3. Chemistry, Functions and Deficiency
Vitamin A
Chemistry, Functions and Deficiency 1

4. Introduction Vitamin A is a fat soluble Vitamin.
Needed in small amounts in diet and is Important for :
Normal Visual function
Maintenance of cell function and 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 Pakistan

5. Lipid soluble vitamins - common features
They cannot be synthesized by the body except Vitamin D.
Supplied by the diet and Absorbed along with fats.
Transported by LP & Specific binding proteins
If Extra, are stored in liver and adipose tissue.
Excess consumption leads to accumulation and can be toxic .

6. Two groups of compounds have Vitamin A activity.
Retinoids and Carotenoids 2

7. Vitamin A, in the strictest sense, refers to retinol. 
Vitamin A, in the strictest sense, refers to retinol.
However, the oxidized metabolites, retinaldehyde and retinoic acid, are also biologically active compounds. 
The term Retinoids includes all
molecules
(including
synthetic retinol.
molecules)
that
are
chemically
related to 3

8. More than 600 carotenoids in nature, and approximately 50 of these can be metabolized to vit. A.
The α-, β-, and γ-carotenes are quantitatively the most important provitamin A carotenoids.
β-Carotene is the most prevalent carotenoid in the food supply that has provitamin A activity.
In humans, carotenoids are absorbed intact and are stored in liver and fat. 4

9. Moderate enhances uptake in •
Liver, fish, and eggs are excellent food sources for preformed vitamin A.
Vegetable sources of provitamin A carotenoids include dark green and deeply colored fruits and vegetables. • •
Moderate enhances uptake in
cooking of vegetables carotenoid release for the gut. 7

10. Recommended Dietary Allowance (RDA) Vitamin A for Adults
Women: 700 µg or 2,330 IU µg
Men: 900 µg or 3,000 IU
UL Men or Women: 3,000 µg or 10,000 IU

11. Unsaturated Isoprenoid side chain (all trans)
Attaching group
β – Ionone ring
Unsaturated Isoprenoid side chain (all trans) 5

12. •One molecule of β carotene yields two molecules of vit A retinol
•Site of β cleavage of carotene is shown by *
•One molecule of β carotene yields two molecules of vit A retinol
•6 μg of β carotene is equivalent to 1μ g of preformed retinol.
•The total amount of vitamin A in foods is therefore expressed as micrograms of retinol equivalents (RE). 6

13. Vitamin A, in animal sources is in the form of Retinyl esters.
It is hydroly zed to retinol and fatty acid by pancreatic hydrolases.
Absorption requires the presence of bile salts.
In intestinal cells, retinol is esterified back and secreted with chylomicrons.
Carotenoid absorption is also aided by some fat in meal.
90% of retinoids can be absorbed 8

14. It yields retinal, which is reduced to retinol.
β-Carotene is cleaved in the intestinal mucosa by carotene dioxygenase.
It yields retinal, which is reduced to retinol.
Retinol is esterified and secreted in chylomicron together with esters formed from dietary retinol. 9

15. Absorption of Carotenoids
Absorbed intact, absorption rate much lower
Intestinal cells can convert carotenoids to retinoids.
It is passed along with fat through the lymphatic system into blood stream.
Absorption increases if taken with fat.
Approximately 80% is absorbed
Vitamin A which is not absorbed is excreted within 1 or 2 days in feces .

16. Transport Chylomicrons from intestinal cells to the liver
From liver to target tissue as retinol via retinol-binding protein (RBP)
The retinol-binding protein complex interacts with a second protein, Transthyretin.

17. This trimolecular complex functions to prevent vitamin A
From being filtered by the kidney glomerulus
To protect the body against the toxicity of retinol and
To allow retinol to be taken up by specific cell- surface receptors that recognize retinol-binding protein. 10

18. 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 9 months or more.

20. Excretion of Vitamin A Not readily excreted
Aging increase risk of toxicity because excretion is impaired

21. Vitamin A is essential for vision (especially dark adaptation), •
Vitamin A is essential for vision (especially dark adaptation),
Immune response, Bone growth, Reproduction, •
Maintenance of the
surface linings of the
eyes, epithelial cell growth and repair, and the epithelial integrity of the respiratory, urinary, and intestinal tracts.
Vitamin A is also important for embryonic development and the regulation of adult genes. • 12

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: Retinol and retinal are essential for normal reproduction
Maintenance of epithelial cells: Essential for normal differentiation of epithelial tissues and mucus secretion

24. Role in Vision Visual Cycle (Wald’s Visual Cycle)
A process by which light falling 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

25. Role in Vision Retina is a light-sensitive layer of cells of the eye
Retina consists of: Rod and cone cells (photosensitive cells)
Rod cells process black ad white image
Cone cells process color image

26. Role of Vitamin A in Vision
Normal vision depends on the retina and on 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. 16

28. Wald’s Visual Cycle

29. The Visual Cycle

30. 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

31. Role of Vitamin A in Vision
Dark Adaptation time
Bright light depletes rhodopsin (photo bleaching)
Sudden shift from bright to dim light, causes difficulty in seeing.
Rhodopsin is synthesized in few minutes and vision is improved in the dark

32. 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

33. In the retina, retinaldehyde functions •
In the retina, retinaldehyde functions
prosthetic group of the light-sensitive proteins, forming Rhodopsin (in rods)
iodopsin (in cones).
as the
opsin and •
Any one cone cell contains only one type of
opsin, and is sensitive to only one color.
The absorption of light by Rhodopsin causes isomerization of the retinaldehyde from 11-cis • to
all-trans, and a conformational change in opsin.
This results in the release of retinaldehyde from the protein, and the initiation of a nerve impulse. • 13

34. The formation of the initial excited form of 
The formation of the initial excited form of
Rhodopsin, bathorhodopsin, occurs within picoseconds of illumination.
There are then a series of conformational 
changes leading to the formation
metarhodopsin II, which initiates nucleotide amplification cascade nerve impulse. of
a guanine
and
then a 14

35. The final step is hydrolysis to release all- 
The final step is hydrolysis to release all-
trans-retinaldehyde and opsin.
The key to initiation of the visual cycle is the availability of 11-cis-retinaldehyde, and hence vitamin A.
In deficiency, both the time taken to adapt  
to darkness and the
light are impaired.
ability to
see in
poor 15

36.  Vitamin A deficiency can result from inadequate intake, fat malabsorption, or liver disorders.
 Deficiency impairs immunity and hematopoiesis and causes skin rashes and typical ocular effects (e.g., xerophthalmia, night blindness).
 Diagnosis is based on typical ocular findings and low vitamin A levels.
 Treatment consists of vitamin A given orally or, if symptoms are severe or malabsorption
is the cause, parenterally. 23

37. Primary vitamin A deficiency Prolonged dietary deprivation
Vegetarians,
Chronic alcoholics,
Toddlers and
Preschool children. 24

38. Pancreatic insufficiency, Duodenal bypass, Chronic diarrhea,  o
Secondary
Sprue,
vitamin A deficiency
Cystic fibrosis,
Pancreatic insufficiency,
Duodenal bypass,
Chronic diarrhea,
Bile duct obstruction, Cirrhosis. 25

39. Bitot spots - Areas of abnormal squamous cell proliferation and 
Bitot spots - Areas of abnormal squamous cell proliferation and
keratinization of the conjunctiva
can be seen in young children with
VAD.
Blindness due to retinal injury - Vitamin A has a major role in 
photo transduction. VAD leads to lack of visual pigments;
this reduces the absorption
of various wavelengths of light,
resulting in blindness. a 26

40. Poor adaptation to darkness (nyctalopia),
which can lead to night blindness, is an early symptom.
Xerophthalmia results from keratinization of the conjunctiva.
Keratomalacia- In advanced deficiency; the cornea becomes hazy and can develop erosions, which can lead to its destruction ( 27

41. since it is a negative ‘Acute phase protein’,
Increased susceptibility to infections- Keratinization of the mucous membranes of respiratory tracts and urinary tract takes place, increasing the susceptibility to infections.
During infection the synthesis of retinol binding protein is reduced in response to infection
since it is a negative ‘Acute phase protein’,
that results in decreased circulatory
concentration of the vitamin deterioration of the immune
with further system. 28

42. Respiratory infections
Fatigue
Anemia
Diarrhea
Respiratory infections
Decreased
Infertility
growth rate
bone
development 29

43. Serum retinol level-Normal range is 28 to 86
μg/dL (1 to 3 µmol/L). The level decreases
vitamin A deficiency.
Serum RBP level
Serum zinc level is useful because zinc deficiency interferes with RBP production.
An iron panel is useful because iron in
deficiency can affect the metabolism
vitamin A. of 30

44. Albumin levels are indirect measures of vitamin A levels.
Complete blood count (CBC) with differential if anemia, infection, or sepsis is a possibility.
An electrolyte evaluation and liver function
studies should be performed to
nutritional and volume status.
evaluate
for 31

45. VITAMIN- A

46. Effects 1. Night blindness (nyctalopia)
Inability to see well in dim light easily when
entering a dark space form bright light
2. Night blindness occurs when there is insufficient Vit A
in the blood to quickly regenerate visual purple .
3. Alcoholic liver disease (cirrhosis) causes
night blindness which is due to hepatic damage affecting Vit A release.

47. Effects
In the eye, the 1st symptom of Vit A deficiency include photophobia (sensitivity to bright light)
Inflammation of eyes and eyelids due to impaired functioning of lacrimal glands
Xerophthalmia (dry, inflamed and edematous cornea)
Keratomalcia – permanent blindness results when infection leads to ulceration and softening of cornea

48. Skin and mucous membrane changes
Keritinization of the epithelial tissues
Increase susceptibility to infections of all membranes, protected by mucous
Follicular hyperperatosis – The sebceous glands becomes clogged and skin takes on a gooseflesh like appearance.

49. Toxic effects Drying and desquamation of skin Anorexia Loss of hair
Bone pain and fragility
Enlargement of liver and spleen

50. Vitamin A is Toxic in Excess
There is only a limited capacity to metabolize vitamin A, and excessive intakes lead to accumulation beyond the capacity of binding proteins, so that unbound vitamin A causes tissue damage.

51. Thanks