deficient infants are abnormally fragile, as a result of unchecked oxidative radical attack. This may lead to hemolytic anemia if they are not give supplements of the vitamin.

• It is difficult to establish vitamin E requirements, partly because deficiency is more or less unknown.
• But also because the requirement depends on the intake of PUFAs. It is generally accepted, albeit with little experimental evidence, that an acceptable intake of vitamin E is 0.4 mg αtocopherol equivalent/g dietary PUFA.

• Tolerable upper intake level for adults 1.000mg αtocopherol.
• Increased bleeding
• Gastrointestinal distress (nausea, diarrhea, and flatulence).
• Respiratory infections
• Muscle weakness
• Fatigue
• Double vision
• If intake in excess amounts (3000IU+) people may experience intestinal caps and diarrhea, fatigue, double vision and muscle weakness.