Vitamin a

1. PRESENTER- Dr. UTKARSH BARANWAL
MODERATOR- DR. NEETU GAUTAM
VITAMIN A

2. WHAT ARE VITAMINS ?
Essential organic compounds that are required in small amounts for
normal growth, maintenance of good health and for the proper utilization
of other nutrients.
Nutrients that our body does not make on its own. Thus we must obtain
them from the foods we eat, or via vitamin supplements.

3. VITAMINS
Fat Soluble
Vitamin A
Vitamin D
Vitamin E
Vitamin K
Water Soluble
B-Complex
Energy
releasing
Thiamine
Riboflavin
Niacin
Pyridoxine
Biotin
Pantothenic
acid
Hematopoietic
Folic acid
Vitamin B12
Non B-
Complex Vitamin C
Classification of
Vitamins

4. Fat soluble vitamins
DIFFERENCE BETWEEN FAT SOLUBLE AND WATER SOLUBLE
VITAMINS
 Soluble in fat
 Absorbed along with other lipids
 Requires carrier proteins
 Stored in liver
 Deficiency manifests only when stores
are depleted
 Toxicity - Hypervitaminosis may result
 Single large dose may prevent deficiency
 E.g. A,D,E & K
 Soluble in water
 Absorption is simple
 No requirement of carrier protein
 Excreted in urine
 Deficiency manifests rapidly as there is no
storage
 Unlikely , since excess is excreted
 Regular dietary supply is required
 E.g. B complex & C
Water soluble vitamins

5. Hydrophobic
Isoprene derivatives
They cannot be synthesized by the body
Supplied by the diet
Absorption along with fat
Transport: By lipoprotein & Specific binding protein
Surplus amount stored – liver & adipose tissue
Excess consumption leads to accumulation & toxic effects.
Lipid soluble vitamins - common features

6. VITAMIN A

7. Introduction
• Vitamin A is an essential nutrient needed in small
amounts for the normal functioning of the visual
system, and maintenance of cell function for growth,
epithelial integrity, red blood cell production,
immunity and reproduction.
• Vitamin A deficiency (VAD) is a major nutritional
concern in poor societies, especially in lower income
countries like INDIA.

8. WHERE DOES IT COME FROM?
Animal Sources
 Eggs
 Meat
 Cheese
 Milk
 Liver
 Kidney
 Fish liver oils
Plant Sources
 Carrots
 Sweet Potatoes
 Apricots
 Broccoli
 Spinach
 Pumpkin
 Papaya
 Mango

9. VITAMIN A
(PREFORMED AND PROVITAMIN)
• Retinoids: Natural & synthetic forms of Vitamin A
• Preformed: Three preformed compounds that are metabolically
active and found in animal products
– Retinol – alcohol form
– Present in animal tissues as retinyl ester with long chain
fatty acid
– Retinal or retinaldehyde – aldehyde form
– Obtained by oxidation of retinol
– Retinal & Retinol are interconvertible
– Retinoic acid – acid form
– Produced by oxidation of Retinal

10. • Provitamin: Carotenoids (β-carotene) can yield 2
retinols when metabolized in the body
• β -carotene
found in plants
Has 2 β-ionone rings connected by a polyprenoid chain

13. RECOMMENDED DAILY ALLOWANCE:
 The recommended daily allowance of vitamin A is as follows:
(i) Infants 300-400 μg;
(ii) children 400-600 μg;
(iii) adolescents 750 μg;
(iv) pregnant women 800 μg.
 1 μg retinol equivalent (RE) = 3.3 international units (IU) of vitamin A. Hence,
30 mg retinol = 100,000 IU vitamin A.

14. RDA:
Normal plasma levels of retinol are 20-50 μg/dL in infants and increase gradually as
children become older.
Median serum retinol values :
• 1.19 μmol/L in both boys and girls ages 4-8 yr
• 1.4 and 1.33 μmol/L in boys and girls, respectively, ages 9-13
• 1.71 and 1.57 μmol/L in boys and girls, ages 14-18 (for conversion, 1 μmol/L = 28.6
μg/dL).
• 1.96 and 1.85 μmol/L are found in 19-30 yr old adult men and women.

15. ABSORPTION
 Retinoids
 Retinyl esters broken down to free retinol & FA in small
intestine - requires bile, digestive enzymes, integration into
micelles
 Once absorbed, retinyl esters reformed in intestinal cells
 90% of retinoids can be absorbed
 Carotenoids
 Absorbed intact, absorption rate much lower
 Intestinal cells can convert carotenoids to retinoids

16. Approximately 80% is absorbed.
It is passed along with fat through the lymphatic
system into blood stream.
Absorption is poor in case of diarrhea, jaundice and
abdominal disorder.
Absorption increases if taken with fat.
 Vitamin A which is not absorbed is excreted within 1
or 2 days in feces .

17. TRANSPORT
Transported via chylomicrons from intestinal cells to
the liver
Transported from the liver to target tissue as retinol
via retinol-binding protein (RBP; MW. 21,000).

18. Summary of Vitamin A
absorption

19. Summary of the functions of Vitamin A
compounds

20. STORAGE
The liver has enormous capacity to store in the
form of retinol palmitate.
Under normal conditions a well-fed person has
sufficient Vitamin A reserves to meet his need for
6 to 9months or more.

21. EXCRETION OF VITAMIN A
Not readily excreted
Kidney disease and aging increase risk of toxicity
because excretion is impaired

22. FUNCTIONS OF VITAMIN A
 Vision: Vitamin A is a component of the visual pigment
rhodopsin. Retinal is bound to the protein opsin.
 Growth: Vitamin A deficiency causes loss of appetite. Slow bone
growth. Affects CNS.
 Reproduction: Essential for spermatogenesis, oogenesis,
placental development, fetal & embryonic growth.
 Maintenance of epithelial cells: Essential for normal
differentiation of epithelial tissues and mucus secretion

23. ROLE OF VITAMIN A IN VISION
Visual Cycle (Wald’s Visual Cycle)
A process by which light impacting on the retina of
the eye is converted to an electrical signal
The optic nerve carries the electrical signal to the
brain (nerve impulse)
The brain processes the signal into an image

24. ROLE OF VITAMIN A IN VISION
 Retina is a light-sensitive layer of cells at the back of
the eye where an image is formed
 Retina consists of: Rod and cone cells (photosensitive
cells)
 Rod cells process black & white image
 Cone cells process color image

25. Rod Cell
Cone Cell

26. ROLE OF VITAMIN A IN VISION
 Normal vision depends on the retina and on
adequate vitamin A
 In the retina, vitamin A in the form of retinal binds to
a protein called opsin to make rhodopsin [11-cis –
retinal- opsin] in rod cells
 Rhodopsin is a light-sensitive pigments

27. ROLE OF VITAMIN A IN VISION
 The human retina contains 2 distinct photoreceptor systems: the rods, in
which rhodopsin senses light of low-intensity, and the cones, in which
iodopsins detect different colors; 11-cis-retinal is the prosthetic group on
both these visual proteins.
 The mechanism of vitamin A action is similar for rods and cones, based on
photoisomerization of 11-cis to all-trans retinal (change shape when
exposed to light), which initiates signal transduction via the optic nerve to
the brain, resulting in visual sensation.
 After isomerization (also known as photobleaching), a series of reactions
serves to regenerate the 11-cis retinal for resynthesis of rhodopsin and
iodopsin.

29. Wald’s Visual
Cycle

30. THE VISUAL
CYCLE

31. ROLE OF VITAMIN A IN VISION
When stimulated by light, vitamin A isomerizes from
its bent ‘cis’ form to a straighter ‘trans’ form and
detaches from opsin
The opsin molecule changes shape, which sends a
signal to the brain via optic nerve and an image is
formed
Most retinal released in this process is quickly
converted to trans-retinol and then to cis-retinal, to
begin another cycle

32. ROLE OF VITAMIN A IN VISION
Dark Adaptation time
Bright light depletes rhodopsin (photobleaching)
Sudden shift from bright light to darkness causes
difficulty in seeing
Rhodopsin is synthesized in a few minutes and
vision is improved in the dark

33. ROLE OF VITAMIN A IN VISION
The time required to synthesize rhodopsin in the
dark is called dark adaptation time
It is increased in vitamin A deficiency

34. FUNCTIONS OF VITAMIN A:
GROWTH AND DIFFERENTIATION OF CELLS
• Retinoic acid is necessary for cellular differentiation
• Important for embryo development, gene expression
• Retinoic acid influences production, structure, and function
of epithelial cells that line the outside (skin) and external
passages (mucus forming cells) within the body.

35. EPITHELIAL CELL ‘INTEGRITY’
Many epithelial cell require Vitamin A for proper
differentiation and maintenance
Lack of Vitamin A leads to dysfunction of epithelia
 The skin becomes keratinized and scaly, and mucus secretion is suppressed

37. FUNCTIONS OF VITAMIN A: IMMUNITY
Deficiency leads to decreased resistance to infections
Supplementation may decrease severity of infections in
deficient person

38. Role in Prevention of cardiovascular disease
 Antioxidant capabilities
Role in Cancer prevention
 Antioxidant capabilities
 Lung, oral, and prostate cancers
 Studies indicate that vitamin A-containing foods are
more protective than supplements

39. VITAMIN A DEFICIENCY AND DISEASES
 Nyctalopia (night blindness)
 Xerophthalmia
 Bitot’s spots
 Keratomalacia
 Complete blindness (in severe deficiency)

40. WHO CLASSIFICATION OF XEROPTHALMIA AS
FOLLOWING:
a) X1A – conjunctiva Xerosis (ocular epithelium becomes dry.)
b) X1B- Bitots spots (foam like hyper keratinized silvery lesions)
c) X2- corneal xerosis
d) X3A – corneal ulceration
e) X3B – Keratomalacia (hyper keratinization of cornea with corneal
opacity, which can progress to ulceration and infection)
f) XN- night blindness
g) XS – corneal scarring
h) XF- fundoscopic changes

41. NIGHT BLINDNESS
 Visual acuity is diminished in dim
light
 Occurs as a result of inadequate
pigment in the retina.
 The dark adaptation time is
increased
 Found in pregnant women in some
instances, especially during the last
trimester of pregnancy when the
vitamin A needs are increased.

42.  It is the most specific VAD, and
is the leading preventable
cause of blindness
 Conjunctiva becomes dry,
thick and wrinkled
 Conjunctiva gets keratinized
and loses its normal
transparency
 Cornea becomes glazy &
lusterless
XEROPHTHALMIA

43. BITOT’S SPOT
Tissue spots that develop around the
eye ball, causing severe dryness in
the eyes.
Seen as grayish-white triangular
plaques firmly adherent to the
conjunctiva.

44. KERATOMALACIA
 One of the major cause for
blindness in India.
 Cornea becomes soft and may
burst
 Prolonged xerophthalmia leads
to keratomalacia (softening of
the cornea)
 If the eye collapses vision is lost.

45.  Follicular hyperkeratosis
 Anorexia
 Growth retardation
 Increased respiratory & intestinal infection
 Defective tooth enamel
 Reproductive failure.
OTHER SYMPTOMS OF VAD

46. TREATMENT:
 More often, higher doses of 30-60 mg of retinol (100,000-200,000
IU/child) are given once or twice, under careful monitoring to avoid
toxicity associated with excess vitamin A.
 Xerophthalmia is treated by giving 1,500 μg/kg body weight orally
for 5 days, followed by intramuscular injection of 7,500 μg of vitamin
A in oil, until recovery.
 < 6 months: 50,000 IU
 6 months – 12 months: 1,00,000 IU
 >12 months: 2,00,000 IU

48. PREVENTION:
 Vitamin A deficiency is a public health problem in India.
 The Ministry of Health and Family Welfare initiated the 'National
Prophylaxis Program against Nutritional Blindness' in 1970.
 According to this scheme, children between 9 months and 3 years
were given oral doses of vitamin A every six months. It was later
expanded to cover children of ages 6-59 months.
 Under this program, a dose of vitamin A 100,000 IU is given with
measles vaccine at 9 months and 2,00,000 IU with DPT booster at 15-
18 months and then 6monthly till 5 years of age.
 Children with measles or severe malnutrition should receive vitamin
A at 100000 IU if < 1 year old and 200000 IU if older. As it decreases
mortality.

49. ASSESSMENT OF DEFICIENCY
Dark adaptation test
Serum RBP
Serum vitamin A
25 – 50 µg/dl

50. 1) Eating of polar bear liver
2) Excess supplementation of
Vitamin A
When?
TOXICITY
One ounce of polar bear liver contains
enough vitamin A (retinol) to kill a
person!

51. TOXICITY
Hepatomegaly
Increased cerebrospinal fluid pressure
Disturbance in calcium homeostasis – skletal decalcificaion
– tendrness of long bones
Skin - Excessive dryness, desquamation

52. HYPERVITAMINOSIS A:
 Chronic daily intakes of 15,000 μg (adults) and 6,000 μg (children) can
be toxic. Because there is no antidote for hypervitaminosis A, and
vitamin A is readily stored in liver and other tissues.
 Extreme hypervitaminosis A is fatal.
 Signs of subacute or chronic toxicity can include:
 headache, vomiting (early signs), anorexia, dry itchy desquamating
skin, and seborrheic cutaneous lesions.
 With chronic hypervitaminosis A,
 fissuring at the corners of the mouth, alopecia and coarsening of the
hair, bone abnormalities and swelling, enlargement of the liver and
spleen, diplopia, increased intracranial pressure, irritability, dryness
of the mucous membranes, and desquamation of the palms and the
soles of the feet.

53.  Less common symptoms include diplopia, papilledema,
cranial nerve palsies, and other symptoms suggesting
pseudotumor cerebri.
 Teratogenicity has been associated with therapeutic doses
(0.5-1.5 mg/ kg) of oral 13-cis-retinoic acid, generally taken
for the treatment of acne or cancer, during the 1st trimester
of pregnancy.
 A high incidence (>20%) of spontaneous abortions and
birth defects, including characteristic craniofacial
abnormalities.
 Carotenoids can cause yellowing of the skin
(carotenodermia).

54. .