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Dr.
P.
N.
ANSIL
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.
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
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
 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
VITAMIN A
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.
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
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
• 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
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
• 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 .
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
Summary of Vitamin A
absorption
Summary of the functions of Vitamin A
compounds
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.
Excretion of Vitamin A
• Not readily excreted
• Kidney disease and aging increase risk of toxicity because
excretion is impaired
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
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
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
Rod Cell
Cone Cell
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
Wald’s Visual Cycle
The Visual
Cycle
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
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
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
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
• 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
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
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
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
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
Functions of Vitamin A: Immunity
• Deficiency leads to decreased resistance to infections
• Supplementation may decrease severity of infections in
deficient person
• 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
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
Vitamin A Deficiency and Diseases
 Nyctalopia (night blindness)
 Xerophthalmia
 Bitot’s spots
 Keratomalacia
 Complete blindness (in severe deficiency)
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.
 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
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.
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.
Other Symptoms of VAD
• Alteration of skin and mucous membrane
• Hepatic dysfunction
• Headache
• Drowsiness
• Peeling of skin
• Dark adaptation test
• Serum RBP
• Serum vitamin A
25 – 50 µg/dl
ASSESSMENT OF DEFICIENCY
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!
• Hepatomegaly
• Increased cerebrospinal fluid pressure
• Disturbance in calcium homeostasis – skletal
decalcificaion – tendrness of long bones
• Skin - Excessive dryness, desquamation
TOXICITY
1.Dietary Deficiency
2. Retinoic acid
a. Psoriasis
b. Pro-myelocytic leukemia
c. Acne
THERAPEUTIC USES
Thank you

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Vitamina 151219041057

  • 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
  • 16.
  • 17. Summary of Vitamin A absorption
  • 18. Summary of the functions of Vitamin A compounds
  • 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
  • 24.
  • 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
  • 51. 1.Dietary Deficiency 2. Retinoic acid a. Psoriasis b. Pro-myelocytic leukemia c. Acne THERAPEUTIC USES