vit A for bachelor level

1. Vitamin ‘A’

2. Vit A activity : is shown by retinoids and
carotenoids
Retinoids: preformed vit A found only in foods of animal origin.
They are three types:
1. Retinol: alcohol with beta ionone ring. Side chain and one OH grp. +nt
in animal tissue as retinyl ester with long chain FA.
2. Retinal: oxidation of retinol retinal ( aldehyde)
3. Retinoic acid: oxidation of retinal retinoic acid ( acidic)

3. Carotenoids : Provitamin A; found in plants.
• β-carotene and related compounds
• β-carotene (provitamin A): found in plants cleaved in intestinal
mucosa by carotene dioxygenase  retinal.
• Theoretically, produces 2 moles of retinal.
• But in practical; is inefficient in humans, β-carotene has 1/6th vitamin A
activity compared to that of retinol. (6 μg of β-carotene is equivalent to 1
μg of preformed retinol)

4. Recommended dietary allowance
• Retinol equivalents (RE) rather than International units(IU)
• 1 RE= 1 μg retinol
• Woman= 800 RE
• Man= 1000 RE
• One IU equals = 0.3 mg of retinol
• The requirement increases in growing children, pregnant
women and lactating mothers

5. Dietary sources
• Animal source contain preformed vit A
• The best sources are liver, kidney, egg yolk, milk,
cheese, butter. 🧀🍼🧀
• Fish liver oils are very rich in vitamin A. 🐟🐠
• Vegetable sources contain the provitamin A-carotene
• Yellow and dark green vegetables: tomato,carrots,
spinach, pumpkins, 🧀🍅🧀
• fruits are good sources: mango, papaya etc. 🧀

6. 👉🏻👉🏻Absorption
and
transport
of
vitamin A👍👍

7. 1. Dietary retinyl esters hydrolysed by pancreatic and intestinal
hydrolases retinol and FFA.
2. Whereas beta carotene retinal reduced to retinol
3. In intestinal mucosal cell both retinol get esterified again retinyl
esters.
4. Carried by chylomicrons  transferred to lymph
5. Retinol esters is taken up by liver and stored.
6. When needed vit A is released from liver as free retinol.
7. Retinol is bound with RBP in circulation form complex
8. At peripheral target tissue binds with specific receptor on cell
membrane enters into cell.
9. Retinol  retinoic acid enters into nucleus binds with nucleus
retinoid receptor regulate gene transcription.

9. 👀👀Rhodopsin / Wald’s visual cycle🏻
Retina>>> retinal. 🏻 🏻
Two types of cell rods cell ( dim) and cones cell ( color and
day)
rhodopsin iodopsin
11-cis retinal ( CHO- grp) + opsin (NH2- of lysine) rhodopsin
(rods) and iodopsin (in cones).

11. Wald's visual cycle
How does this light
strikes create vison in
our brain?
What is actually
happening?
What is visual cascade&
cGMP?
🏻
🏻

12. • When light strikes, the following reaction occurs in actual
💥👉🧀Visual cascade and cGMP
• This results in hyperpolarization
• Which is an excitatory response transmitted
through the neuron network to the visual cortex of
the brain
• image is formed😃😎
Breaks
cGMP
Bleachingaction

13. COLOR VISION
• Cones cell are specialized in bright and color vision
• Visual cycle comparable to rodes is seen in cones too.
• Governed by color sensitive pigments:
• Porphyropsin ( red)
• Iodopsin (green )
• Cyanopsin (blue)
• Splitting of these three pigments in different proportion results in
perception of different color by brain.
•👠🧀🌹🌼

14. Retinol ,Retinoic Acid : Regulation of Gene
Expression & Tissue Differentiation
• Retinoic acid growth, development and tissue
differentiation.
• Like steroid hormone and vit D, it binds with nuclear
receptor  that binds with response element of DNA.
• And regulate transcription of different genes.
• Two nuclear receptor: Retinoid Acid Receptor ( RARs) and
Retinoid X Receptor ( RXR).
• RAR: all trans and 9-cis
• RXR: 9-cis

16. Other
functions of vitamin A
• Cell growth and differentiation
• Maintain healthy epithelial cells
• Synthesis of certain glycoproteins required for growth and mucus
secretion
• The synthesis of transferrin, the iron transport protein
• To maintain proper immune system( fight bacterial infection)
• Cholesterol synthesis require vit A
• Carotenoid acts as anti oxidants.( cancer and heart attack)

17. Usually not immediate coz Hepatic stores can meet body
requirements : 2-4 months
In eyes: earliest symptoms night blindness ( nyctalopia)
Severe deficiency xerophthalmia
Dryness in cornea, conjunctiva and keratinization of epithelial
cells
Certain area of conjunctiva triangular plaques aka Bitot’s
spots.
If xerophthalmia persists for longer timecorneal ulceration and
degeneration occurs keratomalacia causing total blindness
Vitamin A deficiency: in eye

18. xerophthalmia
keratomalacia
Bitot’s spots.

19. Other deficiency
• Effect on growth : retardation due to impairment in skeletal formation.
• Effect on reproduction: Degeneration of germinal epithelium leads to
sterility in male
• Effect on skin and epithelial cells : rough and dry skin.
• Keratinization of epithelial cells of gastro intestinal tract, urinary tract
and respiratory tract is noticed
The plasma level of retinol binding protein is decreased in vitamin A
deficiency (negative acute phase protein)

20. Hypervitaminosis A
• There is only a limited capacity to metabolize vitamin A, and
excessive intakes lead to toxicity.
• Dermatitis
• Hepatomegaly with hyperlipidemia
• Skeletal decalcification
• Hypercalcemia and calcification of soft tissue.
• CNS ( headache, nausea, ataxia, anorexia, ↑ CSF pressure)
• Excessive dry skin and alopecia
🙏⏰🙏