\ 'IT A.

\flNS
\ ll,H1 lll b arc a grou p ol unrd ,ll ed orgamc suh::it aucc~ nccu 1nng ,,, mJm fooJ:, m :-.Ill.di .1n 1unt,
11
an d 11ccl'.s-,a1y m trace am0 ums fo r the normal metabolic fu1h.'t 1u11111g of the body flt c~ c.inn11T lw
sy11thc:, iz\!d in the body and m \J.$1 be supplied through the diet Stm1c \ 11amins like\ 1tan , "- , nd
111 1
\'it a:n m l3 arc synthes ized by bacteria in the intest ine. V11am 111 :, are classified into [\\,() - tat
soluble and \\lat er soluble.
FAT SOLUBLE VITAMINS
These are vitamins that can dissolve in fats and oils . Fat-soluble vitamins are ab:,urbcd alnng
with fats in the diet and can be stored in the body's fatt y ti ss ue Vitamin A. D, E and 1--:. :i re the
different fat sol ubl e vita mins.

v\,ITAMTN A
Vitamin A was discovered in 1909 by Mc Collum and Davis. But the chemical fom, st ructure
was determined in l 931 .1 1he chemical name is retinol and is an organic alcohol with hr d:-oxyl
-
groups of alcohol being attached to polyunsaturated hydrocarbon chair~ Vitamin A is found in
-
the body as retinal (aldehydic form_L and retinoic acid (acidic fOJm) . Retinal and retimd arc easily
inter conve11ible but retinoic acid cannot be converted back Lo retinol or retinal. Vit_&min A is
found in food as retinal and P-carote°:~
~ :::::>

CONVERSION FACTORS
l µg P-carotene = 0.16 µg retinal
If diet contains both retinol and P-carotene, its vitamin A content can be expressed as follows :
Retinal Equivalent (!1.g) = µg Retinal + µg P-carotene x 0.16 (if retinal and P-carotene are
expressed in µg)
The conversion of one molecule P-carotene to retinol should theoretically result in two molecules
of retinol. But due to physiological inefficiency, the maximum conversion that has been shown
in experimental animals is around 50 per cent. FAO/WHO assumed that about one-third of
dietary P-carotene is absorbed. As a result a factor 0.16 is used to convert P-carotene tO retinal.

FUNCTIONS
Vision: The best characterized function of vitamin A is its role in the retina of the eye.
~ cording to Wald, the retina has two cells, the rod cells and the cone cells which contain the

- ·---,...,-----·-----M-i_n_u_M_a_t_h-ev.-,-s,-A-s_s_t._P_r_ofi-e-ss_o_r_,0-ep_t__-of~C~lin~i~c~al'"".'.N~u-tn~.:-'.ti_o_n-::&~
, ::
D-:-ie_t_ell"..c_s_
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 . . w::w
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.
'liodo!l'>in~ •·ind 10 . d . 111 retin al (\ 1La rnm .'\
Pl t! ll l l'llls
---- -'- ops111 n::-rcct1\c l) . f3 oth this pigm ents cn11ta
·d · d ol dehyd ro!.!enase cnz vmc.
c1ldeh ydcJ · Rc1
_ ..
·
111 0 J is ox, izt: _ ~ ~ 111al rn the rod cel ls by :tlcoh
· d
Relin al .rnmb 1;-- ,,-
1 •s -..,....
· le pigm ent know n as rho ops m.
L c W I 1 ~ i ro!c111 nps,n tu prod uce a purp
retina .
localed in the light sensi ti ve rod cells of the
Rhod opsm. a lso know n as \·is ual puplc is
l and
bleac hed as the rhodo psin spl its lo form retina
Whe n ligh1 strikes the reti na. the rod cell s are
vi sua l
smi lled throu gh the opt ic nerve fibres to the
opsin . Al th e same time a nerve imp ul se 1s tran
At each
vis ion is creat ed and the cycle is n~peated .
centr e of the bra in wher e the sensa ti on of
10 retino ic acid and is lost from th
e rod cells . The
cycle a small amou nt of retino l is co nver! l.!d
--c: : j
od. The. amount of
supp li es of retino l in thee
lost amount of retiool must be repla ced by ircs h
which ~ _psin is reg enera ed . If the rhod opsin
rctin ol in blood deter mine s the_ ratc i!,I_
poor. ~ speed with whic h tl~ e eye reco vers its full
regen erati on .i•s siow , visio n in dim light is
lable to
t ly relate d to the amou nt of vitam in A avai
powe r after expo sure to bngh ! li ght 1s direc
n as dark adap tation beca use it aJlo ws the eye
to
fom1 rho do~ This recove1y proce ss is know
cone
to bright li ght. The retina of eye also con tain
adap t to visio n in dim light after expo s ure .
. . . °'~ . . . .
;{;t"Y lo .sec r v1s10n m good hght. 1:i.e funcuonm.ft of
eel.ls whic h are mvol ved m the perq~prwo
of colou
in A
cone cell s is no! sensi tive to varia tions i11 vitam
use the
tam in A takes much longe r to recov er beca
The eyes of pt;op le who is defic ient in vi
nA
n proce eds more slow ly. This effect of vi tami
-
refor matio n of the rhod opsin requi red fo:- visio
is know n as nigh t blind ness.
of
retino l is nece ssary for the synth esis
Growth: Retin yI phos phate synth esise d from
is loss of
th. rrfarl y symp toms of vitam in A defic iency
g]yc opro teins whic h are requi red for gr~w :
,,., -;:l
p7oc u5 .,.e, encf.inS C ate d~ Vitam in A is
tioE, of grow th, rapid weig ht loss and ultim
1

appe tite, follo wed by ~essa

ge to
ies in the ~ n d spina l colum n do not enlar
essen tial for norm al bone grow th. The cavit
ature bone
m. Defi cienc y may invo lve failu re of imm
make room for the grow ing nerv ous syste
acid can
respo nsibl e for bone remo delin g. Retin oic
cells to matu re into osteo clast s whic h are
n.
supp ort grow th but will not main tain visio
elial cells are conti nuall y shed and repla ced
Cell differentiation and Gene expression: Epith
elial cells .
a is requ ired for the form ation of epith
and henc e a cons tant supp ly of vitam in
g of diges tive tract and respi rator y tract . Thos
e with in
Epitr .elial cells are foun d in skin, eye, linin
linin g of
cove red by h.air l i k e ~ fuc ilia on the
the body norm ally secre te mucu s and are
epith elial
of forei gn mate rial on the surfa ce of the
respi rator y syste m prev ent the accu mula tion

cal Nutrition & Dietetics

q Minu Math ews, Asst. Profe ssor, Dept. of Clini
 cdl s h) th~ir cons tant mot, ~ 111 - .
' Hamm A detic1 cn1 ls.cratm1ze d ce lls t.hc c ilia
kcra trni sat io n and loss o f c ili a l~, c tl1e llod) arc.: ll,:,l I he
more ,1.1 lne rable t,) infect ion. Henc e , 1tamm
"now n as an · ant iinfecti ve · \'itam in . ,\ 1s

Regula t ory function of retinoic acid :

Retin oic acid plays a role in the differenti
emb ryon ation o f
-------=-..:i~:.,!~-~-""~" · , nvers1011 1rom mun
ic stem cell s i e co r. · .
ature precu rsor cells mto matu re spec1. ahze
.
d cells
such as mus cle, skin and nerv e cells . TI1is
proc ess of diffe renti ation is medi ated bv chan
ges in
,&ene activ ity . Reti noic acid is the acti\'e
form of \'itam in A invo lved in cont rolling
ceil
deve lopm ent by influ enc ing gene ar tjyjty .
This is due to horm one, like activ ity of retin oic
acid .
Reti noic acid can dela y or prev ent Lhe deve
lopment of certa in epithelial canc ers. It can
also
regu late the meta bolis m if vi tami n A in the
body . The meta bolis m of vi tami n A in the liver
is
influ ence d by the dieta ry avail abili t) of \'itam
jn A or retin0ic acid.
Imm unit y: Vita min A is requ ired to main tain
the no1mal health and func tion of epith elial layer
s,
whic h prov ide a first line of defe nse again
st invad ing micr oorg anism s . Hum eral imm
une
resp onse whic h is med iated by relea se of
antib odies into blood and cellu lar im.rnune resgg
g;e
whic h invo lves the direc t killin g of infected
cells are regulated by vitan un A or its meta bolit
es.
Vita min A can redu ce the seve ritv of outc omes
of certain infections not the incid ence .
Rep rodu ction : Norm al levels of vitam in
A are required for sperm prod uct ion., norm
al
repro duct ive cycl es in r"ema les. prev entio
n of neoplastic trans form ation s and prem
ature
deliv eries .

DEF ICIE NCY

Ocu lar man ifest ation s
Xero phth almi a refer s to the spec trum of ocul
ar mani festa tions due to syste mic vitam in
A
defic ienc y asso ciate d with exce ssive dryn
ess of the conj unct iva and corn ea, whic h lose
their
lustr e and beco me kera tiniz ed. Whe n xero
phth almi a is due to vitam in A defic iency
, the
cond ition begi ns with nigh t blind ness and
conj unct iva! xero sis (dryn ess of the eye mem
bran es),
prog resse s to corn eal xero sis ( dryn ess of
the corn ea), and in its late stage s deve lops
into
kera toma lacia (soft enin g of the corn ea).
Nigh t blin dnes s or nyct alop ia is the cond1t10n
··
o f the eyes m
· wluc
· h v1S1o
· · 1·s norm al in day licrht
n e,
· · abno rmal
or othe r stron g light but 1s ly w eak or com p lete1Y Ios t a t ru·ght or in dim licrht
0 . It is an
early sym ptom of vitam in A defic ienc y. The
spee d with whic h t.lJ.e eye reco vers its full pow
er

Minu Math ews, Asst. Profe ssor, Dept . of Clini

cal Nutri tion & Dietetics
 ,

a11cr ClC f)Osurc to bri ht rI . .

g ig It 15 directly related to the amount or vitamin A that is avail abl e to
fonn rhodops in The .
.J. a . . . _· _ r~covery process 1s known as dark adaptation because it allows
the eye to
~ ., ·,.i : dapt 10 vis ion m dim light after exposure to bri ght light.

~
iJ-~~.,-;;,,~
. ·'f CODJunc. .
tava l xerosis manifes ts as dry patches of non-wettable conj unctiva. It may
:~• . be associated
~· .
.
~ ~~•\f.· 4I wi
th vanous degrees of thicken ing, wrinklin g and pigmen tation (muddy colourin
~ . g) which gives a
~ • ~ ~ _,. smo ky appeara nce to the coniunc tiva.
/Ii, •• ' ~

'~· : Bitot's spot are ra ised, muddy and dry triangul ar patches which are the
·"f I I build up of kerat in
.J..
•

,t:.. ,,..,__,. t,~ ocated superfic ially in the conj unctiva. These spots are a sign of vi tamin
A deficiency and are
assoc iated wi th conjunc tiva l xerosi s.

Cornea l xerosis is the dryness of cornea and there is a du ll hazy appeara

nce. It is due to the
kerat ini sation due to vi tamin A defi ciency in epithelia l ce ll s. The characte
ristic feature is the loss
of part or whole of the cornea l thickness. lf there is secondary infectio n,
there is inflamm ation.
The lesions only heals by leaving scars. If not properly managed it leads to
keratom alacia .
Kerato malacia is the softenin g and dissolut ion of cornea. If untreate d, perforat
ion of the cornea
leads to the prolaps e of iris, extrnsion of the lens and infection of eyeball.
Healing results in
scarring of whole eye and frequen tly in blindness.
Other sympto ms of deficien cy are increase d suscepti bility to infectio n, growth
retardation due to
impairm ent of skeletal fc mation, sterility in males and termination of
pregnan cy due to still
birth and prema ture deliveri es.

TOXICITY
Sympto ms found in adults are headach e, drowsin ess , nausea, loss of hair,
dry skin~ diarrho ea,
rapid resorpti on of bone, cessatio n of menstru ation in woman . In infants
weight loss, anorexi a,
bulging of head, hydroce phalus, hyperin itability and skeletal pain. The
most serious teratoge nic
effects are foetal resorpt ion, abortio n, birth defects, and learning disabili
ties. The sympto ms
occur in adults on receivin g long term doses of 16000 RE/day for a period
of above 6 months
wherea s in infants 8000 RE/day fo 30 days can lead to toxicity .

The storage of caroten es in subcuta neous fat can give the skin a pale yellow
colour, especia lly on
the so les of feet and the palm of hands. This conditi on is called caroten
odermi a and is absolut ely
hannles s .

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

 ABSORPT ION, METABOLISM AND TRANSPORT
Retino l can be absorbed f t· d . .
m~ o~o~ d1rectly mto the intestinal wa ll cell s. Rctiny l esters are first
-- ~- - - - - - ~~ :.:.r.::..o.::.
hydrol ysed to free t' 1 d • . - . . . - - -- . .
re mo an an organic acid . fh1 s hydrolysis 1s catalysed by enzymes w1th m
pancreatic juice. The organic acid released is usually palmitic acid because retinyl palmitate is

J th
e predominant retinyl ester within food . Approximately 75 % of vitamin A is usually absorbed
compared with 5% P-carotene and 50% other carotenoids. Since vitamin A is fat soluble, its
absorption is enhanced by factors that promote fat absorpt ion and diminished by those hindering
fat absorption . Any condition that reduces bile secretion or obstructs the bile duct leads to
diminished absorption of vitamin A. Only small amounts of retinoic acid are found in food . P-
carotenc is hydrolysed in the intestine to fo nn retinal and about 10% of the retinal is converted
to retinoic acid.

Absorbed vitamin A in the fonn of retinal, retinyl esters, P-carotene or the retinal produced from
P-carotene is transpo11ed from the intestine within chy !omicrons . For this to happen, much of the
retinal must be reesterified back into the form of retinyl esters. The chylomicrons are released
into the lymphatic system, which transports them to blood. Most of the retinal and retinyl esters
are transp.:)ted to the liver and some enter adipose tissue and other tissues.
When vitamin A is required by the rest of the body, it is released from the li·ver and transported
to target tissues in the for:n of retinal bound to Retinal Binding proteirI (RBP) . The RBP within

plasma becomes bound to a protein called Transthyretin (TTR) . lbe proteins RBP and TTR
serve to make vitamin A more soluble in blood plasma . By incorporating vitamin A into a much
larger molecule, they protect it from being filtered from blood and excreted via the kidneys . ~-
carotene is released from the liver as pai1 of VLDL. Once delivered into the cell vitamin A is
picked up by various binding proteins, which are distinct from proteins that serve to transport

vitamin A within the blood.

In the liver, vitamin A is stored irI lipid droplets irI the fonn of retinyl palmitate within the fat
storing cells known as stellate cells. Retinyl esters are also stored irI other tissue including the

adipose tissue, lungs, testes, bone marrow, eye and kidney.

SOURCES
Vitamin A are highest in liver, fish oils and, eggs. Green leafy vegetables , orange -yellow

vegetables and fruits like mango, papaya, carrots, pumpkin are rich in P-carotene.

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

Requirements
-
- --
Age group Retinol (µg) P-carotene (µg) 1

Man 600 4800

Wo man 600 4800
Pregnant woman 800 6400
Lactating mother 950 7600
lnfants (6-12 months) 350 2100
C hildren
1-6 yrs 400 3200

7-9 yrs 600 4800

Boys and girls
10- 17 yrs 600 4800