vitamins a
TRANSCRIPT
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BIOCHEMISTRY OF VISION AND
ROLE OF VITAMIN A
Hira Nath Dahal
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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.
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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.
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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
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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.
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•Plant sources ( -carotene β pro →vitamin)
Carrot, green leafy vegetables
(Spinach), papaya, mango, pumpkin, brinjal .
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• 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
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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)
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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
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SYNTHESIS OF VISUAL PIGMENTS Retinol from RPE pass to outer segments of
photoreceptors 11-Cis
Retinol oxidized Retinene Retinal
opsin + NAD Oxidative system
Rhodopsin (Rods) Photopsin
(for peripheral vision & vision
(for highly discriminating or
of low illumination)
central vision)
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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.
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LIGHT INDUCED CHANGES AS STUDIED IN RODS
CAN BE DESCRIBED UNDER 3-HEADINGS
i. Rhodopsin bleaching
ii.Rhodopsin regeneration
iii.Visual cycle
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I) RHODOPSIN BLEACHING & II)REGENERATION
RhodopsinBathorodhopsin
Lumirhodopsin
Metarhodopsin I
Metarhodopsin II
opsin
isomerase
isomerase
11-Cis-Retinal
11-Cis-Retinol
all-trans-Retinal
all-trans-RetinolNAD NAD
NADHNADH
Light energy
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III) VISUAL CYCLE
Rhodopsin Light energy
all-trans-Retinal11-Cis-Retinal
Retinal isomerase
opsinExcitation of nerve
Rate of photochemical bleaching Rate of rhodopsin regenerationUnder constant
Light condition
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US FOOD & DRUG ADMINISTRATIONRECOMMENDED 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 Unit1 IU= 0.3 μg of retinol
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ROLE OF VITAMIN A IN EYE
•Vision in dim light
• It is the main cause for preventable blindness.
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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 .
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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
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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 ).
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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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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.
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d) Anorexia
e) Injury to nerves and brain.
f) Calcium deposition in urogenital tract & bladder disorders.
g) Atrophy of germinal epithelium of testes.
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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 IUOr 20 thousand IU
Every day once every week
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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
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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.
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- Fortification of skimmed milk and margarine with Vit A.
- Control of malnutrition, ARI , measles & diarrhoea.
- Vit A supplementation.
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HYPERVITAMINOS A
• If exceeds daily intake > 10,000 IU
• Results:
abdominal pain , blurred vision , drowsiness,
headache , irritability , nausea and vomiting.