2.  Vitamin E is naturally occuring anti-
oxidant.
 It is known as “anti-sterility vitamin”
because it helps in normal reproduction
in many animals.
 Vitamin E is a Fat soluble vitamin.
 Also known a beauty vitamin

3.  1922: Evans and Bishop, described Vitamin E
deficiency
 1936: Evans et al, Isolated α-tocopherol
 1960s: Vitamin E deficiency was described in
children with fat mal absorption syndromes.
 1980s: Major symptom of vitamin E
deficiency in Human was a peripheral
neuropathy.
 .

5.  Vitamin E is the name given to a group
of toco pherols and tocotrienols.
 Till now 8 tocopherols have been
identified alpha ,beta,
gamma,delta..etc
 Among this alpha tocopherol is active.
 Tocopherols are derivatives of 6-hydroxy
chromane
 The anti –oxidant property is due to
chromane ring.

6.  Dietary tocopherol is dissolved in fats.
 Absorbed in cell membrane ---distributed
to peripheral tissue------cell membrane
remant----liver----transported in VLDL-------
---------STORED IN ADIPOSE TISSUE.

7.  1.Vitamin E is essential for the membrane
structure and integrity of the cell ,hence it is
regarded as a membrane antioxidant.
 2.It prevents the peroxidation of PUFA in
various tissues and membranes .it prevents
RBC from hemolysis by oxidizing agents eg..
Hydrogenperoxide.
 3.It is closely associated with reproductive
functions and prevents sterility. vit.E
preserves and maintains germinal
epithelium of gonads for proper
reproductive function.

8.  4.Vitamin E protects liver from being
damaged by toxic compounds such as
carbon tetrachloride.
 5.It works in association with vitamin A,C
and beta carotene to delay the onset of
cataract.
 6.RECENT studies have shown that high
intake of vitamin E protects against the
development of heart diseases.It is
believed that vit E prevents oxidation of
LDL. The oxidised LDL Have been
implicated to promote heart diseases .

9.  Vitamin E also inhibits the conversion of
nitrites in the stomach to nitrosamines, which
are cancer promoters.

10.  A daily consumption of 10 mg (15 IU) of
alpha tocopherol for man.
 8mg 12 IU for woman is recommended
 1mg of alpha tocopherol =1.5 IU.
 Vitamin E supplement is advised for
pregnant and lactating women.
 Ref:horwitt m.k, critique of the req.for vit
e.Am.J.CLIN nutr.2001,73:1003-1005

11. • Eggs
• Milk
• Nuts, such as almonds
• Spinach and other green leafy vegetables
• Unheated vegetable oils
• Wheat germ
• Wholegrain foods
• Ref:harper’s biochemistry

12. • People more than 55 years of age
• Very low birth weight infants
• Those who abuse alcohol and other drugs
• Those with:
o cystic fibrosis
o celiac disease
o hyperthyroidism
o malnutrition
o liver, gallbladder, or pancreatic disease
o Ref: harper’s biochemistry..

13.  A severe ,progressive neurological disorder.
 Loss of deep tendon reflexes
 Limb ataxia
 Dysarthria
 Ophthalmoplegia
 Nystagmus
 Positive romberg test
 Edema in premature infant and hemolysis

14.  Vitamin E is an antioxidant that protects
cells in the body from the damaging
effects of unstable molecules called free
radicals. Lack of vitamin E causes
neurological problems, such as difficulty
coordinating movements (ataxia) and
speech (dysarthria), loss of reflexes in the
legs , and a loss of sensation in the
extremities (peripheral neuropathy).

15. 
Ataxia with vitamin E deficiency is a rare
condition; however, its prevalence is
unknown

16.  Mutations in the T T PA gene cause
ataxia with vitamin E deficency.
 The TTPA gene provides instructions for
making the α-tocopherol transfer protein
(αTTP), which is found in the liver and
brain.

17.  This protein controls the distribution of
vitamin E obtained from the diet (also
called α-tocopherol) to cells and tissues
throughout the body.
 Cells neutralize free radicals with the aid
of vitamin E, which prevents damage to
the cell. Mutations in the TTPA gene
impair the activity of the αTTP protein,
resulting in an inability to retain and use
dietary vitamin E. This deficiency leads to
accumulation of free radicals within
cells

18.  Vitamin E (a-tocopherol) has been credited with
a variety of beneficial effects in
the premature newborn infant.
It has been thought that deficiency of vitamin E is
at least partly responsible for the anemia which
often occurs 4 to 6 wk after premature birth, and
routine dietary supplementation with vitamin E is
frequently recommended.

19.  In NEWBORN vitamin E acts free radical
scavenger and natural anti-oxidant that
Protects the cell membranes against lipid
peroxidation.
REQUIRED FOR PREMATURE BABY:
Because there is a significant transfer of
vitamin E during the last trimester of
pregnancy.so , vitamin E is required for
preventing haemolysis ,edema and
anaemia

20.  Serum vit E LEVEL increases in presences
of high serum lipid levels
 Ratio <.8mg/g is abnormal
 Premature infants with hemolysis due to
vit e def.have elevated platelet counts
 Ref:nelson vol 1 .18 th ed ,chp 49 pg263.

21.  In neonates dose 25-50 units/day for
1week
 TOXICITY
 NO TOXIC EFFECT HAS BEEN REPORTED .

22.  Heart Disease: Mixed results
 Cancer: Promising but not conclusive
› Breast cancer: two opposing studies
› Colon and G.I. cancer: probably no benefit
› Prostate and bladder cancer: possible
benefit
 Alzheimer’s: theoretical but not well
studied

23.  1998: “Antioxidant vitamins and nuclear
opacities: the longitudinal study of
cataract”
 Cataract risk reduced by ½ in Vit
E supplement users
 764 participant observational
study (low significance)