VITAMIN A ESSAY

Vitamins may be regarded as organic compounds required in diet in small amounts to perform specific biological
functions for normal maintenance of optimum growth and health of organism

Chemistry

 it is a fat soluble vitamin

 it is present only in foods of animal origin
 provitamins and beta carotenes are found in plants
 the term retinoids is oftern used to include the natural and synthetic forms of vitamin a
 retinol, retinal and retinoic acid are refgarded as vitamers of vitamin a
 retinol=============retinal-------retinoic acid ENZYME REDUCTASE AND NAD TO NADH+H+
VITAMERS OF VITAMIN A
1.RETINOL (VITAMIN A ALCOHOL)
 it si a primary alcohol containing beta ionone ring
 the side chain has two isoprenoid units,4 double bonds and one hydroxyl group
 it s present in animal tissues as retinyl ester with long chain fatty acids

2.RETINAL (VITAMIN A ALDEHYDE)

 This is an aldehyde form obtained by oxidation of retinol

 Retinal and retinol are interconvertible
 Previously the name retinine was used

3. retinoic acid(provitamin a )

 It is produced by oxidation of retinal

 It cannot be converted back to retinal or retinol

4. beta carotene (provitamin a )

 Found in plant foods

 Cleaved in intestine to produce two moles of retinol
 In humans this conversion is inefficient hence beta carotene posses about 1/6 vitamin a activity compared to
that of retinol
ABSORTION TRANSPORT AND MOBILISATION
 Intestine is major site for absorption
 Zinc plays an important role in retinol mobilization
 90% of vitamin a stored in liver as retinyl palmitate
 Transport from liver to target cell as retinol via rbp which is bound to transthyretin
 Incase of vitamin deficiency rbp
 Target cells contain cellular rbp
BIOCEHMICAL FUNCTION

 NECESSARY FOR VARIOUS FUNCTON

 Vision proper growth and differentiation
 Reproduction and maintenance of epithelial cells

Vitamin a and vision

The biochemical function of vitamin a in process of vision is elucidated by George wald the events occur in cyclic
processs known as rhodopsin or wald s visual cycle
Rods and cones

Retina of eye posses 2 tyoes of cells –rods and cones

Human eyes has 10 million rods and 5 million cones

Rods arein periphery while cones are at the centre of retina

Rods are involved in dim light vision

Cones are involved in bright light vision

Cones are responsible for vision in bright light as well as color vision. They contain the photosensitive protein, conopsin
There are 3 types of cones, blue (cyanopsin), green (iodopsin) or red (porphyropsin).

Dark adapatation mechanism

when a person shifts suddenly from bright light to a dimly lit area, there is difficulty in seeing,for example, entering a cinema
theater. After a few minutes, rhodopsin is resynthesized and vision is improved. This period is called dark adaptation time the
dark adaptation time time incrreass for people with deficinecy
Visual cascade and c gmp

When light strikes the retina, a number of biochemical changesleading to membrane hyperpolarization occur
resulting in the genesis of nerve impulse. The hyperpolarization of the membrane is broughtabout by a visual cascade involving cyclic GMP.

Bleaching of rhodopsin:
when exposed to light the color of rhodopsin chsnges from red to yellow
Other biochemical functions of vit a
The gene regulation
Immunological system
Reproductive system
Anti oxidant property
Effect on skin
Daily Requirement of Vitamin A
The recommended daily allowance (RDA) for
i. Children = 400–600 µg/day
ii. Men = 750–1000 µg/day
iii. Women = 750 µg/day
iv. Pregnancy = 1000 µg/day
One international unit = 0.3 mg of retinol.
One retinol equivalent = 1 microgram of retinol

Dietary Sources of Vitamin A

Animal sources include milk, butter, cream, cheese, egg
yolk and liver
Carrot contains
significant quantity of beta carotene
Fish liver oils (cod liver oil and shark liver
oil) are very rich sources of the vitamin

deficiency manifestations of vit a

Deficiency manifestations of the eyes : Night
blindness (nyctalopia) The
individuals have difficulty to see in dim light
since the dark adaptation time is increased.
Xeropthalmia
The conjunctiva becomes dry, thick and wrinkled.
The conjunctiva gets keratinized and loses its normal
transparency. Dryness spreads to cornea. It becomes glazy
and lusterless due to keratinization of corneal epithelium
Bitot's Spots
These are seen as grayish-white triangular plaques firmly
adherent to the conjunctiva. This is due to increased
thickness of conjunctiva in certain areas
Keratomalacia
If xerophthalmia persisits for a long time,
corneal ulceration and degeneration occur. This
results in the destruction of cornea, a condition
referred to as keratomalacia, causing total
blindness.

Biochemical functions and deficiency manifestation of vitamin e

Vitamin E (tocopherol) is a naturally occurring

antioxidant. It is essential for normal reproduction
in many animals, hence known as anti-sterility
vitamin. Vitamin E is described as a ‘vitamin in
search of a disease.’ This is due to the lack of any
specific vitamin E deficiency disease in humans

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 polyunsaturated
fatty acids in various tissues and
membranes. It protects RBC from hemolysis by
oxidizing agents (e.g. H2O2).
3. It is closely associated with reproductive
functions and prevents sterility. Vitamin E
preserves and maintains germinal epithelium of
gonads for proper reproductive function.
4. It increases the synthesis of heme by
enhancing the activity of enzymes 􀁇-
aminolevulinic acid (ALA) synthase and ALA
dehydratase.
5. It is required for cellular respiration–
through electron transport chain (believed to
stabilize coenzyme Q).
6. Vitamin E prevents the oxidation of
vitamin A and carotenes.
7. It is required for proper storage of creatine
in skeletal muscle.
8. Vitamin E is needed for optimal absorption
of amino acids from the intestine.
9. It is involved in proper synthesis of nucleic
acids.
10. Vitamin E protects liver from being
damaged by toxic compounds such as carbon
tetrachloride.
11. It works in association with vitamins

Vitamin E and selenium

The element selenium is found in the enzyme
glutathione peroxidase that destroys free
radicals. Thus, Se is also involved in antioxidant
functions like vitamin E, and both of them act
synergistically. To a certain extent, Se can spare
the requirement vitamin E, and vice versa.

No major disease states have been found to be associated with

vitamin E deficiency due to adequate levels in the average diet.
Vitamin E deficiency is seen in persons (a) who cannot absorb dietary
fat, (b) in premature infants (birthweight less than 1500 grams), (c) in
abetalipoproteinemia and (d) in mutations in the gene for the tocopherol
transfer protein. Vitamin E deficiency causes neurological problems due
to poor nerve conduction. These include neuromuscular problems such as
spinocerebellar ataxia, retinopathy, peripheral neuropathy and myopathies

Biochemical functions and deficiency manifestation of vitamin k

Vitamin K is the only fat soluble vitamin with

a specific coenzyme function. It is required for the production of blood clotting
factors, essential for coagulation (in
German–Koagulation; hence the
name K for this vitamin).

The functions of vitamin K are concerned with

blood clotting process. It brings about the posttranslational
(after protein biosynthesis in the
cell) modification of certain blood clotting
factors. The clotting factors II (prothrombin), VII,
IX and X are synthesized as inactive precursors
(zymogens) in the liver. Vitamin K acts as a
coenzyme for the carboxylation of glutamic acid
residues present in the proteins and this reaction
is catalysed by a carboxylase (microsomal). It
involves the conversion of glutamate (Glu) to
􀁊-carboxyglutamate (Gla) and requires vitamin K,
O2 and CO2 (Fig.7.12). The formation of
􀁊-carboxyglutamate is inhibited by dicumarol,
an anticoagulant found in spoilt sweet clover.
Warfarin is a synthetic analogue that can inhibit
vitamin K action (Fig.7.13).
Vitamin K is also required for the
carboxylation of glutamic acid residues of
osteocalcin, a calcium binding protein present
in the bone.
The mechanism of carboxylation is not fully
understood. It is known that a 2,3-epoxide
derivative of vitamin K is formed as an
intermediate during the course of the reaction.
Dicumarol inhibits the enzyme (reductase) that
converts epoxide to active vitamin K.
Role of Gla in clotting : The 􀁊-carboxyglutamic
acid (Gla) residues of clotting factors
are negatively charged (COO–) and they
combine with positively charged calcium ions
(Ca2+) to form a complex. The mechanism of
action has been studied for prothrombin. The
prothrombin Ca complex binds to the
phospholipids on the membrane surface of the
platelets (Fig.7.14). This leads to the increased
conversion of prothrombin to thrombin.

The deficiency of vitamin K is uncommon,

since it is present in the diet in sufficient quantity
and/or is adequately synthesized by the intestinal
bacteria. However, vitamin K deficiency may
occur due to its faulty absorption (lack of bile
salts), loss of vitamin into feces (diarrheal
diseases) and administration of antibiotics (killing
of intestinal flora).
Deficiency of vitamin K leads to the lack of
active prothrombin in the circulation. The result
is that blood coagulation is adversely affected.
The individual bleeds profusely even for minor
injuries. The blood clotting time is increased.
Hypervitaminosis K
Administration of large doses of vitamin K
produces hemolytic anaemia and jaundice,
particularly in infants. The toxic effect is due to
increased breakdown of RBC.
Antagonists of vitamin K
The compounds—namely heparin, bishydroxycoumarin—
act as anticoagulants and are
antagonists to vitamin K. The salicylates and
dicumarol are also antagonists to vitamin K.