? anti-infertility Vitamin
? Infertile animal + vitamin E conception of
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animal? Vitamin E is lipid soluble antioxidants in cell
membranes, and is important in maintaining the
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fluidity of cell membranes.? Structure of Vitamin E was elucidated by Paul Karr (
Noble prize-1937)
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CHEMISTRYVitamin E a name given to a group of Tocopherols and
Tocotrienols
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? tocopherol (5,7,8 trimethyl tocol)5
Structure of a-tocopherol (various tocopherols differ
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in the substitution of methyl groups on chromanol
nucleus).
.
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? Chemically
it
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isa
substituted
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hydroxychromane derivative or methylated
tocols
? 8 derivatives of Tocopherols identified as
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,,, Tocopherol etc. out of which -
tocopherol is most active physiologically.
? OH group of Tocol is responsible for
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antioxidant property of Vitamin E
? Tocotrienols have 1-50% activity of activity of
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TocopherolsABSORPTION, TRANSPORT AND
STORAGE
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? It is absorbed along with other fats and needs thehelp of bile salts.
? Tocopherol is absorbed and transported as chylo
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microns.
? In the liver, it is incorporated into lipoproteins
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(VLDL and LDL) and transported? It is stored in adipose tissue, liver and muscle.
? During catabolism, the chromane ring and side
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chain may be oxidized and excreted in bile afterconjugation with glucuronic acid
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Don't forget.
TISSUE DISTRIBUTION
? All cell membranes including mitochondrial
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membrane and endoplasmic membrane.
? Retina is specially rich in vitamin E.
? Plasma levels are 0.5 -1 mg/dl
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BIOCHEMICAL ROLEA. Antioxidant Role
? It is a potent natural antioxidant vitamin.
? It is a chain breaking and peroxyl-radical
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scavenging antioxidant
? It protects most lipophilic molecule
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susceptible to oxidant injury like PUFA, andphospholipid having PUFA, present in cell
membranes, lipoproteins, RBC, mitochondrial
membrane, retina etc.
.
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? It acts as an antioxidants by donating a hydrogen
radical H. and terminating the chain reaction of
fatty acid peroxidation.
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? Vitamin E itself becomes phenoxy radical which
is relatively more stable.
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? Its further fate is two fold:1. It is reduced by vitamin C back to original form.
The oxidized vitamin C is maintained in reduced
form through glutathione and NADPH via the
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HMP pathway..
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? The phenoxy radical may undergo a series ofrearrangement
involving
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oxidation
of
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chromane ring and side chain. This is thenconjugated with glucuronic acid and excreted.
.
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2.Synergistic action with glutathione peroxidaseand sparing of selenium
? Lipid peroxides produced by oxidation of
lipids are neutralized by glutathione peroxidase
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as a second line of defence.? vitamin E acts synergistically with Selenium
which is a cofactor of antioxidant enzyme
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Glutathione peroxidase that destroys freeradicals .
? Vitamin E can spare requirement of Selenium
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,and vice versa.Reduction of lipid peroxide by
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glutathione peroxidase3. Anti ? atherogenic effect:
? Oxidation of LDL is an initial and critical
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event in the development of atherosclerosis.Vitamin E is known to prevent this oxidation.
Hence, vitamin E has anti atherogenic role .
4. Ant sterility role
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? Prevents sterility and closely associated withreproductive functions
? maintains germinal epithelium of gonads
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? Anti sterility role in humans is doubtful..
5. Maintaining the structural and functional
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integrity of cells and organs. In that sense, it issaid to have anti ? aging effect.
6. It protects the RBC from hemolysis by
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oxidizing agents (e.g. H2O2) and thus helps in
maintaining RBC membrane integrity.
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7. Enhances activity of aminolaevulinic acid(ALA) synthase and ALA dehydratase
Enhances heme synthesis
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8. Required for cellular respiration through
electron transport chain ( stabilizes coenzyme
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Q)9. Vitamin E encourages .skin healing and reducing
scarring effect after injuries such as burn- extensive
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use in skin creams and lotions.10. It is required for proper storage of creatine in skeletal
muscle
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11..It protects the liver from toxic compounds such as
carbontetrachloride
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12.It works in association with vitamin A,C and beta-carotene, to delay the onset of cataract
13.It is said to be beneficial in Alzheimers disease, skin
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disorders, cancers
14.Trace amount of vitamin E ( hydroquinone),Gallic
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acid and alpha naphthol are added in commercialpreparation of fat and oils to prevent oxidative
rancidity
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Vitamin E Deficiency? Blood levels:
levels below 5 ?g/ml are
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suggestive of vitamin Edeficiency.
? Causes :
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1. Dietary deficiency4. Malabsorption
2. Obstructive jaundice
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syndrome
3. Patients with cystic
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5. Hypolipoproteinemiafibrosis & chronic liver
diseases
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6. Very low birth weight
infants
Manifestation of vitamin E Deficiency
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1. Anaemia due to RBC hemolysis because of
the increased membrane fragility.
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2. Neurological deficiency such as delayedmilestone in premature infant, i.e. late start of
standing, walking, crawling
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3. Degenaration of post. Spinal column tract andspinocerebellar tract causing decreased
vibration sense, demyelination of nerves,
cerebellar ataxia
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Manifestation of vitamin E Deficiency4 . Retinal pigmentation degeneration
5. Retrolental fibroplasia (RLF):a neuropathy
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observed in premature infants with low birthweight due to poor placental transfer of
Vitamin E .
6. Muscular weakness & creatinuria.
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.
.
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RDA
? Adults - 8 -10 mg/day
? Pregnancy & Lactation - 10 - 15 mg/day
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? 15 mg of vitamin E is equivalent to 33 IU? Pharmacological dose is 200-400 IU/day
Hypervitaminosis E
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? Hypervitaminosis E : toxicity at doses above1000 IU
? No toxic effects observed = LEAST TOXIC
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fat soluble vitamin
? Tendency of hemorrhage.
? Neurological symptoms.
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"Vitamin in search of a disease".Clinical use of vitamin E
1. Fibrocystic breast diseases
2. Intermittent claudication ( episodes of
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tingling, numbness and pain in the legs due to
ischemia ).
3. Patients at high risk of free radical ?mediated
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injury ( prescribed along with other
antioxidants)
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