, \TfAMJN E

v· .
ll :, 1111 11 F, is the c ) ]j
. ~ t..:C l I\ ~ lil l l1C j'
· t · or a _group I F .
-
an1ox1 da!1t ~~S. Natur;il lv l) ' ' . . -- () d! -sulubi t' co rnp o i.mds With d i ~ti11et1\ t'
.,. - ccu rnng VJta111in l:. exis ts . . . --
gam111a. and d ~a-tocop herc~ I anct I l , . i~~ght chemical lom1S (alpha, beta.
I , . ____,__.. .: a p ia. beta ,_gamma . and d ~1 - .· - - --
cvcl s of b1oloo ical ,., .1·Iv !\
.t - ·- - -- eta tocott1enol) that have
--
va rving
- - Q.'. ' u._ . a - to e I I . J
requirements . - -- op 1ern is the only fonn that is recognized to I
· _ e, _ _ meet~!_n an
Functions

It is an antioxidant nutrient An . .
; - . _ _ - - -- · -~ n t s are sub~ s that protect other chemicals of the bod
irom ox1datirm reactions b · .. . . . Y
. . . .- - ' Y reacting with ox1d1zmg ageQ_ts within the body. Being a fat soluble
v1tan11n, v1tamm E is bl tO . . . .
- - - -- ..:.....::::_ a e mix with and protect l!r:>id tl}_olecules from oxidation. Vitamin E
protect cell membrane fro ·d · • c: . -----=
_. m oxi 1smgJreJUad1cals and is considered to be the body.'._s first line of
defense a 0 ainst lipid pe ·d · 1 . . . - -
0 • rox1 ation w 1erc peroxide denvatives of lipids are formed . Free radicals
are generally formed during the oxidation of energy yielding nutrients in cell and by the presence
of environmental pollutants and drugs . \Vhen free radicals attack the lipids of cell membranes
they can initiate a highly damaging chain reaction which can lead to damage of structure and
function of membranes. Vitamin E is the main ' chain blocking' antioxidant in the body that is
able to prevent these cham reactions. Vitamin E mhibit s oxidation of low -density lipoprotein
(LDL) thereby preventing atherosclerosis. Vitamin E might also help prevent the fonnation of
blood cJots that could lead to a heart attack or venous tlu-omboembolism (obstruction of a blood
vessel by a blood clol that has become dislodged from another site in the circulation).
Vitamin E inhibjts the fom1ation of lipofuscin, a pigment that accumulate within tissues during
ageing. It leads to formation of brown spots which are indicators of ageing. The other functions
of vitamin E are:

1) Prevents peroxi<lation of polyunsaturated fatty acids in various tissues and membranes.

2) Protects FBC from hemolysis by oxidizing agents
3) Protects damage caused by nitrosamines which are strong tumour promoters
4) Preserves and maintains germinai epithelium of gonads for proper reproductive function
5) It is required for cellular respiration through electron transport chain
6) Pr~vents the oxidation of vitamin A and carotene in the intestine
7) It is involved in the synthesis of nucleic acids
8) Delays the onset of cataract

Minu Mathews, Asst. Professor, Dept. of Clinical Nutrition & Dietetics

 9) p rcve nt s th .
e ox id ation of LDL
10) Re qu ired fior pr op er stora ge of er . .
ab . . ea tme m skeletal mu scle
l I) He lp s in th e . .
so rpt1on of am ino aci.d s m the int es tine
De fic ie ncy
Vi ta m in E d e fi1c.1ency ad I defect in fat absorptio .
n
occur in in fan ts and u ts who ha ve some
h .
De cr ea se on bl oo d t oc op erol level leads to .
rea se m he mo lys is of RBC.
It can lead to
. an mc
I . .
hem ol yt ic an em ia . N euro og1cal disorders includ uncoordmated movement, weakness and
e
D . f . rmanent
se ns or y distu rb ances. efective functio .
o ret ma of ey e (re tinopathy) can cause pe
. ru ng . .
. ease or
bl in dn ess m .
pr em at ur e in fa nt s V t . E
de fic ien cy m ch ild ren with severe liver dis
. I am m
c t' fib . c
pa nc re as is a . ~ . . ed aggreg ati on of platelets
in blood .
ys IC I ros 1s Ot
ss oc iat e wi th m cre as
. .
Tox1c1ty
. n of
lu bl e vita.m i · · •
st tox ic on e. Th e intravenous administratio
A m on g fat so ns , vitamm E 1s the lea
· lation of flu id in
vi ta m in E in pr em at ur e · f. t s l ead s to liver and kidney fa ilure , accumu
ex ce ss - m an . People who
bl oo d pl ate let nu mb ers and eventual death
sc ite s) , decreased
pe rit on ea l ca vi ty (A ris k of haemorrhagic damage
because
ol are at gr ea ter
1000 m g of tocopher
co ns w ne m or e th an
an anticoagulant.
th e nu tri en t ca n ac t as
ab ol ism
A bs or pt io n an d M et aximal absorption.
ted by bi le sa lts . M idgu t is the site of m
E is facilita
Ab so rp tio n of vi ta m in ed by the body. Tocopherol
enters blood
um ed is ab so rb
of vi ta m in E cons
A bo ut 20 -4 0 pe r ce nt DL . W he n vitamin E reaches th
e blood
icr on s an d VL
so ci at ed wi th chylom
via ly m ph wh ic h is as LD L. It is th en exchanged between th
e
teins , prim ar ily
so ci at ed wi th lipopro
plasma it be co m es as br an es of RBC. Ad ip os e tissu
es are the
al ly th e m em
id m em br an es , es pe ci
LD L particles an d lip un da nt sto re s of vitamin E sufficie
nt to
pe op le ha ve ab
m in E sto ra ge . M os t
si te for m ax im al vi ta Pl as m a tocopherol concen
trations are
d th ro ug h die t.
s ev en if no t su pp lie
la st fo r se ve ra l m on th
6 an d 1. 6 m g/ 10 0 ml.
no rm al ly be tw ee n 0.
Requirement ire m en t su gg es te d by
IC M R is 0.8
of PU F A . Th e re qu
en t is lin ke d to th at
V ita m in E re qu ire m day.
ac id s. It is ab ou t 8- 10 m g to co ph er ol pe r
m g/ g of es se nt ia l fa tty
So ur ce s he st so ur ce of
an oi l, nu ts an d wh ol e gr am s ar e th e ric
he at ge rm oi l, ric e br
V eg et ab le oils lik e w
s ar e po or sources.
vitam in E. An im al food
s
of es so r, Dept. of Clinical Nutrition & Diete tic
Pr
H I Minu Mathews, Asst.