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BIOCHEMISTRY OF VISION
AND
ROLE OF VITAMIN A
Hira Nath Dahal
VITAMINS
• Potent organic compounds needed in minute
amount for growth and good health.
• Not used for energy but for utilization of other nutrients like
carbohydrate, proteins and fats.
• Most vitamins act as co-enzymes.
• Most vitamins are not made in the body , they must be taken via food or
vitamin supplements.
CLASSIFICATION OF
VITAMINS
1. Fat soluble vitamins:
Vit A
Vit D : are made in skin
Vit E
Vit K : are synthesized by intestinal bacteria
2. Water soluble vitamins:
Vit B Inositol , choline ,para-amino benzoic acid
Vit C are other water soluble vitamins.
VITAMIN A
• Vitamin A is necessary for a variety of functions such
as vision, proper growth and differentiation,
reproduction and maintenance of epithelial cells.
• Active form is present only in animal tissue.
• Retinoids are the compounds
with vitamin A activity.
• Anti infection vitamin
SOURCES OF VITAMIN A
•Animal sources (Retinal esters and
retinol)
Fish liver oil (Cod and Helibnt)
Egg yolk,milk,liver, butter,cream,cheese)
• Liver is the best source of Vit A.
•Plant sources ( -caroteneβ pro→
vitamin)
Carrot, green leafy vegetables
(Spinach), papaya, mango, pumpkin,
brinjal .
• Plant foods contain Vit A in the form of precursors “ the carotenoid
pigment ( Carotenes).
• Carotenes are converted to Vit A(Retinol) by
metabolic activityin the wall of small intestine.
Types of carotenes
i. α-carotenes: yields 1-molecule of Vit A.
ii.β-carotenes: yields 2-molecule of Vit A.
iii. -carotenes: yields 1-molecule of Vit A.γ
VIT A ABSORPTION AND STORAGE
In intestine Vit A is esterified
Reaches blood stream through intestinal
lymphatics
Most retinol reaches liver (stored as well)
Retinol binds with RBP(Retinol Binding Protein)
TRANSPORT FROM LIVER
TO EYE
Retinol-protein complex enters circulation
Becomes attached to specific receptors
present in basal surface of RPE cells
RBP is left outside and only retinol enters RPE
SYNTHESIS OF VISUAL PIGMENTS
Retinol from RPE pass to outer segments of
photoreceptors
11-Cis
Retinol oxidized Retinene Retinal
opsin +
NADOxidativesystem
Rhodopsin(Rods) Photopsin
(forperipheralvision &vision (forhighlydiscriminatingor
LIGHT INDUCED CHANGES
IN VISUAL PIGMENTS
• Light when falls on eye are absorbed by rods and
cones in retina.
• Initiates photochemical changes which in turn
initiates electrical changes.
LIGHT INDUCED CHANGES AS
STUDIED IN RODS
CAN BE DESCRIBED UNDER 3-
HEADINGS
i. Rhodopsin bleaching
ii.Rhodopsin regeneration
iii.Visual cycle
I) RHODOPSIN BLEACHING &
II)REGENERATION
Rhodopsin
Bathorodhopsin
Lumirhodopsin
Metarhodopsin I
Metarhodopsin II
opsin
isomerase
isomerase
11-Cis-Retinal
11-Cis-Retinol
all-trans-Retinal
all-trans-Retinol
NAD NAD
NADHNADH
Light energy
III) VISUAL CYCLE
Rhodopsin Light energy
all-trans-Retinal11-Cis-Retinal
Retinal isomerase
opsin
Excitation of nerve
Rate of photochemical bleaching Rate of rhodopsin regeneration
Under constant
Light condition
US FOOD & DRUG ADMINISTRATION
RECOMMENDED DAILY
ALLOWANCE(RDA) OF VIT A
Groups RDA (IU)
Infants 1500
Children (< 4yrs) 2500
Children (> 4 yrs) 5000
Lactating or Pregnant
women
8000
IU= International Unit
1 IU= 0.3 μg of retinol
ROLE OF VITAMIN A IN EYE
•Vision in dim light
•It is the main cause for
preventable blindness.
BIOCHEMICAL FUNCTION
1. Vision in dim light
2. Necessary for the maintenance of normal epithelium
3. Necessary for reproduction
4. Acts as an anti-oxidant
5. - carotene prevents heart attackβ .
CAUSES OF VITA DEFICIENCY
a) Inadequate dietary intake.
a) Poor absorbtion due to:
- abnormal fat metabolism (biliary
obstruction or pancreatic disease)
- Chronic diarrhoea
- habitual intake of liquid paraffin
c) Inadequate conversion of -carotene toβ
retinol as in liver or intestinal disease.
d) Exhaustion of Vit A store in liver due to
increased demand/intake ratio eg. In pregnancy or in low birth
weight infants or after measles,diarrhoea.
e) Deficiency of zinc and proteins( in PEM ).
OCULAR
MANIFESTATION(XEROPHTHALMIA)
a) Nigt blindness is first symptom due to
impairment in dark adaption.
b) Conjunctival changes:
- Conjunctival xerosis is first clinical sign.
- Bitot’s spot on bulbar conjunctiva.
c) Corneal changes
- Corneal xerosis
- ulceration
- keratomalacia may lead to blindness.
NON- OCULAR MANIFESTATIONS
a) Hyperkeratinization of epithelium and
follicular hyperkeratosis.
b) Increase in infection of gastrointestinal and
respiratory tract.
c) Cessation of bone growth and changes in
teeth.
d) Anorexia
e) Injury to nerves and brain.
f) Calcium deposition in urogenital tract & bladder disorders.
g) Atrophy of germinal epithelium of testes.
VIT A PROPHYLAXIS SCHEDULE IN
TREATMENT OF XEROPTHALMIA
Individuals oral dose Timing
Children < 12 months
age
1 lakh IU Once every 4-6
months
Children >12 months of
age
2 lakh IU “
New born 0.5 lakh IU At birth
Women of child
bearing age
3 lakh IU Within 1 months of
giving birth
Pregnant and lactating
women
5 thousand IU
Or 20 thousand IU
Every day
once every week
MANAGEMENT OF VITAMIN A DEFICIENCY
IN COMMUNITY/PREVENTION OF
XEROPHTHALMIA IN COMMUNITY
a) Identification of severity by history,ocular and systemic
examination.
b) Short term interventions(treatment)
- Breast feeding & proper supplementary
food.
- Vit A supplementation
c) Long term sustainable solutions:(prevention)
- advocacy for change in dietary behavour, breast-feeding & weaning
through nutrition education.
- support home gardening to increase production of vitamin rich
foods and vegetables.
- improved methods for production, preparation & preservation of Vit
A rich foods.
- Fortification of skimmed milk and margarine with Vit A.
- Control of malnutrition, ARI , measles & diarrhoea.
- Vit A supplementation.
HYPERVITAMINOS A
• If exceeds daily intake > 10,000 IU
• Results:
abdominal pain , blurred vision , drowsiness,
headache , irritability , nausea and vomiting.

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Vitamins a

  • 1. BIOCHEMISTRY OF VISION AND ROLE OF VITAMIN A Hira Nath Dahal
  • 2. VITAMINS • Potent organic compounds needed in minute amount for growth and good health. • Not used for energy but for utilization of other nutrients like carbohydrate, proteins and fats. • Most vitamins act as co-enzymes. • Most vitamins are not made in the body , they must be taken via food or vitamin supplements.
  • 3. CLASSIFICATION OF VITAMINS 1. Fat soluble vitamins: Vit A Vit D : are made in skin Vit E Vit K : are synthesized by intestinal bacteria 2. Water soluble vitamins: Vit B Inositol , choline ,para-amino benzoic acid Vit C are other water soluble vitamins.
  • 4. VITAMIN A • Vitamin A is necessary for a variety of functions such as vision, proper growth and differentiation, reproduction and maintenance of epithelial cells. • Active form is present only in animal tissue. • Retinoids are the compounds with vitamin A activity. • Anti infection vitamin
  • 5. SOURCES OF VITAMIN A •Animal sources (Retinal esters and retinol) Fish liver oil (Cod and Helibnt) Egg yolk,milk,liver, butter,cream,cheese) • Liver is the best source of Vit A.
  • 6. •Plant sources ( -caroteneβ pro→ vitamin) Carrot, green leafy vegetables (Spinach), papaya, mango, pumpkin, brinjal .
  • 7. • Plant foods contain Vit A in the form of precursors “ the carotenoid pigment ( Carotenes). • Carotenes are converted to Vit A(Retinol) by metabolic activityin the wall of small intestine. Types of carotenes i. α-carotenes: yields 1-molecule of Vit A. ii.β-carotenes: yields 2-molecule of Vit A. iii. -carotenes: yields 1-molecule of Vit A.γ
  • 8. VIT A ABSORPTION AND STORAGE In intestine Vit A is esterified Reaches blood stream through intestinal lymphatics Most retinol reaches liver (stored as well) Retinol binds with RBP(Retinol Binding Protein)
  • 9. TRANSPORT FROM LIVER TO EYE Retinol-protein complex enters circulation Becomes attached to specific receptors present in basal surface of RPE cells RBP is left outside and only retinol enters RPE
  • 10. SYNTHESIS OF VISUAL PIGMENTS Retinol from RPE pass to outer segments of photoreceptors 11-Cis Retinol oxidized Retinene Retinal opsin + NADOxidativesystem Rhodopsin(Rods) Photopsin (forperipheralvision &vision (forhighlydiscriminatingor
  • 11. LIGHT INDUCED CHANGES IN VISUAL PIGMENTS • Light when falls on eye are absorbed by rods and cones in retina. • Initiates photochemical changes which in turn initiates electrical changes.
  • 12. LIGHT INDUCED CHANGES AS STUDIED IN RODS CAN BE DESCRIBED UNDER 3- HEADINGS i. Rhodopsin bleaching ii.Rhodopsin regeneration iii.Visual cycle
  • 13. I) RHODOPSIN BLEACHING & II)REGENERATION Rhodopsin Bathorodhopsin Lumirhodopsin Metarhodopsin I Metarhodopsin II opsin isomerase isomerase 11-Cis-Retinal 11-Cis-Retinol all-trans-Retinal all-trans-Retinol NAD NAD NADHNADH Light energy
  • 14. III) VISUAL CYCLE Rhodopsin Light energy all-trans-Retinal11-Cis-Retinal Retinal isomerase opsin Excitation of nerve Rate of photochemical bleaching Rate of rhodopsin regeneration Under constant Light condition
  • 15.
  • 16. US FOOD & DRUG ADMINISTRATION RECOMMENDED DAILY ALLOWANCE(RDA) OF VIT A Groups RDA (IU) Infants 1500 Children (< 4yrs) 2500 Children (> 4 yrs) 5000 Lactating or Pregnant women 8000 IU= International Unit 1 IU= 0.3 μg of retinol
  • 17. ROLE OF VITAMIN A IN EYE •Vision in dim light •It is the main cause for preventable blindness.
  • 18. BIOCHEMICAL FUNCTION 1. Vision in dim light 2. Necessary for the maintenance of normal epithelium 3. Necessary for reproduction 4. Acts as an anti-oxidant 5. - carotene prevents heart attackβ .
  • 19. CAUSES OF VITA DEFICIENCY a) Inadequate dietary intake. a) Poor absorbtion due to: - abnormal fat metabolism (biliary obstruction or pancreatic disease) - Chronic diarrhoea - habitual intake of liquid paraffin
  • 20. c) Inadequate conversion of -carotene toβ retinol as in liver or intestinal disease. d) Exhaustion of Vit A store in liver due to increased demand/intake ratio eg. In pregnancy or in low birth weight infants or after measles,diarrhoea. e) Deficiency of zinc and proteins( in PEM ).
  • 21. OCULAR MANIFESTATION(XEROPHTHALMIA) a) Nigt blindness is first symptom due to impairment in dark adaption. b) Conjunctival changes: - Conjunctival xerosis is first clinical sign. - Bitot’s spot on bulbar conjunctiva. c) Corneal changes - Corneal xerosis - ulceration - keratomalacia may lead to blindness.
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  • 24. NON- OCULAR MANIFESTATIONS a) Hyperkeratinization of epithelium and follicular hyperkeratosis. b) Increase in infection of gastrointestinal and respiratory tract. c) Cessation of bone growth and changes in teeth.
  • 25. d) Anorexia e) Injury to nerves and brain. f) Calcium deposition in urogenital tract & bladder disorders. g) Atrophy of germinal epithelium of testes.
  • 26. VIT A PROPHYLAXIS SCHEDULE IN TREATMENT OF XEROPTHALMIA Individuals oral dose Timing Children < 12 months age 1 lakh IU Once every 4-6 months Children >12 months of age 2 lakh IU “ New born 0.5 lakh IU At birth Women of child bearing age 3 lakh IU Within 1 months of giving birth Pregnant and lactating women 5 thousand IU Or 20 thousand IU Every day once every week
  • 27. MANAGEMENT OF VITAMIN A DEFICIENCY IN COMMUNITY/PREVENTION OF XEROPHTHALMIA IN COMMUNITY a) Identification of severity by history,ocular and systemic examination. b) Short term interventions(treatment) - Breast feeding & proper supplementary food. - Vit A supplementation
  • 28. c) Long term sustainable solutions:(prevention) - advocacy for change in dietary behavour, breast-feeding & weaning through nutrition education. - support home gardening to increase production of vitamin rich foods and vegetables. - improved methods for production, preparation & preservation of Vit A rich foods.
  • 29. - Fortification of skimmed milk and margarine with Vit A. - Control of malnutrition, ARI , measles & diarrhoea. - Vit A supplementation.
  • 30. HYPERVITAMINOS A • If exceeds daily intake > 10,000 IU • Results: abdominal pain , blurred vision , drowsiness, headache , irritability , nausea and vomiting.