This document discusses vitamins, specifically focusing on vitamin A. It begins by defining vitamins and describing their diverse biological functions. It then discusses vitamin A in more detail, covering its chemistry, sources, recommended dietary allowance, absorption and transport, key biochemical functions including in vision and cell differentiation, deficiency and toxicity manifestations. The summary highlights that vitamin A plays important roles in vision, bone growth, reproduction and as an antioxidant, and deficiencies can cause night blindness while too much can be toxic.

1. VITAMINS
Dr UMALAKSHMI
Asst.Prof of Biochemistry
Vydehi medical college, Bangalore

2. VITAMIN- definition
 An organic compound required as a nutrient
in tiny amounts by an organism.
 It cannot be synthesized in sufficient
quantities by an organism, and must be
obtained from the diet.
 Vitamins have diverse biological function:
– hormone-like functions as regulators of mineral
metabolism (vit. D),
– regulators of cell and tissue growth and
differentiation (some forms of vit. A)
– antioxidants (vit. E, C)
– enzyme cofactors (tightly bound to enzyme as a
part of prosthetic group, coenzymes)

3. Definition and
Classification of vitamins
 Non-caloric organic nutrients
 Needed in very small amounts
 Facilitators – help body processes
proceed; digestion, absorption,
metabolism, growth etc.
 Some appear in food as precursors or
provitamins

4. Definition and Classification

5. FAT SOLUBLE
VITAMINS

6. FAT Soluble Vitamins:
Characteristics
 Essential
 Organic Structures
 Non-energy Producing
 Micronutrients
 Stored
 Bioavailability
 Toxicity

7. Fat vs. Water Soluble
Vitamins
Characteristics Water Soluble Fat Soluble
Absorption Directly to
blood
Lymph via CM
Transport free Require carrier
Storage Circulate freely In cells with fat
Excretion In urine Stored with fat
Toxicity Possible w
supplements
Likely w
supplements
Requirements Every 2-3 days Every week

8. Objectives
 Chemistry
 Structures
 Sources of vitamin
 Recommended dietary allowance
 Absorption transport and storage
 Biochemical functions
 Deficiency manifestations
 Toxicity manifestations

9. VITAMIN A
CH3
ǀ
CH2 =CH-C=CH-CH3
Chemistry:
 Biologically active forms – retinoids
 Retinyl esters,β-carotene, a carotene, b
cryptoxanthin, Lycopene, Canthaxanthin,
Zeaxanthin
 Retinol:-it is a primary alcohol
containing β-ionone ring with side chain
having 2 isoprenoid units
(or)
 Retinol is present in animal tissues as
retinyl palmitate.

10. Chemistry
 Retinal:- it is aldehyde form
oxidation oxidation
Retinol ↔ Retinal → Retinoic acid
 Retinoic acid:- this is acid form and it
cannot give Retinal and Retinol.
 β-Carotene(provitamin A):- it is plant
source of Vitamin A. It is cleaved by
intestinal enzyme to 2 moles of retinal.
In humans only it is having 1/6 th of
Vitamin A activity.

11. STRUCTURES

12. Sources of vitamin A
Animal sources
 Liver
 Kidney
 cod liver oil
 Meat
 Egg yolk
 Milk
 dairy products
Plant sources
carrot
 broccoli
 spinach
 papaya
 apricots
Mango
Yellow and
dark green
leafy
vegetables are
rich sources

13. Vitamin A Recommended
dietary allowance(RDA)
RDA for Men :- 1000 RE(3500IU)
Women : 800 RE(2500IU)
Requirement is more in pregnant and
lactating women.
IU (international unit)=0.3mg of Retinol
RE(Retinol equivalent)= 1µg Retinol
= 6µg β-carotene
= 12µg other carotenoids

14. Absorption-Transport
Storage
 Retinol esters → hydrolysis by
pancreatic enzymes or intestinal brush
border hydrolases to retinol.
 b-caroten is cleaved to retinal by b-
carotene 15,15´ dioxygenase
(cofactors iron and bile salts).
 Intestinal cells → esterification of
retinol → transported in chylomicrons.

15. Absorption-Transport
Storage
 Remnants of chylomicrons → liver→
esterification (if the concentration
exceeds 100 mg, esters are stored ).
 Transport of retinol to target organs
tightly bound to retinol-binding protein,
RBP(mol.wt.21000) in association with
pre-albumin.

16. Absorption-Transport
Storage

17. Biochemical functions
 Vision
– Generates pigments for the retina
– Maintains surface lining of eyes
 Bone growth
 Reproduction
 Cell division and differentiation
 Healthy Skin
 Regulate Immune System
 Anti-oxidant property by β -carotene

18. Vitamin A and
vision
 Vitamin A in the process of vision is
elucidated by George Wald(noble
prize 1968).
 The events occur in cyclic process
for vision are called-Rhodopsin
cycle or Wald’s visual cycle.

19. Vitamin A and vision
 Rods are at periphery - responsible for Dim
light vision.
 Cones are at centre – responsible for Bright
light vision and colour vision.

20.  Vit. A is necessary to form
rhodopsin (in rodes, night
vision) and iodopsins
(photopsins, in cones –
color vision) - visual pigment.
 Rhodopsin is conjugated
protein having Retinal as a
prosthetic group linked to ε-
amino group of Lysine of
light-sensitive opsin protein.
 In the retina, all-trans-retinol
is isomerized to 11-cis-retinol
→ oxidized to 11-cis-retinal,
this reacts with opsin (Lys)
→ to form the holoprotein
rhodopsin.
Vitamin A and vision

21.  Exposure and
Absorption of light →
conformation changes of
opsin → photorhodopsin.
 The following is a series
of izomerisation →
bleaching of rhodopsin→
initiation of nerve
impulse.
 The final step is
hydrolysis to release
opsin and all-trans retinal
which participate in the
visual cycle.
Vitamin A and vision

22.  When a photon of light is absorbed leads to
activation of cyclic GMP mediated visual cascade.
 The protein transducin is activated by
metarhodopsin-‫װ‬ this involves conversion of GTP to
GDP.
 Activated transducin inturn activates cyclic GMP
phosphodiesterase which degrades the cyclic GMP
to 5’GMP.
 As decreased cyclic GMP closes Na+ channels in
the membranes of rod cells leads hyperpolarization
 At the end gives a excitatory response to the visual
cortex of brain.
Vitamin A and vision

23. Vitamin A and vision

24. Vitamin A and vision
Wald’s visual cycle
 All trans Retinal is
immediately isomerized
to11-cisRetinal by retinal
Isomerase which is
incomplete. So most of
All- trans retinal is
transported to liver for
conversion by alcohol
dehydrogenase. Then
undergoes isomerization
to 11-cis retinol then
oxidized to 11-cis retinal

25. Vitamin A and vision
Dark adaptation time
 When a person shifts from a bright light to
dim light rhodopsin stores are depleted
vision is impaired within few minutes called
as dark adaptation time.
 Vision is improved when rhodopsin is
resynthesized.
 Dark adaptation time is increased in vit.A
deficient individuals.

26. Vitamin A and vision
 Visual cycle comparable to
that present in Rods is also
seen in cones. The colour
vision is governed by colour
sensitive pigments
(Retinal+opsin).
 When bright light strikes the
retina one or more of these
pigments are bleached
 porphyropsin(red),
 iodopsin (green),
 Cyanopsin(blue)
Different proportions of these
pigments results in perception of
different colours by brain.

27. Vitamin A
other
Biochemical functions

28. Vitamin A in Protein Synthesis and Cell
Differentiation
• Through cell differentiation, vitamin A allows cells to
perform specific functions.
• Retinol and Retinoic Acid are required to prevent keratin
synthesis(responsible for horny surface)Epithelial cells:-
Epithelial tissues on the outside of the body form the
skin.
Epithelial tissues on the inside of the body form the
mucous membranes.

29. Vitamin A and Regulation of protein

30.  Retinoic acid regulates the transcription of
genes - acts through nuclear receptors
(steroid-like receptors).
 By binding to various nuclear receptors, vit.
A stimulates (RAR – retinoid acid receptor)
or inhibits (RXR- retinoid „X“ receptor)
transcription of genes regulate specific
protein synthesis. All-trans-retinoic acid
binds to RAR and 9-cis-retinoic acid binds to
RXR.
Vitamin A and Regulation of
protein

31. Vitamin A in Reproduction
and Growth
 Sperm development in men
 Normal fetal development in women
 Growth in children
 Remodeling of the bone involves
osteoclasts, osteoblasts, and lysosomes.
 Osteoclasts are cells that destroy bone
growth.
 Osteoblasts are cells that build bones.
 Lysosomes are sacs of degradative
enzymes that destroy bones.

32. Vitamin A - functions
 Vitamin A is considered to be essential for
the maintenance of proper immune system
to fight against various infections.
 Vitamin A necessary for the synthesis of
certain Glycoproteins, mucopolysaccharides
which are required for growth and mucus
secretion.
 Carotenoids function as Anti-oxidants and
reduce risk of cancers initiated by free
radicals and strong oxidants.

33. Vitamin A deficiency
causes
 Inadequate dietary intake
 Impaired intestinal absorption
 Reduced storage in Liver
 Chronic Alcoholism
Deficiency symptoms not occurred
immediately as Hepatic stores can meet
the requirements for 2-4 months.

34. Vitamin A Deficiency
manifestations
 Night
blindness(Nyctolopia)
 Xerosis (corneal drying)
 Bitot’s spots
 Xerophtalmia
 Karatomalacia
 Hyperkeratosis

35. Vitamin A Deficiency
manifestations
 Impaired immunity
 Sterility
 Growth retardation
 Rough and dry skin
 Keratanization of Epithelial layer of
GIT,URT,RT leads to infections
 Formation of Urinary stones

36. Hypervitaminosis A
 Total Vitamin A level is elevated in
Hypervitaminosis(Normal 20-50 µg/dl)
 Toxicosis symptoms appear only after
retinol binding capacity exceeds and
only when free Retinol or lipoprotein
attached one is present
 Higher concentration of retinol
increases synthesis of lysosomal
hydrolases leads all tissues destruction
mainly cell membranes.

37. Hypervitaminosis A
Acute toxicity :- Occurs when adults ingest
>100x RDA (children ingest >20x RDA ) of
preformed Vitamin A for a period of hours or
several days.
Acute toxicity symptoms
 Blurred vision
 Nausea, vomiting,
 vertigo
 Increase of pressure
inside skull, mimicking
brain tumor
 Headaches

38. Hypervitaminosis A
Chronic toxicity :- >25,000 IU preformed
Vitamin A for >6 years(>100,000 IU
preformed A for >6 months)
 Chronic toxicity symptoms
– Increased activity of osteoclasts
causing reduced bone density
– Liver abnormalities
– Birth defects

39. fat soluble
vitamins
Vitamin D

40. Vitamin D - chemistry
 Vitamin D also called as sun shine
vitamin or anti-rachitic vitamin
 Biologically available forms
In Plants : Ergocalciferol(vitamin D2)
In Animals :Cholecalciferol(vitamin D3)
Biochemically active form :
1,25 –DihydroxyCholecalciferol(Calcitriol)

41. Vitamin D - chemistry
Ergocalciferol Cholecalciferol
 Except Double bond and methyl group
having similar structure as like
Cholecalciferol

42. Vitamin D synthesis
UV
irradiation
270nm-300nm

43. Vitamin D-Synthesis
Photolysis
Non-enzymatic reaction in the skin
Transport to the liver
Biosynthesis of
Cholesterol formed
as intermediate in the
Skin.On exposure to
sun-light Vitamin D3
is formed.

44. Fig. 11-9, p. 377
1,25-dihydroxy vitamin
D3 (active form) Stepped Art
In the liver:
Ultraviolet
light from
the sun
In the
kidneys:
Vitamin D3
(an inactive form)
Hydroxylation
Foods
In the skin:
7-dehydrocholesterol
(a precursor made in the liver
from cholesterol)
Previtamin D3
25-hydroxy vitamin D3
Hydroxylation

45. Sources of Vitamin D
Vitamin D provided to body
Other than sunlight good sources of Vitamin D fatty
fish, fish liver oil, egg yolk.
By eating fortified
and vit D precursor
containing foods like
yeast,milk,butter etc..
Consumption of
Natural foods
Exposure of
skin To sunlight

46. Vitamin D recommended
dietary allowance(RDA)
 Daily requirement :400 IU or
10 mg cholecalciferol
In India
Daily requirement : 200 IU or
5 mg cholecalciferol

47. Absorption-transport
storage
• Dietary Vitamin D is absorbed
from a micelle, along with other
fats.
• About 50% of dietary D3 is
absorbed. Most absorbed in
distal small intestine.
• Incorporated into chylomicrons
• Cholecalciferol from the skin is
bound to DBP and travels
primarily to the liver, but can be
picked up by other tissues as
well (muscle and adipose)
Diet
Bile
lymph
Chylomicrons
skin
Cholecalciferol
DBP
Biochemical
functions

48. • Blood is the major storage site; half-life of 10-21
days
• Through lymph it enters the circulation and
transported with α2 globulin.
• Small amount of Vit D stores in the liver and other
tissues.
• Cholecalciferol first Hydroxylated at 25 th position by
25 Hydroxylase in the liver.
• 25 hydroxyl cholecalciferol is hydroxylated by 1
hydroxylase in the kidney forms 1,25 Dihydroxy
cholecalciferol(calcitriol).
Absorption-transport
storage

49. • Two hydroxylation reactions are mediated by
cytochrome p 450 system,NADPH, O2.
Regulation :
1.When calcitriol concentration is more leads to
activation of 24 – hydroxylase in the kidney leads to
formation of 24,25 dihydroxy cholecalciferol.
2. Low plasma phosphate leads increased activity of 1
hydroxylase.
3. Low calcium enhances the production of PTH which
inturn activates 1 hydroxylase.
Metabolism of Vit D

50. Metabolism of Vit D

51. Vitamin D –biochemical
functions
 Biochemically active form is Calcitriol
 Three important sites it functions
 On intestine
 On bone
 On kidney

53.  Calcitriol
On intestine
Increases
Calcium&
phosphate

54. Vitamin D –biochemical
functions

55.  Calcitriol action on Bone :
1.When calcium sufficient /high leads to
uptake and deposition of calcium and
phosphate within the osteoblasts cells.
2.When low calcium leads to bone
resorption along with parathyroid
hormone results blood calcium and
phosphate level elevation.
Vitamin D –biochemical
functions

56. Calcitriol action on Kidney :
 Acts on Kidney minimizes the
excretion of calcium and phosphate
 Increases the reabsorption of calcium
and phosphate.
As calcitriol acts on target tissues and binds to
receptors which modifies the mRNA synthesis
just like steroid hormones.
Vitamin D is a hormone.
Vitamin D –biochemical
functions

57. VitaminD deficiency is relatively less common.
Causes :-
 Insufficient exposure to sunlight
 Diet lacking Vitamin D
 Chronic alcoholism
 Liver and kidney diseases
 Fat malabsorption syndrome
 Strict vegetarians
Vitamin D –Deficiency

58. Vitamin D
Vitamin D –Deficiency

59. Deficiency manifestations :-
In children
 Causes Rickets characterized by
bone deformities due to incomplete
mineralization.
 Results in soft pliable bones and delay
formation.
 Weight bearing bones bent and forms
bow legs
Vitamin D –Deficiency

60. In Adults :-
 Causes Osteomalacia (adult Rickets)
 Demineralization of the bones leads to
softer susceptibility to fractures.
Renal Rickets:
 Seen in chronic renal failure patients
 Reduced synthesis of Calcitriol
Vitamin D –Deficiency

61. Vitamin D –Deficiency

62. Hypervitaminosis D
 Vitamin D is most toxic when consumed in
overdosage(10-100 times of RDA)
Symptoms:
 increased bone resorption, increased
calcium absorption from intestine leads to
hypercalcemia.
 Deposition of calcium in many soft tissues,
kidney and arteries.
 Stones in kidney.

64. Fat soluble
vitamins
Vitamin E

65. Vitamin E -chemistry
 Vitamin E also called as Anti-sterility
vitamin as it is important for normal
reproduction.
 Vitamin E active form is Tocopherol
 Biologically α, β, γ, δ etc such eight
varieties of Tocopherols and
Tocotrienols forms are available.

66.  Tocopherols are derivatives of 6-
hydroxyl chromane ring with 3 units of
isoprenoid side chain.
 Different varieties of tocopherols is
depending on the methyl groups
arrangement.
α – Tocopherol : 5,7,8-trimethyl tocol
β – Tocopherol : 5,8-dimethyl tocol
γ – Tocopherol : 7,8-dimethyl tocol
Vitamin E -chemistry

67. Fig. 10-17, p. 353
Only form with
biologic activity
Vitamin E -chemistry

68. Plant sources
Wheat germ oil
Cotton seed oil
Corn oil
peanut oil
Sunflower oil
Animal sources
Meat
Milk
Butter
eggs
Sources of Vitamin E

69. Vitamin E recommended
dietary allowance(RDA)
 Daily requirement :
Men :10 mg(15 IU) of α- tocopherol
Women : 8 mg(12 IU) of α- tocopherol
1 mg of α- tocopherol =1.5 IU
Requirement is more in Lactating and
pregnant women

70. Absorption-transport
storage
 Synthetic forms are de-esterified
• Free alcohol forms are absorbed
passively in micelles; non-saturable
• 20-80% absorption; better with fats
• Incorporated into chylomicrons in
intestinal cell and sent out into lymph
• Transfer between chylomicrons, HDLs
and LDLs occurs in the blood. HDLs
and LDLs contain highest
concentration of the vitamin
• Half-life of about 48 hrs.
• Some stored in adipose, liver, lung,
heart, muscle, adrenals
Diet
Bile
lymph
Biochemical
functions

71. Biochemical functions
 Vitamin E having Anti-oxidant property.
 It prevents non-enzymatic oxidation of
various cell components (unsaturated
fatty acids present in phospholipids) by
Molecular oxygen, Free radicals
-superoxide (O2 ̄ )
-hydrogen peroxide(H2O2)
It protects poly unsaturated fatty acids
from peroxidation reactions by getting
oxidized itself. Selenium required for this.

72. Biochemical functions
 Lipid peroxidation :

73. Vitamin E Anti-oxidant function

+ R
Selenium
+RH
Biochemical functions

74.  Vitamin E prevents oxidation of
polyunsaturated fatty acids, LDL
cholesterol, vitamin A, Carotenes.
 Because of its anti-oxidant property it
maintains membrane integrity and
structure of cells.
 Prevents hemolysis as protects RBC
membrane.
 Prevents sterility as maintains germinal
epithelium of gonads.
Biochemical functions

75.  Increases Heme synthesis by enhancing δ-
aminolevulinic acid synthase and ALA
dehydratase.
 Stabilizes Co-enzyme Q component of
electron transport chain for cellular
respiration
 Protects liver from toxins such CCl4
 Involved in Nucleic acid synthesis,
absorption of amino acids from intestine.
 Proper storage of creatine in skeletal
muscle requires Vitamin E.
Biochemical functions

76. Vitamin E- Deficiency
 Symptoms of Vitamin E deficiency not
seen in humans except in severe
condition increased fragility of RBC
and minor neurological symptoms.
 In animals deficiency leads to sterility.
Toxicity:
Vitamin E least toxic even after ingestion
of 300 mg/day for 23 days also no toxic
symptoms reported.

77. Fat soluble
vitamins
Vitamin K

78. Vitamin K -chemistry
 Vitamin K very important for blood
coagulation (K-german word
Koagulation)
 Biologically Different forms available -
K1: phylloquinone present in plants
K2: menaquinone produced by intestinal
bacteria present animals
K3 : menadione is synthetic form

79. Three varieties of VitaminK are Naphthoquinone deri-
vatives and Isoprenoid side chain present in K1,K2.
K1
K2
 K3
Vitamin K -chemistry

80. Sources of Vitamin K
Plant sources
Cabbage
Cauliflower
Tomatoes
Alfa alfa
Spinach
Green
vegetables
Animal sources
Meat
Liver
Cheese
Egg yolk
Dairy products
Interstinal
bacteria

81. Vitamin K recommended
dietary allowance(RDA)
 Daily requirement :
Adult : 70-140 µg/day
Requirement 50% is provided by diet.
Another 50% is met from intestinal
bacterial synthesis

82. Absorption-transport
storage
Absorption: in micelles;
incorporated into
chylomicrons, then
chylomicron remnants,
then VLDLs, then HDLs
and LDLs.
Found mainly in liver and
heart. Turnover is once
every 2.5 hrs.
Stored mainly in liver and
less extent in other tissues
Diet Bile
+ Intestinal
Bacteria
GUT lymph
Biochemical
functions

83. Biochemical functions
 Vitamin K important for blood clotting
process.
 It brings post translational(after protein
synthesis in the cell) modification of
certain blood clotting factors such as
factor no. ll, vll, lx, x in liver.
 Vitamin K acts as a coenzyme for the
carboxylation of glutamic acid residues of
protein convert into γ-carboxyglutamate.
 The γ-carboxyglutamic acid are negatively
charged (COO-) and they combine with
positively charged Ca2+ to form a complex.

84.  Dicumarol, Warfarin are inhibitors of
Vitamin- K action -anticoagulants.
 Vitamin K required for the
carboxylation of glutamic acid residues
of Osteocalcin, a calcium binding
protein present in the bone.
Biochemical functions

85. Fig. 10-21, p. 363
Blood coagulation process

86. Fig. 10-23, p. 364
Vitamin K cycle
Needed for protein
carboxylation
Vit. K usually only present
in this form in the body
Osteocalcin or Bone Gla protein
Matrix Gla protein
Biochemical functions

87. Deficiency: rare in adults;
newborns, chronic antibiotic
administration, and
malabsorption can result in
deficiency
Bleeding episodes
Osteoporosis
Toxicity: Administration of
Large doses produces
hemolytic anaemia and
jaundice in infants.
Vitamin K- Deficiency