Download MBBS Vitamin E Lecture PPT

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tokos=childbirth, pherin =to bear and ol=alcohol)

? 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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CHEMISTRY

Vitamin 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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is

a

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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Tocopherols
ABSORPTION, TRANSPORT AND

STORAGE

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? It is absorbed along with other fats and needs the

help 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 after

conjugation 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 ROLE

A. 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, and
phospholipid 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 of

rearrangement

involving

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oxidation

of

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chromane ring and side chain. This is then
conjugated with glucuronic acid and excreted.


.

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2.Synergistic action with glutathione peroxidase
and 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 free
radicals .

? Vitamin E can spare requirement of Selenium

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,and vice versa.


Reduction of lipid peroxide by

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glutathione peroxidase
3. 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 with

reproductive 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 is

said 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 commercial

preparation 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 E

deficiency.

? Causes :

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1. Dietary deficiency

4. Malabsorption

2. Obstructive jaundice

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syndrome

3. Patients with cystic

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5. Hypolipoproteinemia

fibrosis & 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 delayed

milestone in premature infant, i.e. late start of
standing, walking, crawling

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3. Degenaration of post. Spinal column tract and

spinocerebellar tract causing decreased
vibration sense, demyelination of nerves,
cerebellar ataxia

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Manifestation of vitamin E Deficiency

4 . Retinal pigmentation degeneration
5. Retrolental fibroplasia (RLF):a neuropathy

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observed in premature infants with low birth
weight 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 above

1000 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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