Transcript Vitamin E deficiency

Vitamin E
Dr. Amani A. Alrasheedi
Associated Professor
Nutrition and food Science
King Abdul Aziz University
Vitamin E
• 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.
Sources
• 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.
Digestion, absorption, transport, &
storage
– 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 sensitivity
• 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 heat also can lead to increased
destruction.
Active form
• 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.
Absorption and metabolism
• 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.
Absorption and metabolism
• There are two mechanisms for tissue uptake
of vitamin E.
• 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.
Storage
• 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.
Metabolic functions of vitamin E
• 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.
Metabolic functions of vitamin E
• 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.
Other roles
• 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.
Interactions with other nutrients
• 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.
Interactions with other nutrients
• 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
Vitamin E deficiency
• 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.
Vitamin E deficiency
• 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.
Vitamin E deficiency
• 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
Vitamin E deficiency
• 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.
Vitamin E requirements
• 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.
Toxicity
• 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.