2. VITAMIN
Vitamins may be defined as organic compounds
occurring in small quantities in the different natural
foods and necessary for the growth and maintenance
of good health in human beings and certain
experimental animals.
5. FAT SOLUBLE VITAMINS
Fat Soluble Vitamins
Vitamin A Vitamin A occurs only in foods of animal origin
vitamin A activity is also possessed by carotenoids found in
plants. Hence carotenoids are called pro vitamin A.
Forms of Vitamin A
Vitamin A - Antixerophthalmic vitamin
Vitamin A1 - Retinol
Vitamin A2 - Dehydroretinol
Vitamin A + Aldehyde - Retinene, retinal
6. Vitamin A + Acid - Retinoic acid
Vitamin A+ esters - Retinyl esters
PHYSIOLOGICAL FUNCTIONS OF VITAMIN A
Vitamin A and vision: Vitamin A is essential for vision in
dim light vitamin A deficient subjects cannot see objects.
The characteristic pigments of the retinal rods and cones in
the retina are rhodopsin and iodopsin.
They differ only in respect of the protein moieties (called
scotopsin and photopsin respectively).
The specific pigment common to both is a cis-isomer of
retinene (vitamin A aldehyde).
Vitamin A alcohol is oxidized to vitamin A aldehyde in the
epithelium of the rods by alcohol dehydrogenase in the
presence of NAD.
.
7. The protein opsin (scotopsin) reacts with retinene to
form rhodopsin. Light initiates a series photochemical
changes in rhodopsin, beginning with bleaching of the
purple pigment and ending with the formation of all-
trans-retinene and it sisomerisation.
Vitamin A & epithelial tissues: Vitamin A is essential
for the integrity of the mucous secreting cells of
epithelial tissues. In vitamin A deficiency, the
epithelial tissues are keratinized. The tissues affected
are salivary glands, respiratory tract, eyes, skin and sex
organs.
8. Vitamin A and nerves: The important observation in
experimental animals that vitamin A deficiency causes
degeneration of the myelin sheath.
Vitamin A and bone: Vitamin A is essential for normal
bone formation. Excess of 53 vitamin A is toxic and causes
brittleness of bones and hence bone fractures.
Vitamin A and protein deficiency: The absorption and
mobilization of vitamin A is impaired in protein
malnutrition. When protein is fed, vitamin A is mobilized
from liver.
Vitamin A and mucoprotein synthesis: Vitamin A is
essential for the synthesis of mucoproteins and
glycoproteins.
9. Vitamin A and reproduction: In vitamin A deficiency,
reproduction does not take place through
infertility in the male
Failure of the female to conveive or resorption or
abortion of the foetus if conceived.
Effects of Vitamin A Deficiency
i. Night blindness
ii. Xerosis conjunctivae
iii. Xerosis cornea
iv. Biot’s Spots
v. Keratomalacia
vi. Follicular hyperkeratosis
10. Night blindness: In early stages of vitamin A deficiency, the
individual cannot see well in dim light.
Difficulty in reading or driving the car in dim light is
experienced. In advanced deficiency, the subject cannot see
objects in dim light.
Night blindness is fairly common in regions where the
vitamin A intake is inadequate.
Xerosis conjunctivae: The conjunctiva is dry, thickened,
wrinkled and pigmented.
This is due to the keratinisation of the epithelial cells. The
pigmentation gives the conjunctiva a smoky appearance.
This condition is extremely common among all age groups
in India and other developing countries where the vitamin
A intake is inadequate.
11. Xerosis cornea: When dryness spreads to cornea, it
takes on a dull, hazy, lusterless appearance.
This is due to the keratinisation of the epithelial tissue
covering the cornea.
Bitots spots: Grayish glistening, white plaques formed
of desquamated thickened conjunctiva epithelium,
usually triangular in shape and firmly adhering to the
conjunctiva are frequently found in children having
other signs of vitamin A deficiency.
Keratomalacia: When xerosis of the conjuctivae and
cornea is not treated, it may develop into the condition
known as ‘keratomalacia’.
.
12. The corneal epithelium becomes opaque and
ulceration and bacterial invasion of the cornea bring
about its destruction resulting in blindness.
Follicular hyperkeratosis (phrynoderma): In this
condition, there is hyperkeralinisation of epithelium
lining the hair follicle.
The skin becomes rough and dry and papillae of
varying sizes are observed. Earlier workers showed that
this condition respond to treatment with vitamin A.
More recent studies however, indicate that the above
condition can be cured by the administration of
essential fatty acids and pyridoxine.
15. Dietary sources
SOURCE VITAMIN A
CONTENT(Mu g/100g)
Rich sources Fish liver oil 6,660-1000,000
Liver (sheep) 6,600-10,000
Good sources Butter and ghee 600-800
Ghee (clarified butter
fat)
600-700
Egg (hen) whole egg 300-400
Egg yolk 600-800
Milk power, full cream 400-450
Fair Sources Milk (cow’s or buffala or
human)
50-60
Red palm oil (carotene) 25,000-30,000
GLV (carotene) 1,500-6,000
Carrots (carotene) 1,500-2,000
16. Requirements:
Age groups Vit.A (mug) Carotene(mug)
Infants(1-6months) 400
7-12months 300 1200
Children 1-3yrs 250 1000
4-6 years 300 1200
7-9 years 400 1600
10-12 years 600 2400
Adolescents(boys and girls) 750 3000
Men 750 3000
Women 750 3000
Pregnant women 750 3000
Lactation 1150 4600
17. Treatment and Prevention of Vitamin A Deficiency:
Mild to moderate cases of vitamin A deficiency can be
treated by the daily oral dose of 10,000 mug of fat
soluble vitamin A for a period of 10 days.
In severe cases, large oral doses of 50,000 mug of fat
soluble vitamin A will have to be administered daily for
one week.
Toxic Effects of Excess of Vitamin A
The children have been receiving 30,000 to 1,50,000 g
of water soluble vitamin A for several months.
The characteristics signs and symptoms observed
were anorexia, headache, a dry itching skin and
swelling over the long bones due to bony exostosis.
