This document discusses vitamins A and E. It defines vitamins and classifies them as fat-soluble or water-soluble. For vitamin A, it describes the different forms, absorption, transport and storage in the body, and functions including vision, gene expression, cell growth and differentiation. Deficiency causes night blindness and can lead to blindness. Vitamin E is an antioxidant that protects cells and prevents sterility.

2. What are vitamins?

3. CLASSIFICATION OF VITAMINS

4. DIFFERENCE BETWEEN FAT SOLUBLE &
WATER SOLUBLE VITAMINS

6. VITAMIN A

8. CHEMISTRY
 Term Vitamin A is collectively used to represent 3
biologically active forms :
1) Retinol ( Vitamin A – alcohol)
2) Retinal (Vitamin A- aldehyde)
3) Retinoic Acid (Vitamin A acid)
 These forms are referred to as “RETINOIDS”
 Vit-A is also derivative of Carotenoids
- hydrocarbon pigments (yellow & red)
- Called as Provitamins
- Most important is β-carotene

13. Interconversion of Vitamin-A metabolites

14. ABSORPTION, STORAGE & TRANSPORT OF VITAMIN A
Absorption-
 Ingested β-carotene in the intestine by β-carotene
dioxygenase to give retinal.
 Retinal is reduced to retinol by retinaldehyde reductase,
an NADPH requiring enzyme within the intestine.

15. Storage-
 Retinol is esterified with palmitic acid incorporated into
chylomicrons together with dietary lipid and delivered to the
liver for storage.
Transport-
 Transport of retinol from the liver to extrahepatic tissues,
occurs by binding of retinol to retinol-binding protein (RBP).
 Transport of retinoic acid is done by binding to albumin.

17. FUNCTIONS OF VITAMIN A
 Different forms of Vitamin A have different functions
- Retinal & Retinol involved in vision
- Retinoic acid for growth and cellular
differentiation
- β-Carotene have an antioxidant role.

18. 1) ROLE IN VISION
- Biochemical function of vitamin A in visual cycle was
discovered by George Wald
- Events occur in cyclic process known as “Wald’s
visual cycle”
 Retina of eyes contain 2 types of receptor cells:
- Rods – involved in dim light vision
- Cones – involved in bright light and color vision

19.  In retinal rod cells, light sensing protein Rhodopsin
is present
 Rhodopsin is made up of – 11-cis-retinal & protein
opsin
 11-cis retinal serves as light absorbing part.

20.  When light falls on Rhodopsin,a series of
photochemical isomerizations occurs, splits into
Opsin and all -trans retinal
 This trigger a nerve impulse that is transmitted by
optic nerve to the brain.
WALD’S VISUAL CYCLE

21.  The all-trans-retinal is immediately isomerized by
retinal isomerase to 11-cis-retinal.
 11-cis-retinal combines with opsin to regenerate
rhodopsin and complete the visual cycle.

22. IN LIVER-
 The conversion of all-trans-retinal to 11-cis-retinal is
incomplete.
 Remaining all-trans-retinal which is not converted to
11-cis-retinal is converted to all-trans-retinol by
alcohol dehydrogenase, gets stored in liver.

23.  When needed, all-trans-retinol re-enters circulation
which is taken up by retina.
 All-trans-retinol is converted back to 11-cis retinal,
which combines with Opsin & again to form Rhodopsin
 This completes- WALD’S VISUAL CYCLE.

25. DARK ADAPTATION TIME
 When person shifts from bright light to dark, there is
difficulty in seeing and after a few minutes the vision
improves
 During these few minutes Rhodopsin is
resynthesized and vision is improved.

26.  The time taken for regeneration of rhodopsin is
referred to as the Dark Adaptation Time
 Deficiency of vitamin A
Increase in dark adaptation time
 Night blindness

29.  Retinoic acid is important regulator of gene
expressionbinds to response elements of DNA
regulate transcription of genes.
3) Cell Growth And Differentiation
 Retinoic acid is required for cell differentiation in
spermatogenesis & epithelial cells.
2) Role In Gene Expresssion

30. 4) Required For Maintenance Of Healthy Epithelial Cells
- Deficiency leads to keratinization of epithelial cells
5) Role In Glycoprotein & Mucopolysaccharide Synthesis
- Necessary for mucus secretion
6) Antioxidant Role-
- β carotene is an antioxidant traps free radicals in
tissues.
- Prevent the development of Cancer and cardiovascular
diseases

31. DIETARY SOURCES
 Animal sources –
- Liver, kidney, Egg yolk, milk, cheese, butter
- fish liver oils are very rich in vitamin A
 Plant foods – contain provitamin-β carotenes
- Carrots, spinach, pumpkins, mango, papaya etc.

32. RDA

Requirement increases in growing children , pregnant women & lactating mothers
= 6 µg of β-carotene

33. DEFICIENCY OF VITAMIN A:
Causes-
 May be Primary or secondary
 Primary causes – Inadequate dietary intake
 Secondary causes-
- Failure to cleave β-carotene because of enzyme
defect
- Failure to synthesize chylomicrons
- Impaired storage in hepatic cells due to liver
disease
- Failure to synthesize RBP

34. DEFICIENCY MANIFESTATIONS
Deficiency manifestations of Eyes
 NIGHT BLINDNESS - is one of the earliest signs of vitamin A
deficiency.
- have difficulty to see in dim light since dark adaptation
time is increased.
 XEROPHTHALMIA- leads to severe deficiency .
-changes occur in lacrimal glands leading to dryness of
conjunctiva & Cornea

35.  BITOT’S SPOTS - In conjunctiva, greyish- white triangular
plaques.
-This is due to increased thickness of conjunctiva in
certain areas.
 KERATOMALACIA- If Xerophthalmia persists for long time,
- corneal epithelium becomes keratinized, opaque and
becomes softened and ulcerated.
- ultimate result is blindness.

37.  Effect on growth – growth retardation due to
impairment in skeletal formation
 Effect on reproduction – degeneration of germinal
epithelium leads to sterility in males
- incidence of miscarriage and malformed
offspring
 Effect on skin – dry , rough and scaly skin.
 Effect on epithelial cells - keratinization of GIT,
Urinary tract & respiratory tract- leads to increased
bacterial infection

38. ASSESSMENT OF DEFICIENCY
1. Dark adaptation test
2. RBP level in serum
3. Vitamin A level in serum
 Normal blood level of vitamin A is
25 to 30 µgm/dl.

39. VITAMIN A TOXICITY
 Excessive intake of vitamin A produces a toxic syndrome
called hypervitaminosis A syndrome
 Symptoms are :
- dermatitis(dryness and redness of skin)
- hepatic dysfunction
- skeletal decalcification
- joint pains
- loss of weight
- loss of hair
 During pregnancy -congenital malformation of foetus.

41. VITAMIN-E
 Vitamin-E is chemically known as Tocopherol
(tocos means childbirth).
 It plays a role in cellular respiration.
 It is an antioxidant that acts as a scavenger for
molecular oxygen and free-radicals.
 It is known as anti-sterility vitamin.

42. CHEMISTRY
 α-tocopherol is the most active form.
 The tocopherol are derivatives of 6-hydroxy chromane
(tocol) ring with isoprenoid side chain.
 The antioxidant property is due to the chromane ring.

43. ABSORPTION, TRANSPORT, & STORAGE
Absorption-
 Vitamin E is absorbed from intestine together with dietary lipid.
 It is delivered to the liver via chylomicron.
Transport-
 The liver can export vitamin E into VLDL to target cells.
 In cells, tocopherols are distributed where antioxidant activity is
required.
Storage-
 The major site of vitamin E storage is in adipose tissue.

44. BIOCHEMICAL FUNCTIONS
 Vitamin E act as a natural antioxidant by scavenging free radicals
and singlet molecular oxygen.
 It protects the RBCs from hemolysis by oxidizng agents(e.g H2O2)
 Vitamin E also help to prevent oxidation of LDL(oxidized LDL
promotes heart disease)
 Vitamin E is required for normal reproduction and prevent
sterility.
 It controls metabolism of PUFA (such as –linoleic acid , linolenic
acid)