2. What are vitamins ?
Essential organic compounds that are required in small
amounts for normal growth, maintenance of good health
and for the proper utilization of other nutrients.
Nutrients that our body does not make on its own. Thus
we must obtain them from the foods we eat, or via vitamin
supplements.
3. VITAMINS
Fat Soluble
Vitamin A
Vitamin D
Vitamin E
Vitamin K
Water Soluble
B-Complex
Energy
releasing
Thiamine
Riboflavin
Niacin
Pyridoxine
Biotin
Pantothenic
acid
Hematopoietic
Folic acid
Vitamin
B12
Non B-
Complex Vitamin C
Classification of
Vitamins
4. Fat soluble vitamins
• Soluble in fat
• Absorbed along with other lipids
• Requires carrier proteins
• Stored in liver
• Deficiency manifests only when
stores are depleted
• Toxicity - Hypervitaminosis may
result
• Single large does may prevent
deficiency
• E.g. A,D,E & K
• Soluble in water
• Absorption is simple
• No requirement of carrier protein
• Excreted in urine
• Deficiency manifests rapidly as
there is no storage
• Unlikely , since excess is excreted
• Regular dietary supply is required
• E.g. B complex & C
Difference between fat soluble and water soluble vitamins
Water soluble vitamins
5. Hydrophobic
Isoprene derivatives
They cannot be synthesized by the body
Supplied by the diet
Absorption along with fat
Transport: By lipoprotein & Specific binding protein
Surplus amount stored – liver & adipose tissue
Excess consumption leads to accumulation & toxic effects.
Lipid soluble vitamins - common features
7. Introduction
• Vitamin A is an essential nutrient needed in small amounts
for the normal functioning of the visual system, and
maintenance of cell function for 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
INDIA.
8. Where does it come from?
Animal Sources
Eggs
Meat
Cheese
Milk
Liver
Kidney
Fish liver oils
Plant Sources
Carrots
Sweet Potatoes
Apricots
Broccoli
Spinach
Pumpkin
Papaya
Mango
9. Vitamin A
(Preformed and Provitamin)
• Retinoids: Natural & synthetic forms of Vitamin A
• Preformed: Three preformed compounds that are metabolically
active and found in animal products
– Retinol – alcohol form
– Present in animal tissues as retinyl ester with long chain
fatty acid
– Retinal or retinaldehyde – aldehyde form
– Obtained by oxidation of retinol
– Retinal & Retinol are interconvertible
– Retinoic acid – acid form
– Produced by oxidation of Retinal
10. • Provitamin: Carotenoids (β-carotene) can yield 2
retinols when metabolized in the body
• β -carotene
found in plants
Has 2 β-ionone rings connected by a polyprenoid
chain
11.
12.
13. Absorption
• Retinoids
– Retinyl esters broken down to free retinol & FA in small
intestine - requires bile, digestive enzymes, integration into
micelles
– Once absorbed, retinyl esters reformed in intestinal cells
– 90% of retinoids can be absorbed
• Carotenoids
– Absorbed intact, absorption rate much lower
– Intestinal cells can convert carotenoids to retinoids
14. • Approximately 80% is absorbed.
• It is passed along with fat through the lymphatic system
into blood stream.
• Absorption is poor in case of diarrhea, jaundice and
abdominal disorder.
• Absorption increases if taken with fat.
• Vitamin A which is not absorbed is excreted within 1 or 2
days in feces .
15. Transport
• Transported via chylomicrons from intestinal cells to the
liver
• Transported from the liver to target tissue as retinol via
retinol-binding protein (RBP; MW. 21,000).
From intestine to Liver
From liver to tissue
Plasma retinol binding protein(RBP)– to cell membrane-
Cellular retinoic-acid binding protein(CRBP) –retinol—
cytoplasm—HRE—GENE EXPRESSION
Chylomicron
19. 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 9months or
more.
20. Excretion of Vitamin A
• Not readily excreted
• Kidney disease and aging increase risk of toxicity because
excretion is impaired
21. 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
22. Role of Vitamin A in Vision
Visual Cycle (Wald’s Visual Cycle)
A process by which light impacting 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
23. Role of Vitamin A in Vision
Retina is a light-sensitive layer of cells at the back of the
eye where an image is formed
Retina consists of: Rod and cone cells (photosensitive
cells)
Rod cells process & image
Cone cells process color image
26. Role of Vitamin A in Vision
Normal vision depends on the retina and on adequate
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
29. 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
30. Role of Vitamin A in Vision
Dark Adaptation time
Bright light depletes rhodopsin (photobleaching)
Sudden shift from bright light to darkness causes
difficulty in seeing
Rhodopsin is synthesized in a few minutes and vision is
improved in the dark
31. 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
32. Bleaching of Rhodopsin
• Bleaching - When exposed to light, the colour of
rhodopsin changes from red to yellow
• Occurs in a few milliseconds
• Unstable intermediates are formed
Rhodopsin Prelumirhodopsin Lumirhodopsin
Metarhodopsin I
Metarhodopsin II
All-trans-retinal +
Opsin
33. • Light strikes the retina – biochemical changes –
membrane hyperpolarization – generate nerve impulse.
• Hyperpolarization of the membrane is brought about by
a visual cascade involving cGMP
Visual cascade and cGMP
34. Visual cascade involving cGMP
• Decrease in cGMP closes
the Na+ channels in the
membranes of the rod
cells
• Result in
hyperpolariztion – an
excitatory response
transmitted through the
neuron network to the
visual cortex of the
brain
35. Colour vision
• Cones are specialized in bright and colour vision
• Governed by colour sensitive pigmens
iodopsin – green
cyanopsin – blue
porphyropsin – red
• These pigments are complexes of protein & Vitamin A
• Bright light strikes retina – depending on the
particular colour of the light – one or more pigments
are bleached – passes nerve impulse to brain as
specific colour
36. Functions of Vitamin A:
Growth and Differentiation of Cells
• Retinoic acid is necessary for cellular differentiation
• Important for embryo development, gene expression
• Retinoic acid influences production, structure, and
function of epithelial cells that line the outside (skin)
and external passages (mucus forming cells) within the
body
37. Epithelial cell ‘integrity’
• Many epithelial cell require Vitamin A for proper
differentiation and maintenance
• Lack of Vitamin A leads to dysfunction of epithelia
– The skin becomes keratinized and scaly, and mucus
secretion is suppressed
38.
39. Functions of Vitamin A: Immunity
• Deficiency leads to decreased resistance to infections
• Supplementation may decrease severity of infections in
deficient person
40. • Role in Prevention of cardiovascular disease
– Antioxidant capabilities
• Role in Cancer prevention
– Antioxidant capabilities
– Lung, oral, and prostate cancers
– Studies indicate that vitamin A-containing foods are more
protective than supplements
41. What does RDA mean?
• Recommended Dietary Allowances
• These are suggested levels of essential nutrients
considered adequate to meet nutritional needs of healthy
individuals.
Infants and children - 400-600µg/day
Men -750-1000µg/day
Women -750µg/day
Pregnancy -1000µg/day
Lactation -1200µg/day
42. Vitamin A Deficiency and Diseases
Nyctalopia (night blindness)
Xerophthalmia
Bitot’s spots
Keratomalacia
Complete blindness (in severe deficiency)
43. 1. Night Blindness
• Visual acuity is diminished in dim
light
• Occurs as a result of inadequate
pigment in the retina.
• The dark adaptation time is
increased
• Found in pregnant women in
some instances, especially during
the last trimester of pregnancy
when the vitamin A needs are
increased.
44. It is the most specific VAD,
and is the leading
preventable cause of
blindness
Conjunctiva becomes dry,
thick and wrinkled
Conjunctiva gets keratinized
and loses its normal
transparency
Cornea becomes glazy &
lusterless
2. Xerophthalmia
45. 3. Bitot’s Spot
• Tissue spots that develop around
the eye ball, causing severe
dryness in the eyes.
• Seen as grayish-white triangular
plaques firmly adherent to the
conjunctiva.
46. 4.Keratomalacia
• One of the major cause for
blindness in India.
• Cornea becomes soft and may
burst
• Prolonged xerophthalmia
leads to keratomalacia
(softening of the cornea)
• If the eye collapses vision is
lost.
47. Other Symptoms of VAD
• Alteration of skin and mucous membrane
• Hepatic dysfunction
• Headache
• Drowsiness
• Peeling of skin
48. • Dark adaptation test
• Serum RBP
• Serum vitamin A
25 – 50 µg/dl
ASSESSMENT OF DEFICIENCY
49. 1) Eating of polar bear liver
2) Excess supplementation of
Vitamin A
When?
TOXICITY
One ounce of polar bear
liver contains enough
vitamin A (retinol) to kill a
person!
50. • Hepatomegaly
• Increased cerebrospinal fluid pressure
• Disturbance in calcium homeostasis – skletal
decalcificaion – tendrness of long bones
• Skin - Excessive dryness, desquamation
TOXICITY