2. Introduction:
⦿ In 1911, Funk provide clear evidence of the
validity of vitamin hypothesis.
⦿ Funk has isolated an anti beri-beri factor from
yeast.
3. ⦿ Define:-
• The naturally occurring micronutrients present in food and
are required for normal functioning and growth of the
living organisms are called as a vitamins.
⦿ Classification
A) Fat soluble vitamins: these are soluble in fat and are
stored in liver.
• Their absorption requires presence of bile salts and fats.
I. Vitamin A,
II. Vitamin D,
III. Vitamin E and
IV. Vitamin K
B) Water soluble vitamins: These are soluble in water and
are not stored in body.
-- Water soluble vitamin includes
I. B-complex group and
II. vitamin C.
5. 1. VITAMIN A:-
⦿ Vit A is bright eye vitamin.
⦿ It is of 2 type: i)vit. A1 = Retinol
Ii) Vit. A2 = Dehydroretinol
⦿ Sources:- Carotenoids are chief source of vit A.
➢ Liver of various fishes are the richest natural
sources.
➢ Other sources are butter, milk, egg, pigmented
vegetable, fruits, egg yolk, etc.
⦿ Structure:- Vit A1
6. ⦿ Vit A2:-
⦿ Both these form are unsaturated alcohol contain
B-ionone ring
⦿ Vit A2 contain additional double bond between
3 & 4 carbon.
⦿ Precursor of Vit A is carotenoids in alpha, beta
& gamma form.
⦿ Vit A2 is less active than Vit A1
8. • Function of Vit. A:-
1. Vit A is needed for formation of rhodopsin or
visual pigment which is concerned with vision in
dim light.
2. Vit A maintain epithelial cells of the skin & the
linings of digestive , respiratory & genitourinary
system.
3. Vit A acts as an antioxidant thus helpful in
cancer.
4. It stimulate mucous & tear secretion.
5. It act as an factor in tooth & bone formation.
10. ❑ Role of Vitamin A in vision:
• The retina of the eye contains two types of receptor
cells, Rod cells which are responsible for dim light
vision & the cones, responsible for bright light vision .
• Cones are also responsible for colour perception. The
deficiency of cone pigments makes the individual
colour blind.
• In retinal pigments, the rod cells contain rhodopsin.
Under the influence of light, rhodopsin is converted to
lumirhodopsin which is further converted into
metarhodopsin.
• Then hydrolysed to protein opsin & trans retinal.
Trans-Retinal(trans- retinene) is inactive in the
synthesis of rhodopsin, it must be coverted to the
active cis- isomer.
11. ⦿ In the eye, the trans-retinal is reduced to
trans-retinol by the enzyme retinal reductase &
NADH.
⦿ The trans retinol which is too inactive in rhodopsin
synthesis is passed into blood stream, then carried
to liver .
⦿ It is then converted to cis -isomer. In dim light
active cis-retinol from the blood enters the retina
where it is oxidized to cis-retinal by reverse action
of retinal reductase in the presence of NAD+.
⦿ Finally the cis-retinal combines with protein opsin
to give back rhodopsin and thus cycle is repeated.
⦿ The individual having vitamin A deficiency are
unable to resynthesise rhodopsin and thus unable to
see in the dim light and the condition is called
night blindness.
15. ⦿ VitaminA Deficiency:-
1.Xeophthalmia: ( Dryness of eyes )
⦿ Deficiency of vit A causes dryness of eye called as
Xerophthalmia, in which there is thickening & loss of
transparency of conjunctiva with yellowish pigment.
2. Kertomalacia:
⦿ It is a corneal disease in which cornea becomes soft & the
corneal epithelium becomes dry scaly rough & opaque.
⦿ Vit A deficiency causes defective teeth formation.
3. Night blindness/ Nyctalpia:
⦿ As retinol is required in the formation of rhodopsin, in
deficiency of Vit A the capacity to look in dark decreases
hence called as Night Blindness.
4.Growth retardation.
5.Susceptibility to respiratory tract infections.
6. Skin becomes dry, scaly & rough.
16. 2. VITAMIN D:
⦿ Vit D is called as calciferol.
⦿ It is steroidal hormones.
⦿ It is of 3 type:-
i)Vit D1:- Calciferol
Ii) Vit D2 :-Ergocalciferol
Iii) Vit D3:- Cholecalciferol
⦿ Sources- The best natural source of vit D are fish
liver oil.
⦿ Structure- Two nutritionally imp Vit D : Vit D2 &
Vit D3
18. ⦿ Biological active form:
• On exposure to sunlight
• Ergosterol Sunlight Ergocalciferol (plants)
• 7-dehydrocholesterol Sunlight – UV rays cholecalciferol
( D3) which then gets converted to calcidiol.
• Calcidiol in kidney gets converted to calcitriol
which is an active form of vitamin D.
⦿ Biological Functions :
1. It increases intestinal absorption of calcium &
phosphate
2. It causes elevation in plasma calcium & phosphate
levels.
3. It helps in formation of bones
19. 4. It minimizes excretion of calcium & phosphate
through kidneys.
5. It increases citrate level of blood, bone, kidney &
heart tissue as well as excretion of citric acid.
⦿ Deficiency diseases Of Vit D:
1. Rickets in children: The calcification of bone is
affected & density of bone is decreases.
2. Osteomalacia, osteoporosis in adults: Defective
mineralization & bones get soften.
3. Skeletal deformity
4. Growth disturbance
5. Hypocalcemia (Tetany)
20. 3. VITAMIN E:-
⦿ Vit E is also called as tocopherol
⦿ It is also known as antisterility factor.
⦿ Sources– vegetable oils, wheat germ.
⦿ Structure– It consist of alpha beta & delta
tocopherol from which only alpha tocopherol has
greatest biological activity.
21. • Function—
1. It protect vit A & carotene from destruction by
oxidation in the body.
2. It prevents formation of peroxide by
polyunsaturated fatty acid.
3. It protect enzymes in muscle, nerves from
destruction.
4. It prevent hepatic necrosis produced by the lack
of sulphur containing amino acid in diet.
5. Most of above action of Vit E are due to its
antioxidant property.
22. ⦿ Deficiency diseases Vitamin E--
1. Degenerative changes in muscles.
2. Minor neurological symptoms.
3. Changes in CNS.
4. Increased fragility of erythrocytes.
5. Megaloblastic anaemia.
6. Sterility.
23. ❑ VitaminK
⦿ It is an antihaemorphagic vitamin.
⦿ Source– green vegetable like spinach, cabbage
contain Vit k1 & Vit K2 is synthesized by bacteria
present in human intestine.
⦿ It is of 3 type– i) Vit K1= Phylloquinone
Ii) Vit K2= Menaquinone
Iii) Vit K3= Menadione
⦿ Structure--
25. ⦿ Deficiency
1. Lack of active prothrombin in the circulation.
2. Blood coagulation gets adversely affected.
3. Profuse bleeding even on minor injuries.
4. Blood clotting time is increased.
5. Uncontrolled hemorrhages, etc.
26. ⦿ Hypervitaminosis: (↑Fat soluble Vitamins)
⦿ Hypervitaminosis refers to a condition of
abnormally high storage levels of vitamins, which
can lead to toxic symptoms. The medical names of
the different conditions are derived from the
vitamin involved.
⦿ With few exceptions, like some vitamins from B
complex, hypervitaminosis usually occurs more
with fat-soluble vitamins which are stored in the
liver and fatty tissues of the body. These vitamins
build up and remain for a longer time in the body
than water-soluble vitamins.
⦿ Eg. Hypervitaminosis A, Hypervitaminosis D,
Hypervitaminosis E, Hypervitaminosis K,
27. WATER SOLUBLE VITAMINS
1. Thiamine (B1) –
⦿ Anti beri-beri substance.
⦿ Active form thiamine pyrophosphate
⦿ Sources- grains, meat (liver, heart), unrefined
cereals.
⦿ Structure—
29. ⦿ Function-
1.Thiamine pyrophosphate (TPP) play imp role in
following reaction:
⦿ Oxidative decarboxylation of pyruvic acid
⦿ Transketolase reaction in HMP pathway of
glucose metabolism.
2.It is essential for growth.
3.It is essential for maintaining the nerves in
normal condition.
4. Biosynthesis of fat from carbohydrate, Protein.
30. ⦿ Deficiency—
● It primarily affect nervous system & circulatory
system.
● Its deficiency causes peripheral neuritis develop
results into paralysis.
● CVS symptoms like edema, loss of appetite are
seen during deficiency commonly called as
beri-beri–
● Types
I )Wet beri-beri
Ii) Dry beri-beri
31. 2. Riboflavin (B2) —
⦿ It is required for redox system
⦿ Source—milk, whole grain, leafy vegetable, liver,
kidney, fermenting bacteria are best source.
⦿ Structure--
32. ⦿ There are two coenzyme–
i) Flavin mononucleotide (FMN)
ii) Flavin adenine dinucleotide (FAD)
⦿ FAD & FMN are prosthetic group of oxidation
reduction enzyme.
Eg: succinate dehydrogenase requires FAD as a
prosthetic group.
33. ⦿ These prosthetic group are also required for
amino acid oxidase which is needed for
deamination of amino acid.
⦿ Eg:
34. ⦿ Riboflavin is converted to its active form i.e.
FMN by an enzyme flavokinase
⦿ FAD is synthesized from FMN with the help of
ATP
35. 3. Nicotinic acid (Vit B3) :
⦿ It is also called as P-P factor or niacin.
⦿ Source– husk of cereals, yeast, green vegetables,
tomato, egg, milk.
⦿ Structure--Niacin
36. ⦿ Its active forms are-
--Dinucleotide= Niacinamide adenine nucleotide
(NAD)
⦿ Its phosphorylate form= Niacinamide adenine
nucleotide phosphate (NADP)
⦿ Functions
1. Helps in maintaining healthy skin, healthy nerves
& healthy digestive system.
2. Reduced coenzyme helps in production of high
energy compounds like ATP.
3. NADP+ helps in pentose phosphate pathway.
4. NADPH is involved in biosynthesis of fatty acids.
38. • Deficiency
• Pellagra is a vitamin deficiency disease caused by
dietary lack of niacin
• The symptoms of pellagra include:
1. Dermatitis, oedema ,Red skin lesions
2. Dementia
3. Diarrhoea
⦿ The main results of pellagra can easily be
remembered as
"the three D's": diarrhea,
dermatitis and dementia.
39. 4. Pantothenic acid (B5):
⦿ It is required for formation of co-enzyme A
⦿ co-enzyme A require for all acetate & fatty acid
metabolism in body.
40. ⦿ Eg:
⦿ Deficiency –
1. Growth failure.
2. Dermatitis
3. Graying & loss of hair.
4. Tissue necrosis, etc.
41. 5. Pyridoxine (B6):
⦿ It include pyridoxine, pyridoxal & pyridoxamine.
⦿ The active form is Pyridoxal phosphate
42. ⦿ It is involved in number of reaction such as
amino acid decaxboxylase, tranaminase,
tryptophanase cytothionase.
i) Transamination
⦿ In transamination, the NH2 group on one
molecule is exchanged with the C=O group on
the other molecule. The amino acid becomes a
keto acid, and the keto acid becomes an amino
acid
⦿ In this example alpha keto-glutaric acid
becomes glutamic acid, amino acid becomes
keto acid.
--This reaction is reversible.
44. ⦿ Deficiency—
⦿ Dermatitis with swelling & edema.
6. Biotin (Vit B7):
⦿ It is also called as vit H.
⦿ It is needed for
carboxylation
reaction.
45. ⦿ Deficieny:
Egg white injury:
⦿ It’s a deficiency disease of biotin which is rare and
generally observed when large quantities of raw
eggs are consumed.
⦿ Egg white contains large amount of protein avidin
which binds to biotin very tightly and prevents its
absorption in the intestine.
⦿ The avidin in egg white may be a defense
mechanism inhibiting growth of bacteria.
⦿ When eggs are cooked avidin gets denatured along
with other egg white proteins.
46. ⦿ biochemical role of pyridoxine/ function of
Pyridoxine:
⦿ The active form of pyridoxal phosphate as a
coenzyme involved in the number of reactions such
as
I. ---amino acid Decarboxylation,
II. ---Transamination,
III. ---Racemisation and Elimination reactions.
⦿ It is essential for growth of infants.
⦿ It is involved in Immune function.
⦿ It is useful in the dermatitis.
47. 7. Folic acid (Vit B9) —
⦿ It consist of = Pteridine ring + p-aminobenzoic
acid + Glutamic acid
⦿ Structure--
⦿
48. ⦿ Active form of folic acid is tetrahydrofolate
(THF).
⦿ THF act as co-enzyme for transferase enzyme.
49. FUNCTION OF FOLIC ACID:
1. Folic acid is used in the treatment of anaemia
due to folic acid deficiency.
2. Tetrahydrofolate, coenzyme of folic acid is
involved in one carbon group transfer reactions.
3. It is involved in biosynthesis of nucleic acid.
4. It is involved in synthesis of amino acids like
methionine, serine
5. It is essential for growing & multiplying cells.
6. Folic acid is required for synthesis of RBC in
bone marrow.
50. 8. Cyanocobalamin (Vit B12) :
⦿ Vit B12 is necessary for blood formation.
⦿ Active form of it is co-enzyme B12.
⦿ Reaction which need co-enzyme B12 are:
i) 1, 2 shift of hydrogen:
52. ⦿ Absorption of Vit B12 need mucoprotein of
gastric juice called intrinsic factor, that bind
to Vit B12 & transport the nutrient into
intestinal cell.
⦿ Due to lack of intrinsic factor / defective
mucoprotein result into Vit B12 deficiency.
⦿ Deficiency of Vit B12 causes= Pernicious
Anaemia.
❑ Lipoic acid: active supporting growth factor
for bacteria & protozoa.
⦿ It is needed for of pyruvic acid & alpha-
ketoglutaric acid.
53. ❑ Ascorbic acid (Vit C) :
⦿ It is antisorbutic factor.
⦿ Source: Amla, citrus fruits like orange,
tomato, cabbage, etc
⦿ Structure:
54. FUNCTIONS OF VIT. C
⦿ Vitamin C plays important role in:
1. Collagen formation
2. Bone formation
3. Iron & haemoglobin metabolism
4. Tryptophan,Tyrosine, & Folic acid metabolism
5. Synthesis of immunoglobulins (antibodies)
6. Synthesis of peptide hormone & corticosteroid
hormones
7. Reduces risk of cataract formation
8. As an antioxidant reduces risk of cancer, coronary
heart disease.
9. it is a strong antioxidant agent
10. it enhances iron absorption by keeping it in the
ferrous form
55. • Deficiency :- i) Scurvy
• Symptoms: Weakness, pain in bones and joints ,
loosening of teeth, poor healing of wound, internal
haemorrhage, swelling of long bone, Easy
factorability of bones.
• Scurvy leads to the formation of spots on the skin,
spongy gums, and bleeding from all mucous
membranes.
• The spots are most abundant on the thighs and
legs, and a person with the ailment looks pale,
feels depressed, and is partially immobilized.
• In advanced scurvy there are open, suppurating
wounds and loss of teeth, sluggish hormonal
function of adrenal cortex, swollen joints,
osteoporosis.
56. ▪ Treatment:
• Treatment involves taking vitamin C
supplements and eating citrus fruits, potatoes,
broccoli and strawberries.
• Co-enzyme: The non-protein, low molecular
weight & organic substances associated with
functions of enzymes are called as co-enzyme.
58. ❑ Name the respective vitamins responsible for
nutritional deficiency cause:
1. Osteoporosis: Vitamin D
2. Blood clotting disorder/ Haemorrhage: Vitamin K
3. Beri-beri: Vitamin B1( Thiamin)
4. Night blindness: Vitamin A ( Retinol)
5. Pernicious anaemia: Vitamin B12 (Cyanocobalamine).
6. Scurvy: Vitamin C (Ascorbic acid)
7. Rickets: Vitamin D (Calciferol)
8. Egg white injury: Vitamin H (Biotin).