Vitamins .......,..............................

Vitamins mbbs biochemistry

1. VITAMINS

2. Learning Objectives
Define, classify vitamins and enumerate the difference
between fat soluble and water soluble vitamins
Describe the metabolism, biochemical functions,
deficiency diseases associated with inadequate intake,
and toxicity of excessive intakes of the vitamins
Learning Objectives
Define, classify vitamins and enumerate the difference
between fat soluble and water soluble vitamins
Describe the metabolism, biochemical functions,
deficiency diseases associated with inadequate intake,
and toxicity of excessive intakes of the vitamins

3. Definition and classification of vitamins
Vitamins are organic nutrients that are required in small
quantities for a variety of biochemical functions and
which generally cannot be synthesized by the body and
must, therefore, be supplied by the diet.
Some vitamins can be synthesized by intestinal
microorganisms, but in quantities that are not sufficient to
meet our needs.
Definition and classification of vitamins
Vitamins are organic nutrients that are required in small
quantities for a variety of biochemical functions and
which generally cannot be synthesized by the body and
must, therefore, be supplied by the diet.
Some vitamins can be synthesized by intestinal
microorganisms, but in quantities that are not sufficient to
meet our needs.

4. Classification of vitamins
1.Water soluble vitamins
2. Fat soluble vitamins
Classification of vitamins
1.Water soluble vitamins
2. Fat soluble vitamins

5. Water soluble vitamins
Vitamin B complex, e.g.
– Thiamine (vitamin B1)
– Riboflavin (vitamin B2)
– Niacin (vitamin B3)
– Pantothenic acid (vitamin B5)
– Pyridoxine (vitamin B6)
– Biotin
– Folic acid
– Cobalamin (vitamin B12)
Vitamin C or ascorbic acid.
Water soluble vitamins
Vitamin B complex, e.g.
– Thiamine (vitamin B1)
– Riboflavin (vitamin B2)
– Niacin (vitamin B3)
– Pantothenic acid (vitamin B5)
– Pyridoxine (vitamin B6)
– Biotin
– Folic acid
– Cobalamin (vitamin B12)
Vitamin C or ascorbic acid.

6. Fat soluble vitamins
– Vitamin A or retinol
– Vitamin D or cholecalciferol
– Vitamin E or tocopherol
– Vitamin K.
Fat soluble vitamins
– Vitamin A or retinol
– Vitamin D or cholecalciferol
– Vitamin E or tocopherol
– Vitamin K.

7. Fat Soluble Vs. Water Soluble Vitamins
Fat soluble vitaminsWater soluble vitamins
Function as coenzymes,
hormones and
antioxidants
Function as precursor for
coenzymes and
antioxidants
Function as coenzymes,
hormones and
antioxidants
Function as precursor for
coenzymes and
antioxidants
Toxicwhen taken in
excessive quantities
Usuallynon-toxic
Can be stored Not stored extensively
except vitamin B
12,

8. Thiamine (Vitamin B1)
Thiamineconsists of a pyrimidine ring attached to a thiazole
ringbymethylene bridge.
Structureof thiamin.

9. Active Form ofThiamine
Thiamine pyrophosphate (TPP) is an active coenzyme
form of vitamin thiamine

10. Sources
Itis present in all natural foods but particularlygood
dietarysources are unrefined cereals, meat, nuts,green
vegetables, eggs, etc.
Whitebread and polished rice are very poor sources of
thevitaminthiamine.
Sources
Itis present in all natural foods but particularlygood
dietarysources are unrefined cereals, meat, nuts,green
vegetables, eggs, etc.
Whitebread and polished rice are very poor sources of
thevitaminthiamine.

11. Functions
Thiamineis required mainly for carbohydrate
metabolism
Thiaminepyrophosphate (TPP) is a coenzyme involved
inoxidativedecarboxylationandtransketolase
reactions.
Functions
Thiamineis required mainly for carbohydrate
metabolism
Thiaminepyrophosphate (TPP) is a coenzyme involved
inoxidativedecarboxylationandtransketolase
reactions.

12. 1.Oxidative Decarboxylation
TPP is a coenzyme forpyruvate dehydrogenasecomplex
which catalyzes the conversion of pyru­vate into acetyl
CoA.
Acetyl-CoA is a precursor for the synthesis of
neurotransmitter acetylcholine and also for the synthesis
of myelin. Thus, thiamine is required for the normal
functioning of the nervous system.
1.Oxidative Decarboxylation
TPP is a coenzyme forpyruvate dehydrogenasecomplex
which catalyzes the conversion of pyru­vate into acetyl
CoA.
Acetyl-CoA is a precursor for the synthesis of
neurotransmitter acetylcholine and also for the synthesis
of myelin. Thus, thiamine is required for the normal
functioning of the nervous system.

13. 2.TPP is a coenzyme forα-ketoglutarate dehydro­genase
which catalyzes the conversion ofα-ketoglutarate to
succinyl-CoA in TCA cycle
3. TPP is a coenzyme for the enzymetransketolase, in the
pentose phosphate pathway of glucose oxidation
2.TPP is a coenzyme forα-ketoglutarate dehydro­genase
which catalyzes the conversion ofα-ketoglutarate to
succinyl-CoA in TCA cycle
3. TPP is a coenzyme for the enzymetransketolase, in the
pentose phosphate pathway of glucose oxidation

14. Nutritional Requirements
NutritionalResearchCouncil recommends daily intake
of1.0 to1.5 mgof thiamine for adults which is increased
with increased muscular activity, dietarycarbohydrates
andin pregnancy and lactation.
Nutritional Requirements
NutritionalResearchCouncil recommends daily intake
of1.0 to1.5 mgof thiamine for adults which is increased
with increased muscular activity, dietarycarbohydrates
andin pregnancy and lactation.

15. DeficiencyManifestations
Thedeficiency of vitamin B1 results in a condition called
beriberi.
Deficiencyof thiamine occurs in population who consume
exclusively polished rice as staple food.
Theearly symptoms of thiamine deficiency areanorexia
(lackofappetite) ,nausea, mental confusion, peripheral
neuritis,and muscle fatigue.
DeficiencyManifestations
Thedeficiency of vitamin B1 results in a condition called
beriberi.
Deficiencyof thiamine occurs in population who consume
exclusively polished rice as staple food.
Theearly symptoms of thiamine deficiency areanorexia
(lackofappetite) ,nausea, mental confusion, peripheral
neuritis,and muscle fatigue.

16. Beriberi
Beriberiis dividedinto threetypes,relating to the body
system involvedi.e.Nervousorcardiovascularorage of
patient (infantile).
1. Dry beriberi (neuritic beriberi):affects the nervous system
2. Wet beriberi(cardiac beriberi):affectscardiovascular system
3. Infantile beriberi:affectschildrenof malnourished mothers.
Beriberi
Beriberiis dividedinto threetypes,relating to the body
system involvedi.e.Nervousorcardiovascularorage of
patient (infantile).
1. Dry beriberi (neuritic beriberi):affects the nervous system
2. Wet beriberi(cardiac beriberi):affectscardiovascular system
3. Infantile beriberi:affectschildrenof malnourished mothers.

17. Dry beriberi (neuritic beriberi)
Itdevelops when the diet chronically contains slightly less
thanrequirements.Itis characterized by:
–Vomiting.
–Poor appetite
–Peripheralneuritis
–Difficulty inwalking
–Tingling or loss of sensation, numbness in hands
and feet
Dry beriberi (neuritic beriberi)
Itdevelops when the diet chronically contains slightly less
thanrequirements.Itis characterized by:
–Vomiting.
–Poor appetite
–Peripheralneuritis
–Difficulty inwalking
–Tingling or loss of sensation, numbness in hands
and feet

18. –Severemuscular weakness and fatigue.
–Mental confusion/speech difficulties
–Dry skin
–Involuntary eye movements (nystagmus)
–Severemuscular weakness and fatigue.
–Mental confusion/speech difficulties
–Dry skin
–Involuntary eye movements (nystagmus)

19. Wet beriberi (cardiac beriberi)
Itdevelops when the deficiency is more severe in which
cardiovascular system is affected in addition to
neurological symptoms.
Wetberiberi is characterizedby:
−PeripheralEdema (swelling of lower legs)
−Heartenlargement and cardiac insuffi­ciency.
−Increasedheartratetachycardia
−Itis sometimes fatal
Wet beriberi (cardiac beriberi)
Itdevelops when the deficiency is more severe in which
cardiovascular system is affected in addition to
neurological symptoms.
Wetberiberi is characterizedby:
−PeripheralEdema (swelling of lower legs)
−Heartenlargement and cardiac insuffi­ciency.
−Increasedheartratetachycardia
−Itis sometimes fatal

20. Infantileberiberi
Infantileberiberi is observed in breast fed infants
(betweentwo and six months ofage) whose
mothers have inadequate thiamineintake.The
breast milk of these mothers is deficient in
thiamine.
Infantileberiberi
Infantileberiberi is observed in breast fed infants
(betweentwo and six months ofage) whose
mothers have inadequate thiamineintake.The
breast milk of these mothers is deficient in
thiamine.

21. Itis characterizedby
−GI disturbances such as vomiting ,diarrhea
−Cardiac dilation (enlargement of heart),
−Tachycardia (rapid heart rate)
−Convulsions,
−Edema
−In acute condition, the infant may die due to
cardiac failure.
Itis characterizedby
−GI disturbances such as vomiting ,diarrhea
−Cardiac dilation (enlargement of heart),
−Tachycardia (rapid heart rate)
−Convulsions,
−Edema
−In acute condition, the infant may die due to
cardiac failure.

22. Wernicke-Korsakoff Syndrome
Wernicke-Korsakoff Syndrome (WKS) is aneurological
disordercaused by a deficiency of vitamin thiamine
(vitamin B1)duetochronic alcoholconsumption
It is also known ascerebral beriberi.
In chronic alcoholics, the nutritional deficiencies result
from either poor intake of food or malabsorp­tion of
nutrients from intestine.
Wernicke-Korsakoff Syndrome
Wernicke-Korsakoff Syndrome (WKS) is aneurological
disordercaused by a deficiency of vitamin thiamine
(vitamin B1)duetochronic alcoholconsumption
It is also known ascerebral beriberi.
In chronic alcoholics, the nutritional deficiencies result
from either poor intake of food or malabsorp­tion of
nutrients from intestine.

23. Symptoms
Mentalconfusion and impaired short-term memory.
Impairedperson’s ability to learn new information or tasks.
Ataxia(Loss of muscle coordination that can cause weakness
inlimbsand leg tremor)
Paralysisof eye muscles
Nystagmus(Abnormal eyemovements back & forth
movements of eye)
Double vision, eyelid drooping
Symptoms
Mentalconfusion and impaired short-term memory.
Impairedperson’s ability to learn new information or tasks.
Ataxia(Loss of muscle coordination that can cause weakness
inlimbsand leg tremor)
Paralysisof eye muscles
Nystagmus(Abnormal eyemovements back & forth
movements of eye)
Double vision, eyelid drooping

24. Antimetabolites
Thiamine can be destroyed if the diet containsthiaminase.
Thiaminase is present in raw fish and seafood.
Thiamine Assay
Whole blood or Erythrocyte transketolase (requiring TPP
as a coenzyme) activity is used as a measure of thiamine
deficiency.
Antimetabolites
Thiamine can be destroyed if the diet containsthiaminase.
Thiaminase is present in raw fish and seafood.
Thiamine Assay
Whole blood or Erythrocyte transketolase (requiring TPP
as a coenzyme) activity is used as a measure of thiamine
deficiency.

25. Riboflavin (Vitamin B2)
Riboflavinis a yellow compound (Flavus =yellowin
Latin) consisting of aisoalloxazine ringwith aribitol
(sugar alcohol) side chain

26. ActiveForm ofRiboflavin
 Flavin mononucleotide(FMN)
 Flavin adenine dinucleotide(FAD)
ActiveForm ofRiboflavin
 Flavin mononucleotide(FMN)
 Flavin adenine dinucleotide(FAD)

27. Structureof riboflavin and its active coenzyme forms FMN and
FAD.

28. Sources
Themain dietary sources of riboflavin are yeast,
germinating seeds, green leafy vegetables milk and milk
products, eggs, liver, meat etc.
Cerealsare a poorsource
Sources
Themain dietary sources of riboflavin are yeast,
germinating seeds, green leafy vegetables milk and milk
products, eggs, liver, meat etc.
Cerealsare a poorsource

29. NutritionalRequirements
TheRDA for vitamin B
2is1.3 to 1.7 mgfor adults.
Itis related to protein use and increases during growth,
pregnancy, lactation and wound healing.
NutritionalRequirements
TheRDA for vitamin B
2is1.3 to 1.7 mgfor adults.
Itis related to protein use and increases during growth,
pregnancy, lactation and wound healing.

30. Functions
Riboflavinis a precursor of coenzymesFMNandFAD, which
are required by severaloxidation-reductionreactions in
metabolism.
FMNand FAD serve as coenzymes for oxidoreductase
enzymes involved incarbohydrate,protein,lipid,nucleic acid
metabolism andelectron transport chain.
Decarboxylation of pyruvate andα-ketoglutarate requires FAD
Fatty acyl CoA dehydrogenase requires FAD in fatty acid
oxidation
Functions
Riboflavinis a precursor of coenzymesFMNandFAD, which
are required by severaloxidation-reductionreactions in
metabolism.
FMNand FAD serve as coenzymes for oxidoreductase
enzymes involved incarbohydrate,protein,lipid,nucleic acid
metabolism andelectron transport chain.
Decarboxylation of pyruvate andα-ketoglutarate requires FAD
Fatty acyl CoA dehydrogenase requires FAD in fatty acid
oxidation

31. Synthesis ofactiveform of folate(5-methyl THF) requires
FADH
2
FADis required to converttryptophantoniacin(vitB
3)
Reduction of the oxidized form ofglutathione (GSSG)to
itsreduced form (GSH)is also FADdependent. Thus they
are also involved indetoxification reactions
It is needed for maintenance ofmucosal epithelial&
ocular tissues.
Synthesis ofactiveform of folate(5-methyl THF) requires
FADH
2
FADis required to converttryptophantoniacin(vitB
3)
Reduction of the oxidized form ofglutathione (GSSG)to
itsreduced form (GSH)is also FADdependent. Thus they
are also involved indetoxification reactions
It is needed for maintenance ofmucosal epithelial&
ocular tissues.

32. DeficiencyManifestations
Riboflavindeficiency (ariboflavinosis) is quite
rare. Itis most commonly seen in chronic
alcoholics.
DeficiencyManifestations
Riboflavindeficiency (ariboflavinosis) is quite
rare. Itis most commonly seen in chronic
alcoholics.

33. Thecharacteristic symptoms of riboflavin deficiency are:
Cheilosis:Cracksattheanglesofthemouth,
Glossitis:Inflammationofthetonguethatbecomes
swollenandmagentacolored
Dermatitis:Roughandscalyskin
Vascularization(thedevelopmentofbloodvessels)
ofcornea.Theeyesbecomered,itchy,wateryand
sensitivetobrightlight.
Thecharacteristic symptoms of riboflavin deficiency are:
Cheilosis:Cracksattheanglesofthemouth,
Glossitis:Inflammationofthetonguethatbecomes
swollenandmagentacolored
Dermatitis:Roughandscalyskin
Vascularization(thedevelopmentofbloodvessels)
ofcornea.Theeyesbecomered,itchy,wateryand
sensitivetobrightlight.

34. Niacin (Vitamin B
3)
Structure
Niacin is a general name for thenicotinic acidand
nicotinamide, either of which may act as a source of the
vitamin in the diet. Niacin is a simple derivative of
pyridine.
Niacin (Vitamin B
3)
Structure
Niacin is a general name for thenicotinic acidand
nicotinamide, either of which may act as a source of the
vitamin in the diet. Niacin is a simple derivative of
pyridine.

35. ActiveForm
Active forms of niacin are:
Nicotinamideadenine dinucleotide(NAD+)
Nicotinamideadenine dinucleotide phosphate(NADP+)
ActiveForm
Active forms of niacin are:
Nicotinamideadenine dinucleotide(NAD+)
Nicotinamideadenine dinucleotide phosphate(NADP+)

38. Sources
Yeast, liver, legumes and meats are major sources of niacin.
Limitedquantities of niacin can also be obtained from the
metabolism of tryptophan.For every 60 mg of tryptophan, 1
mg equivalent of niacin can be generated.
NutritionalRequirement
TheRDA for niacin is15 to 20 mg.
Tryptophancan only provide10% of the totalniacin
requirement.
Sources
Yeast, liver, legumes and meats are major sources of niacin.
Limitedquantities of niacin can also be obtained from the
metabolism of tryptophan.For every 60 mg of tryptophan, 1
mg equivalent of niacin can be generated.
NutritionalRequirement
TheRDA for niacin is15 to 20 mg.
Tryptophancan only provide10% of the totalniacin
requirement.

39. Functions
Niacinis a precursor of coenzymes,nicotinamide adenine
dinucleotide (NAD+)andnicotinamide adenine
dinucleotide phosphate (NADP+).
NAD+ and NADP+ are involved in variousoxidationand
reductionreactions.
Theyare, therefore involved in many metabolic pathways
of carbohydrate, lipid and protein.
Functions
Niacinis a precursor of coenzymes,nicotinamide adenine
dinucleotide (NAD+)andnicotinamide adenine
dinucleotide phosphate (NADP+).
NAD+ and NADP+ are involved in variousoxidationand
reductionreactions.
Theyare, therefore involved in many metabolic pathways
of carbohydrate, lipid and protein.

40. Generally,NAD+catalyze oxidation-reduction reactions
inoxidative path­ways, e.g. citric acid cycle and
glycolysis.
WhereasNADP+are oftenfound in pathways concerned
withreductive synthesis, e.g. synthesis of cholesterol,
fatty acid and pentose phosphate pathways.
Generally,NAD+catalyze oxidation-reduction reactions
inoxidative path­ways, e.g. citric acid cycle and
glycolysis.
WhereasNADP+are oftenfound in pathways concerned
withreductive synthesis, e.g. synthesis of cholesterol,
fatty acid and pentose phosphate pathways.

42. Deficiency Manifestation
Pellagra
Deficiencyof niacin in human causes pellagra, a
disease involving:
Skin
Gastrointestinaltract
Centralnervous system.
Deficiency Manifestation
Pellagra
Deficiencyof niacin in human causes pellagra, a
disease involving:
Skin
Gastrointestinaltract
Centralnervous system.

43. The symptoms of pellagra are characterized by three‘Ds’:
1.PhotosensitiveDermatitis
2. Diarrhea
3.Depressive psychosis (dementia) andif nottreateddeath.
Untreated pellagrais fatal.
The symptoms of pellagra are characterized by three‘Ds’:
1.PhotosensitiveDermatitis
2. Diarrhea
3.Depressive psychosis (dementia) andif nottreateddeath.
Untreated pellagrais fatal.

44. Niacindeficiency occurs in:
Populationdependent on maize (corn) or sorghum
(jowar)as the staple food.
In maize, niacin ispresent inboundformniacytin.
Sorghum contenthighamount ofleucine. Excess of
leucineinhibit conversionoftryptophantoniacin
Niacindeficiency occurs in:
Populationdependent on maize (corn) or sorghum
(jowar)as the staple food.
In maize, niacin ispresent inboundformniacytin.
Sorghum contenthighamount ofleucine. Excess of
leucineinhibit conversionoftryptophantoniacin

45. Deficiency of vitamin B6(pyridoxal phosphate) leads to
niacin deficiencyas it is involved as a coenzyme in the
pathway of synthesis of niacin from tryptophan.
Malignantcarcinoid syndromein which tryptophan is
diverted to formation of serotonin.
InHartnup disease, a genetic disorder in which tryptophan
absorption and trans­portation is impaired.
Deficiency of vitamin B6(pyridoxal phosphate) leads to
niacin deficiencyas it is involved as a coenzyme in the
pathway of synthesis of niacin from tryptophan.
Malignantcarcinoid syndromein which tryptophan is
diverted to formation of serotonin.
InHartnup disease, a genetic disorder in which tryptophan
absorption and trans­portation is impaired.

46. Theconversion of tryptophan into nicotinic acid.

47. Pantothenic Acid (Vitamin B5)
The name pantothenic acid is derived from the Greek word
‘pantothene,’meaning from“everywhere”and gives an
indication of the wide distribution of the vitamin in foods.

48. Structure
Pantothenic acid is formed by combination of
pantoic acidandβ-alanine
Structure
Pantothenic acid is formed by combination of
pantoic acidandβ-alanine
Structureof pantothenic acid.

49. Activeform
1. Coenzyme-A(CoA-SH)
2. Acylcarrier protein (ACP).
Source
Eggs, liver, yeast, wheat germs, cereals, etc. are impor­tant
sources of pantothenic acid, although the vitamin is widely
distributed.
Activeform
1. Coenzyme-A(CoA-SH)
2. Acylcarrier protein (ACP).
Source
Eggs, liver, yeast, wheat germs, cereals, etc. are impor­tant
sources of pantothenic acid, although the vitamin is widely
distributed.

50. NutritionalRequirement
The RDA of pantothenic acid is not well established. A
daily intake of about 5–10 mg is advised for adults

51. Functions
Pantothenicacid is a component ofcoenzyme-A (CoA-
SH)andacyl carrier protein (ACP).
Thethiol (-SH) group of CoA-SH and ACP acts as a
carrier ofacyl groups.
Coenzyme-Aparticipates in reactions concerned with:
– Reactions of citric acidcycle
– Fatty acid synthesis and oxidation
– Synthesis of cholesterol
– Utilization of ketone bodies.
ACPparticipate in reactions concerned with fatty acid
synthesis.
Functions
Pantothenicacid is a component ofcoenzyme-A (CoA-
SH)andacyl carrier protein (ACP).
Thethiol (-SH) group of CoA-SH and ACP acts as a
carrier ofacyl groups.
Coenzyme-Aparticipates in reactions concerned with:
– Reactions of citric acidcycle
– Fatty acid synthesis and oxidation
– Synthesis of cholesterol
– Utilization of ketone bodies.
ACPparticipate in reactions concerned with fatty acid
synthesis.

52. DeficiencyManifestations
No clear-cut case of pantothenic acid deficiency has been
reported.
Clinical signs observed in experimentally induced
deficiencies are:
Paraesthesia(abnormal tingling sensation)
Headache
Dizziness
Gastrointestinal malfunction.
DeficiencyManifestations
No clear-cut case of pantothenic acid deficiency has been
reported.
Clinical signs observed in experimentally induced
deficiencies are:
Paraesthesia(abnormal tingling sensation)
Headache
Dizziness
Gastrointestinal malfunction.

53. Pyridoxine (Vitamin B
6)
Structure
Vitamin B
6consists of a mixture of three different closely
related pyridine derivativesnamely:
1.Pyridoxine
2.Pyridoxal
3.Pyridoxamine.
Allthe three have equal vitamin activity, as they can be
interconverted in the body.
Pyridoxine (Vitamin B
6)
Structure
Vitamin B
6consists of a mixture of three different closely
related pyridine derivativesnamely:
1.Pyridoxine
2.Pyridoxal
3.Pyridoxamine.
Allthe three have equal vitamin activity, as they can be
interconverted in the body.

54. Structureof three different forms of vitamin B

55. Active Form of Vitamin B
6
Pyridoxal phosphate (PLP) is the active form of vitamin
B
6.

56. Sources
Pyridoxineoccurs mainly in plants, whereas pyridoxal
and pyridoxamine are present mainly in animal
products.
Majordietary sources of vitamin B6 are yeast,
unrefined cereals, pulses, meat, poultry fish, potatoes
and vegetables.
Dairyproducts and grains contribute lesser amounts.
Sources
Pyridoxineoccurs mainly in plants, whereas pyridoxal
and pyridoxamine are present mainly in animal
products.
Majordietary sources of vitamin B6 are yeast,
unrefined cereals, pulses, meat, poultry fish, potatoes
and vegetables.
Dairyproducts and grains contribute lesser amounts.

57. NutritionalRequirement
The RDA for vitamin B
6is1.6to2.0 mg.
Requirementsincrease during pregnancy and lactation

58. Functions
Activeform of vitamin B6, pyridoxal phosphate(PLP)
acts as coenzyme inaminoacid metabolism. For
example:
– Transamination
– Decarboxylation
– Nonoxidative deamination
– Trans-sulfuration
– Condensation reactions of amino acids.
Functions
Activeform of vitamin B6, pyridoxal phosphate(PLP)
acts as coenzyme inaminoacid metabolism. For
example:
– Transamination
– Decarboxylation
– Nonoxidative deamination
– Trans-sulfuration
– Condensation reactions of amino acids.

59. Transaminationreactions
Transaminationreactionsare catalyzedby transaminases
andPLPacts as coenzyme converting amino acid to keto
acid, e.g. aspartate transaminase(AST)and alanine
transaminase(ALT)
Non-oxidativedeamination
Hydroxyl group contain­ing amino acids (serine,
threonine) arenon-oxidativelydeaminated toα-ketoacids
and ammonia, which requiresPLP.
Transaminationreactions
Transaminationreactionsare catalyzedby transaminases
andPLPacts as coenzyme converting amino acid to keto
acid, e.g. aspartate transaminase(AST)and alanine
transaminase(ALT)
Non-oxidativedeamination
Hydroxyl group contain­ing amino acids (serine,
threonine) arenon-oxidativelydeaminated toα-ketoacids
and ammonia, which requiresPLP.

60. Decarboxylation reaction
PLPacts as coenzyme in decarboxylation of some amino
acids. The amino acids are decarboxylated to corresponding
amines.
–γ-Aminobutyric acid(GABA)
–Serotoninandmelatonin
–Histamine
–Catecholamines(dopamine, norepinephrine and
epinephrine)
Decarboxylation reaction
PLPacts as coenzyme in decarboxylation of some amino
acids. The amino acids are decarboxylated to corresponding
amines.
–γ-Aminobutyric acid(GABA)
–Serotoninandmelatonin
–Histamine
–Catecholamines(dopamine, norepinephrine and
epinephrine)

61. Trans-sulfurationreaction:
PLPis a coenzyme for cystathionine synthase involved in
synthesis of cysteine from methionineInthese reactions
transfer of sulfur from methionine to serine occurs to
produce cysteine.
Condensationreactions
Pyridoxalphosphate is required for the condensation
reaction of L-glycine and succinyl CoAin the synthesis of
heme.
Trans-sulfurationreaction:
PLPis a coenzyme for cystathionine synthase involved in
synthesis of cysteine from methionineInthese reactions
transfer of sulfur from methionine to serine occurs to
produce cysteine.
Condensationreactions
Pyridoxalphosphate is required for the condensation
reaction of L-glycine and succinyl CoAin the synthesis of
heme.

62. Other reactions requiringPLPare:
–Forniacin coenzyme(NAD+/NADP+)synthesis
from tryptophan
–Forsynthesis of serine fromglycine
–FORthesynthesisofsphingomyelin.
Other reactions requiringPLPare:
–Forniacin coenzyme(NAD+/NADP+)synthesis
from tryptophan
–Forsynthesis of serine fromglycine
–FORthesynthesisofsphingomyelin.

63. Deficiency Manifestations
VitaminB
6deficiency causes neurological disorders such
asdepression,nervousnessandirritability.
Severedeficiency of pyridoxine causes epileptic seizures
(convulsions) ininfants.
Demyelinationof nerves causesperipheral neuro­pathy.
VitaminB
6deficiency causeshypochromic micro­cytic
anemiadue to decreased heme synthesis.
Deficiency Manifestations
VitaminB
6deficiency causes neurological disorders such
asdepression,nervousnessandirritability.
Severedeficiency of pyridoxine causes epileptic seizures
(convulsions) ininfants.
Demyelinationof nerves causesperipheral neuro­pathy.
VitaminB
6deficiency causeshypochromic micro­cytic
anemiadue to decreased heme synthesis.

64. The commonest cause of pyridoxine deficiency is:
Drugantagonism,e.g.isoniazide (INH),used in the
treatment of tuberculosis andpenicillamideused in the
treatment of Wilson’s disease and rheumatoid arthritis can
combine with pyridoxal phosphate forming an inactive
derivative with pyridoxal phosphate.
Alcoholism:Alcoholics may be deficient owing to
metabolism of ethanol to acetaldehyde, which stimulates
hydrolysis of the phosphate of the pyridoxal phosphate
The commonest cause of pyridoxine deficiency is:
Drugantagonism,e.g.isoniazide (INH),used in the
treatment of tuberculosis andpenicillamideused in the
treatment of Wilson’s disease and rheumatoid arthritis can
combine with pyridoxal phosphate forming an inactive
derivative with pyridoxal phosphate.
Alcoholism:Alcoholics may be deficient owing to
metabolism of ethanol to acetaldehyde, which stimulates
hydrolysis of the phosphate of the pyridoxal phosphate

65. Biotin
Biotin was known formerly as vitaminH.
Structure
It consists of atetrahydro-thiopheneringbound to an
imidazole ringand avaleric acidside chain.
Biotin
Biotin was known formerly as vitaminH.
Structure
It consists of atetrahydro-thiopheneringbound to an
imidazole ringand avaleric acidside chain.

66. Structureof biotin.

67. Sources
Itis widely distributed in foods.
Liver, kidneys, vegetables and egg yolk are the
important sources of biotin.
Biotinis also synthesized by intestinal bacteria.
Sources
Itis widely distributed in foods.
Liver, kidneys, vegetables and egg yolk are the
important sources of biotin.
Biotinis also synthesized by intestinal bacteria.

68. ActiveForm of Biotin
Enzyme-bound biotin, biocytinis an active form of biotin.
Biotin is covalently bound toε-aminogroup of lysine of an
enzyme to form biocytin.
NutritionalRequirements
A daily intake of about 150–300 mg is recommended for
adults. Biotin is synthesized by intestinal micro­organisms in
such a large quantities that a dietary source is probably not
necessary.
ActiveForm of Biotin
Enzyme-bound biotin, biocytinis an active form of biotin.
Biotin is covalently bound toε-aminogroup of lysine of an
enzyme to form biocytin.
NutritionalRequirements
A daily intake of about 150–300 mg is recommended for
adults. Biotin is synthesized by intestinal micro­organisms in
such a large quantities that a dietary source is probably not
necessary.

69. Functions
Biotin is a coenzyme ofcarboxylase reactions, where it is a
carrier ofCO2.
Conversion ofacetyl-CoAintomalonyl-CoAcatalyzed
by acetyl-CoA carboxylase in fatty acid synthesis.
Conversionofpyruvateintooxaloacetate, catalyzed by
pyruvate carboxylasein gluconeogenesis.
Functions
Biotin is a coenzyme ofcarboxylase reactions, where it is a
carrier ofCO2.
Conversion ofacetyl-CoAintomalonyl-CoAcatalyzed
by acetyl-CoA carboxylase in fatty acid synthesis.
Conversionofpyruvateintooxaloacetate, catalyzed by
pyruvate carboxylasein gluconeogenesis.

70. Conversionofpropionyl-CoAtoD-methyl malonyl-CoA
catalyzed bypropionyl-CoA carboxylasein the pathway
of conversionofpropionatetosuccinate.
Catabolismofbranched chain amino acidcatalyzed byβ-
methylcrotonyl-CoA carboxylase
Conversionofpropionyl-CoAtoD-methyl malonyl-CoA
catalyzed bypropionyl-CoA carboxylasein the pathway
of conversionofpropionatetosuccinate.
Catabolismofbranched chain amino acidcatalyzed byβ-
methylcrotonyl-CoA carboxylase

71. BiotinIndependent Carboxylation Reaction
Formationof carbamoyl phosphate by carbamoyl
phosphate synthetase in urea cycle.
Additionof CO2 to form C6 in purine ring.
Conversionof pyruvate to malate by malic enzyme.
BiotinIndependent Carboxylation Reaction
Formationof carbamoyl phosphate by carbamoyl
phosphate synthetase in urea cycle.
Additionof CO2 to form C6 in purine ring.
Conversionof pyruvate to malate by malic enzyme.

72. Deficiency Manifestation
Sincebiotin is widely distributed in plant and animal
foods and intestinal bacterial flora supply adequate
amounts of biotin, the natural deficiency of biotin is not
well characterized inhumans.
Theexperimentally induced symptoms of biotin
deficiency arenausea, anorexia, glossitis, dermatitis,
alopecia (loss of hair), depression and muscular pain.
Deficiency Manifestation
Sincebiotin is widely distributed in plant and animal
foods and intestinal bacterial flora supply adequate
amounts of biotin, the natural deficiency of biotin is not
well characterized inhumans.
Theexperimentally induced symptoms of biotin
deficiency arenausea, anorexia, glossitis, dermatitis,
alopecia (loss of hair), depression and muscular pain.

74. Deficiency of biotin occurs in:
Thepeople with the unusual dietary habit of consuming
large amounts of uncooked eggs. Egg white contains the
glycoproteinavidin,which binds the imidazole group of
biotin and prevents biotin absorption.
Useof antibiotics, that inhibit the growth of intestinal
bacteria, eliminates this source of biotin and leads to
deficiency of biotin.
Deficiency of biotin occurs in:
Thepeople with the unusual dietary habit of consuming
large amounts of uncooked eggs. Egg white contains the
glycoproteinavidin,which binds the imidazole group of
biotin and prevents biotin absorption.
Useof antibiotics, that inhibit the growth of intestinal
bacteria, eliminates this source of biotin and leads to
deficiency of biotin.

75. Folic Acid
Structure
Folic acid consists of three components:
1. Pteridinering,
2. P-aminobenzoic acid (PABA) and
3. L-glutamicacid
Ina folic acid molecule, the numberof glutamicacid
residues varies from one to seven. Folicacid usually
has one glutamic acid residue.
Folic Acid
Structure
Folic acid consists of three components:
1. Pteridinering,
2. P-aminobenzoic acid (PABA) and
3. L-glutamicacid
Ina folic acid molecule, the numberof glutamicacid
residues varies from one to seven. Folicacid usually
has one glutamic acid residue.

76. Thestructure and numbering of atoms of folic acid.

77. Active Form of FolicAcid
Tetrahydrofolate (THF)is the active form of folic acid.
Source
Folic acid is found in green leafy vegetables, liver, yeast.
Theword folate is related to folium which meansleafin
Latin.
Active Form of FolicAcid
Tetrahydrofolate (THF)is the active form of folic acid.
Source
Folic acid is found in green leafy vegetables, liver, yeast.
Theword folate is related to folium which meansleafin
Latin.

78. NutritionalRequirements
TheRDA of folate is200 mg.
Requirementsincrease during pregnancy and
lactation.

79. Formationoftetrahydrofolate fromfolic acid.

82. Functions
Tetrahydrofolate (THF)acts as a carrier of one-
carbonunits.The one carbon units are:
Methyl CH
3
Methylene CH
2
Methenyl CH
Formyl CHO
Formimino CH = NH
Functions
Tetrahydrofolate (THF)acts as a carrier of one-
carbonunits.The one carbon units are:
Methyl CH
3
Methylene CH
2
Methenyl CH
Formyl CHO
Formimino CH = NH

83. Onecarbon unit binds to THF throughN
5
orN
10
or both
N
5
, N
10
position.
TheTHF coenzymes serve as acceptors or donors of one
carbon units in a variety of reactions involved inamino
acidandnucleic acid metabolism.
Onecarbon unit binds to THF throughN
5
orN
10
or both
N
5
, N
10
position.
TheTHF coenzymes serve as acceptors or donors of one
carbon units in a variety of reactions involved inamino
acidandnucleic acid metabolism.

84. Five major reactions in which THF is involved are:
1. Conversion of serine to glycine:
The conversion ofserineto glycineis accompanied
by the formation of N
5
,N
10
-methylene THF.
2.Synthesis of thymidylate (pyrimidine nucleo­tide):
The enzymethymidylate synthasethat converts
deoxyuridylate(dUMP) into thymidy­late (TMP)
usesN
5
, N
10
-methylene THF as the methyl donor
for this reaction.
Five major reactions in which THF is involved are:
1. Conversion of serine to glycine:
The conversion ofserineto glycineis accompanied
by the formation of N
5
,N
10
-methylene THF.
2.Synthesis of thymidylate (pyrimidine nucleo­tide):
The enzymethymidylate synthasethat converts
deoxyuridylate(dUMP) into thymidy­late (TMP)
usesN
5
, N
10
-methylene THF as the methyl donor
for this reaction.

85. 3.Catabolismof histidine :
Histidinein the course of its catabolismis convertedinto
formimino­ glutamate(FIGLU).Thismolecule donatethe
formiminogroup to THF to produceN
5
formimino THF.
4. Synthesisof purine:
N
5
-FormylTHFinter­ mediate formedin histidine
catabolismis used in the biosyn­ thesis of purineand
thereforein theformationof bothDNAandRNA.
5.Synthesisof methionine from homocysteine:
Homocysteine is convertedtomethioninein presenceof
N
5
-methylTHF,and vitamin B
12
.
3.Catabolismof histidine :
Histidinein the course of its catabolismis convertedinto
formimino­ glutamate(FIGLU).Thismolecule donatethe
formiminogroup to THF to produceN
5
formimino THF.
4. Synthesisof purine:
N
5
-FormylTHFinter­ mediate formedin histidine
catabolismis used in the biosyn­ thesis of purineand
thereforein theformationof bothDNAandRNA.
5.Synthesisof methionine from homocysteine:
Homocysteine is convertedtomethioninein presenceof
N
5
-methylTHF,and vitamin B
12
.

86. –Inthis reaction the methyl group bound to cobalamin
(Vitamin B
12) istransferredto homocysteine to form
methionine and the cobalaminthenremoves the methyl
group from N
5
-methyl THF to form THF.
–Thisstep is essential for the liberation of freeTHFand
for itsrepeated usein one carbon metabolism. In B
12
deficiency, conversion ofN
5
-methylTHFto freeTHFis
blocked.
–Inthis reaction the methyl group bound to cobalamin
(Vitamin B
12) istransferredto homocysteine to form
methionine and the cobalaminthenremoves the methyl
group from N
5
-methyl THF to form THF.
–Thisstep is essential for the liberation of freeTHFand
for itsrepeated usein one carbon metabolism. In B
12
deficiency, conversion ofN
5
-methylTHFto freeTHFis
blocked.

87. Thecombined roleof vitamin B
12and folateand folate
trap.

89. DeficiencyManifestations
Megaloblasticor macrocyticanemia
Accumulationand excretion of FIGLU in theurine
Hyperhomocysteinemia
Neural tube defect in foetus
DeficiencyManifestations
Megaloblasticor macrocyticanemia
Accumulationand excretion of FIGLU in theurine
Hyperhomocysteinemia
Neural tube defect in foetus

90. Excretionof FIGLU in folicacid deficiency.

91. Cobalamin (Vitamin B
12)
Structure
Vitamin B
12bears a complexcorrin ring(containing
pyrrols similar to porphyrin), linked to a cobalt atom
held in the center of the corrin ring, by four coordination
bonds with the nitrogen of the pyrrole groups.
Cobalamin (Vitamin B
12)
Structure
Vitamin B
12bears a complexcorrin ring(containing
pyrrols similar to porphyrin), linked to a cobalt atom
held in the center of the corrin ring, by four coordination
bonds with the nitrogen of the pyrrole groups.

92. Theremaining coordination bonds of the cobalt are
linked with the nitrogen ofdimethylbenzimidazole
nucleotideand sixth bond is linked to eithermethylor
5'-deoxy­adenosylorhydroxygroup to form
methyl­cobalamin, adenosylcobalamin or
hydroxycobalamin respectively
Theremaining coordination bonds of the cobalt are
linked with the nitrogen ofdimethylbenzimidazole
nucleotideand sixth bond is linked to eithermethylor
5'-deoxy­adenosylorhydroxygroup to form
methyl­cobalamin, adenosylcobalamin or
hydroxycobalamin respectively

94. StructureofVit B
12.
(R:either
methyl
or
deoxyadenosyl
or
hydroxygroup)
StructureofVit B
12.
(R:either
methyl
or
deoxyadenosyl
or
hydroxygroup)

95. Active form of VitaminB12
Methylcobalamin
Deoxyadenosylcobalamin.
Sources
Dietarysources of vitamin B12 are of animal origin;
meat, eggs, milk, dairy products, fish, poultry, etc.
VitaminB12 is absent in plant foods.
Humansobtain small amounts ofB12fromintestinal
flora.
Active form of VitaminB12
Methylcobalamin
Deoxyadenosylcobalamin.
Sources
Dietarysources of vitamin B12 are of animal origin;
meat, eggs, milk, dairy products, fish, poultry, etc.
VitaminB12 is absent in plant foods.
Humansobtain small amounts ofB12fromintestinal
flora.

96. NutritionalRequirements (RDA )
3μgwith higherallowancesfor pregnancy and
lactatingwomen.
NutritionalRequirements (RDA )
3μgwith higherallowancesfor pregnancy and
lactatingwomen.

97. Absorption, Transport and Storage

98. •The intestinal absorption of vitamin B12requires an
intrinsic factor (IF),a glycoprotein secreted by parietal
cells of the stomach.
•Instomach IF binds the dietary vitamin B12to form
vitamin B12-IF complex.
•Thiscomplex binds to specific receptors on the surface of
the mucosal cells of the ileum.
•Afterbinding to the receptor, the bound vitamin B12is
released from the complex and enters the illeal mucosal
cells through a Ca
2+
dependent process.
•The intestinal absorption of vitamin B12requires an
intrinsic factor (IF),a glycoprotein secreted by parietal
cells of the stomach.
•Instomach IF binds the dietary vitamin B12to form
vitamin B12-IF complex.
•Thiscomplex binds to specific receptors on the surface of
the mucosal cells of the ileum.
•Afterbinding to the receptor, the bound vitamin B12is
released from the complex and enters the illeal mucosal
cells through a Ca
2+
dependent process.

99. Functions
There are only two human enzyme systems that are
known to require vitamin B
12coenzyme.
1. Isomerizationof methylmalonyl-CoA tosuccinyl-CoA
2. Conversion of homocysteine to methionine
Functions
There are only two human enzyme systems that are
known to require vitamin B
12coenzyme.
1. Isomerizationof methylmalonyl-CoA tosuccinyl-CoA
2. Conversion of homocysteine to methionine

100. Roleofvit B
12in
isomerizationof
methylmalonyl-CoA to
succinyl-CoA

101. Role of vit B
12conversionof homocysteine to methionine
Thisis the only mammalian reactionrequireboth vitamins

102. Deficiency Manifestations
Perniciousanemia
Megaloblasticanemia
Methylmalonicaciduria
Neuropathy (sub acute combined degeneration,
SCD)
Folatetrap
Deficiency Manifestations
Perniciousanemia
Megaloblasticanemia
Methylmalonicaciduria
Neuropathy (sub acute combined degeneration,
SCD)
Folatetrap

103. Vitamin B12Deficiency Causes
FunctionalFolate Deficiency: The FolateTrap
S-adenosyl methionine forms homocysteine, which may
be remethylated by methyltetrahydrofolate catalysed by
methionine synthase, a vitamin B12 dependentenzyme.
Impairment of methionine synthase in vitamin B12
deficiency results in the accumulation of
methyltetrahydrofolate that cannot be used and cannot be
converted to free THF.
Vitamin B12Deficiency Causes
FunctionalFolate Deficiency: The FolateTrap
S-adenosyl methionine forms homocysteine, which may
be remethylated by methyltetrahydrofolate catalysed by
methionine synthase, a vitamin B12 dependentenzyme.
Impairment of methionine synthase in vitamin B12
deficiency results in the accumulation of
methyltetrahydrofolate that cannot be used and cannot be
converted to free THF.

104. Thus, most of THF is irreversibly “trapped” as methyl
THF.
Thereis therefore functional deficiency of folate,
secondary to the deficiency of vitamin B12.
Folatetrap creates folate deficiency and an adequate
supply of free THF is not available for the synthesis of
purine and pyrimidine bases.
Thus, most of THF is irreversibly “trapped” as methyl
THF.
Thereis therefore functional deficiency of folate,
secondary to the deficiency of vitamin B12.
Folatetrap creates folate deficiency and an adequate
supply of free THF is not available for the synthesis of
purine and pyrimidine bases.

106. Vitamin C (Ascorbic Acid)
Structure
Itis a six-carbonsugar derivative.
Humanscannot synthesize ascorbic acid, due to lack of
the enzymegluconolactoneoxidase.
Vitamin C (Ascorbic Acid)
Structure
Itis a six-carbonsugar derivative.
Humanscannot synthesize ascorbic acid, due to lack of
the enzymegluconolactoneoxidase.

107. Structureof ascorbic acid.

108. Active Form of Ascorbic Acid
Ascorbic acid itself is an active form.
Sources
Themain dietary sources of vitamin C are leafy
vegetables and fruits, especially citrus fruits, strawberries,
tomatoes, spinach and potatoes.
Cerealscontain no vitaminC.
Animaltissues and dairy products are very poor sources.
Active Form of Ascorbic Acid
Ascorbic acid itself is an active form.
Sources
Themain dietary sources of vitamin C are leafy
vegetables and fruits, especially citrus fruits, strawberries,
tomatoes, spinach and potatoes.
Cerealscontain no vitaminC.
Animaltissues and dairy products are very poor sources.

109. NutritionalRequirements
The recommended daily allowance is about60–70 mg.
Additional intakes are recommended for women during
pregnancy and lactation.

110. Functions
Vitamin C is the coenzyme for two groups of
hydroxylases.
–Copper containing hydroxylases
–α-ketoglutaratelinked iron containing
hydroxylases
Ascorbic acid has specific roles inthenumberofnon-
enzymatic effectsas result of its action as a reducing
agent and oxygen radical quencher.
Functions
Vitamin C is the coenzyme for two groups of
hydroxylases.
–Copper containing hydroxylases
–α-ketoglutaratelinked iron containing
hydroxylases
Ascorbic acid has specific roles inthenumberofnon-
enzymatic effectsas result of its action as a reducing
agent and oxygen radical quencher.

111. Role of Ascorbic acid in the copper containing hydroxylases
Dopamine β-hydroxylaseis acopper containingenzyme
involved in the synthesis of thecatecholamines
(norepinephrine and epinephrine), from tyrosine in the
adrenal medulla and central nervous system.
Anumber ofpeptide hormoneshave a carboxy terminal
amide that is derived from a terminal glycine residue. This
glycine is hydroxylated on the α-carbon by a copper
containing enzyme,peptidylglycine hydroxylase, which
again, requires ascorbate for reduction of Cu
2+
.
Role of Ascorbic acid in the copper containing hydroxylases
Dopamine β-hydroxylaseis acopper containingenzyme
involved in the synthesis of thecatecholamines
(norepinephrine and epinephrine), from tyrosine in the
adrenal medulla and central nervous system.
Anumber ofpeptide hormoneshave a carboxy terminal
amide that is derived from a terminal glycine residue. This
glycine is hydroxylated on the α-carbon by a copper
containing enzyme,peptidylglycine hydroxylase, which
again, requires ascorbate for reduction of Cu
2+
.

112. Role of Ascorbic acid in the iron containinghydroxylases
Prolinehydroxylasesandlysine hydroxylasesare required for the
postsynthetic modification ofprocollagentocollagen.
Aspartateβ-hydroxylaseis required for the postsynthetic
modification of the precursor ofproteinC.
VitaminK-dependent proteasethat hydrolyses activated factor V
in the blood clotting cascade.
Trimethyllysineandγ-butyrobetain hydroxylasesare required for
the synthesis ofcarnitine.
Role of Ascorbic acid in the iron containinghydroxylases
Prolinehydroxylasesandlysine hydroxylasesare required for the
postsynthetic modification ofprocollagentocollagen.
Aspartateβ-hydroxylaseis required for the postsynthetic
modification of the precursor ofproteinC.
VitaminK-dependent proteasethat hydrolyses activated factor V
in the blood clotting cascade.
Trimethyllysineandγ-butyrobetain hydroxylasesare required for
the synthesis ofcarnitine.

113. Non-enzymatic effects as result of its action as areducing
agentand oxygen radicalquencher
Ascorbicacid is a water solubleantioxidant:
–Itreduces oxidized vitamin E (tocopherol)to
regeneratefunctional vitamin E.
–VitaminC thought to be involved in theprevention of
atherosclerosis and coronary heart diseaseby
preventingoxidation of LDL.
Non-enzymatic effects as result of its action as areducing
agentand oxygen radicalquencher
Ascorbicacid is a water solubleantioxidant:
–Itreduces oxidized vitamin E (tocopherol)to
regeneratefunctional vitamin E.
–VitaminC thought to be involved in theprevention of
atherosclerosis and coronary heart diseaseby
preventingoxidation of LDL.

114. –Antioxidantproperty of vitamin C is alsoassociated
withprevention of cancer by inhibitingnitrosamine
formationfrom naturally occurring nitratesduring
digestion.
•In addition to other roles of vitamin C, it enhancesthe
absorptionof inorganic iron. Ascorbic acidfacilitates the
absorption of iron from intestine by reducing itto the
Fe++ (ferrous) state.
–Antioxidantproperty of vitamin C is alsoassociated
withprevention of cancer by inhibitingnitrosamine
formationfrom naturally occurring nitratesduring
digestion.
•In addition to other roles of vitamin C, it enhancesthe
absorptionof inorganic iron. Ascorbic acidfacilitates the
absorption of iron from intestine by reducing itto the
Fe++ (ferrous) state.

115. Deficiency Manifestation
Deficiencyhas been observed in infants receivingun-
supplementedcow’s milk and in infants receiving breast
milk from deficientmother.
Deficiencyoccurs most commonly in the elderly,
especially those who do not eat fresh fruits and vegetables
and who tend to cook in frying pans, the combination of
heat and large area of food in contact with air irreversibly
oxidizes the vitamin and loses its biologicalactivity.
Deficiencyalso can occur in iron overload.
Deficiency Manifestation
Deficiencyhas been observed in infants receivingun-
supplementedcow’s milk and in infants receiving breast
milk from deficientmother.
Deficiencyoccurs most commonly in the elderly,
especially those who do not eat fresh fruits and vegetables
and who tend to cook in frying pans, the combination of
heat and large area of food in contact with air irreversibly
oxidizes the vitamin and loses its biologicalactivity.
Deficiencyalso can occur in iron overload.

116. Scurvy
Deficiencyof ascorbic acid causesscurvy.
VitaminC is required for formation of collagen, where it is
needed for the hydroxylation ofprolineandlysineresidues, of
protocollagen.
Hydroxyprolineand hydroxylysine are essential for the
collagen cross-linking and collagen strength andstability.
Sincevitamin C is required for normal collagen formation,
vitamin C is also involved in bone and dentin formation as well
as wound healing process.
Scurvy
Deficiencyof ascorbic acid causesscurvy.
VitaminC is required for formation of collagen, where it is
needed for the hydroxylation ofprolineandlysineresidues, of
protocollagen.
Hydroxyprolineand hydroxylysine are essential for the
collagen cross-linking and collagen strength andstability.
Sincevitamin C is required for normal collagen formation,
vitamin C is also involved in bone and dentin formation as well
as wound healing process.

117. Symptoms ofscurvy
Symptomsof scurvy are related todeficient collagen
formation.These include:
–Fragilityof vascular walls causing bleeding tendency,
muscle weakness, soft spongy, swollen bleeding
gums, loosening of teeth.
–Abnormalbone development and osteoporosis. In
children bone formation is impaired.
Symptoms ofscurvy
Symptomsof scurvy are related todeficient collagen
formation.These include:
–Fragilityof vascular walls causing bleeding tendency,
muscle weakness, soft spongy, swollen bleeding
gums, loosening of teeth.
–Abnormalbone development and osteoporosis. In
children bone formation is impaired.

118. –Poorwound healing.
–Anemiadue to impaired erythropoiesis.
–Milderforms of vitamin C deficiency are more
common and manifestation of such includeeasy
bruising (contusion)andformation of petechiaeboth
due toincreased capillary fragility.
–Poorwound healing.
–Anemiadue to impaired erythropoiesis.
–Milderforms of vitamin C deficiency are more
common and manifestation of such includeeasy
bruising (contusion)andformation of petechiaeboth
due toincreased capillary fragility.

119. Vitamin A
Structure
Vitamin A contains a single 6-membered ring to which is
attached an 11-carbon sidechain.
VitaminA is analcohol (retinol),but can be converted
into analdehyde (retinal),oracid(retinoic acid).
Vitamin A
Structure
Vitamin A contains a single 6-membered ring to which is
attached an 11-carbon sidechain.
VitaminA is analcohol (retinol),but can be converted
into analdehyde (retinal),oracid(retinoic acid).

120. Structureof vitamin A, retinol.

121. Active Form
Vitamin A consists of three biologically active molecules
which are collectively known asretinoids.
1. Retinol:Primaryalcohol (CH2OH) containing form
2. Retinal:Aldehyde(CHO) containing form
3. Retinoicacid:Carboxyl(COOH) containing form
Active Form
Vitamin A consists of three biologically active molecules
which are collectively known asretinoids.
1. Retinol:Primaryalcohol (CH2OH) containing form
2. Retinal:Aldehyde(CHO) containing form
3. Retinoicacid:Carboxyl(COOH) containing form

122. Each of these compounds are derived from the plant precursor
molecule,β-carotene.
β-carotenewhich consists of two molecules ofretinallinked
at their aldehyde ends is also referred to as theprovitamin
form of vitamin A.
Theretinol and retinal are interconverted by enzymeretinal
aldehyde reductase.
Theretinoic acid is formed by oxidation of retinal. The
retinoic acidcan notbe reduced to either retinol or retinal
Each of these compounds are derived from the plant precursor
molecule,β-carotene.
β-carotenewhich consists of two molecules ofretinallinked
at their aldehyde ends is also referred to as theprovitamin
form of vitamin A.
Theretinol and retinal are interconverted by enzymeretinal
aldehyde reductase.
Theretinoic acid is formed by oxidation of retinal. The
retinoic acidcan notbe reduced to either retinol or retinal

123. Conversionof β-carotene (provitamin) tobiologically activeforms of
vitamin A.

124. Sources
Therichest dietary sourcesarefish liver oils(cod liver
oil). Meatis rather low in vitamin A.
Othergood sources aremilkanddairy products,dark-
green leaves, such asspinachandyellowandred fruits
and vegetables, such ascarrots,tomatoes, andpeaches
etc.
Sources
Therichest dietary sourcesarefish liver oils(cod liver
oil). Meatis rather low in vitamin A.
Othergood sources aremilkanddairy products,dark-
green leaves, such asspinachandyellowandred fruits
and vegetables, such ascarrots,tomatoes, andpeaches
etc.

125. NutritionalRequirements
The RDA of vitamin A for adults is800–1000 retinol
equivalents.(1 retinol equivalent = 1 mg retinol = 6 mgβ-
carotene).
NutritionalRequirements
The RDA of vitamin A for adults is800–1000 retinol
equivalents.(1 retinol equivalent = 1 mg retinol = 6 mgβ-
carotene).

126. Functions of Vitamin A
VitaminA is required for a variety of functions suchas
–Vision
–Celldifferentiation andgrowth
–Mucus secretion
–Maintenanceof epithelialcells
Functions of Vitamin A
VitaminA is required for a variety of functions suchas
–Vision
–Celldifferentiation andgrowth
–Mucus secretion
–Maintenanceof epithelialcells

127. Differentforms of the vitamin have different functions.
–Retinaland retinol are involved invision.
–Retinoicacid is involved incellular differentiation
and metabolic processes.
–β-caroteneis involved in antioxidant function.
Differentforms of the vitamin have different functions.
–Retinaland retinol are involved invision.
–Retinoicacid is involved incellular differentiation
and metabolic processes.
–β-caroteneis involved in antioxidant function.

128. Role of Vitamin A inVision
The role of vitamin A in vision has been known through
the studies ofG Wald,who received the Nobel Prize in
1943
The cyclic events occur in the process of vision, known
asrhodopsin cycleorWald’s visualcycle
Role of Vitamin A inVision
The role of vitamin A in vision has been known through
the studies ofG Wald,who received the Nobel Prize in
1943
The cyclic events occur in the process of vision, known
asrhodopsin cycleorWald’s visualcycle

129. Bothrod and cone cells of retina contain a photoreceptor
pigment in their membrane and vitamin A is a component
of these pigments.
Rhodopsinorvisual purple,the visual pigment of rod
cells in the retina consists of11-cis-retinalbound to
proteinopsin.
Bothrod and cone cells of retina contain a photoreceptor
pigment in their membrane and vitamin A is a component
of these pigments.
Rhodopsinorvisual purple,the visual pigment of rod
cells in the retina consists of11-cis-retinalbound to
proteinopsin.

130. Wald’svisual cycle

131. When rhodopsin absorbs light, the 11-cis-retinal is
converted toall-trans retinal.
The isomerization is associated with a conforma­tional
change in the proteinopsin.
Conformational changes in opsin generates anerve
impulsethat is trans­mitted by the optic nerve to the brain.
This is followed by dissociation of the all-trans retinal
from opsin
When rhodopsin absorbs light, the 11-cis-retinal is
converted toall-trans retinal.
The isomerization is associated with a conforma­tional
change in the proteinopsin.
Conformational changes in opsin generates anerve
impulsethat is trans­mitted by the optic nerve to the brain.
This is followed by dissociation of the all-trans retinal
from opsin

132. Theall-trans retinal is immediately isomerized by retinal
isomerase to11-cis-retinal.
This combines with opsin to regenerate rhodopsin and
complete the visual cycle.
The conversion of all-trans retinal to 11-cis-retinal is
incomplete and therefore remaining all-trans retinal
which is not converted to 11-cis-retinal is converted to all-
trans retinol byalcohol dehydrogenaseand is stored in the
liver.
Theall-trans retinal is immediately isomerized by retinal
isomerase to11-cis-retinal.
This combines with opsin to regenerate rhodopsin and
complete the visual cycle.
The conversion of all-trans retinal to 11-cis-retinal is
incomplete and therefore remaining all-trans retinal
which is not converted to 11-cis-retinal is converted to all-
trans retinol byalcohol dehydrogenaseand is stored in the
liver.

133. Whenneeded, retinol re-enters thecirculationand is taken
up by the retina, where it is converted back to 11-cis-
retinal which combines with opsin again to form
rhodopsin
Whenneeded, retinol re-enters thecirculationand is taken
up by the retina, where it is converted back to 11-cis-
retinal which combines with opsin again to form
rhodopsin

134. Darkadaptationtime
Thetime taken for regeneration of rhodopsin is known as
dark adaptation time. Dark adaptation time is increased in
vitamin A deficient individuals

135. Role of Vitamin A in Color Vision
Colorvision is mediated bythreepigmentscalled
porphyropsin,iodopsinandcyanopsinand are sensitive to
the three essentialcolours:red,greenandblue
respectively.
Allthese pigments consist of 11-cis-retinal bound to
proteinopsin.
Whenlight strikesretina, it bleaches one or more of these
pigments, depending on the color quality of the light.
Thepigments are converted to all-trans retinal, and the
protein moiety opsin is released as in the case of
rhodopsin.
Role of Vitamin A in Color Vision
Colorvision is mediated bythreepigmentscalled
porphyropsin,iodopsinandcyanopsinand are sensitive to
the three essentialcolours:red,greenandblue
respectively.
Allthese pigments consist of 11-cis-retinal bound to
proteinopsin.
Whenlight strikesretina, it bleaches one or more of these
pigments, depending on the color quality of the light.
Thepigments are converted to all-trans retinal, and the
protein moiety opsin is released as in the case of
rhodopsin.

136. This reaction gives rise to the nerve impulse that is read
out in the brain as color:
– Red if porphyropsin is split
– Green if iodopsin is split
– Blue if cyanopsin is split.
If mixtures of the three are converted, the color read out
in the brain depends on the proportions of the three split.
This reaction gives rise to the nerve impulse that is read
out in the brain as color:
– Red if porphyropsin is split
– Green if iodopsin is split
– Blue if cyanopsin is split.
If mixtures of the three are converted, the color read out
in the brain depends on the proportions of the three split.

137. Cellular Differentiation and MetabolicEffect
Retinoic acid is an important regulator of gene
expression especially during growth and development.
Retinoicacid is essential for normal gene expression
during embryonic development such as cell
differentiationin spermatogenesis and in the
differentiation of epithelial cells.
Cellular Differentiation and MetabolicEffect
Retinoic acid is an important regulator of gene
expression especially during growth and development.
Retinoicacid is essential for normal gene expression
during embryonic development such as cell
differentiationin spermatogenesis and in the
differentiation of epithelial cells.

138. Retinoic acids exert a number of metabolic effects on tissues.
These include:
–Controlof biosynthesis of membraneglycoproteins
and glycosaminoglycans (mucopolysaccharide)
necessary for mucus secretion. The normal mucus
secretion maintains the epithelial surface moist and
prevents keratinization of epithelial cell.
–Controlof biosynthesis of cholesterol.
Retinoic acids exert a number of metabolic effects on tissues.
These include:
–Controlof biosynthesis of membraneglycoproteins
and glycosaminoglycans (mucopolysaccharide)
necessary for mucus secretion. The normal mucus
secretion maintains the epithelial surface moist and
prevents keratinization of epithelial cell.
–Controlof biosynthesis of cholesterol.

139. Antioxidant Function
β-caroteneis an antioxidant and may play a role in
trappingfreeradicalsin tissues.
Theantioxidant property of lipid soluble vitamin A may
account for its possibleanticanceractivity.
Highlevels of dietary carotenoids have been associated
with adecreased risk of cardiovascular disease
Antioxidant Function
β-caroteneis an antioxidant and may play a role in
trappingfreeradicalsin tissues.
Theantioxidant property of lipid soluble vitamin A may
account for its possibleanticanceractivity.
Highlevels of dietary carotenoids have been associated
with adecreased risk of cardiovascular disease

140. Deficiency Manifestation
Clinically, degenerative changes ineyesandskinare
observed commonly in individuals with vitamin A
deficiency.
Vitamindeficiency may beprimary(dietary
insufficiency) orsecondary.
Deficiency Manifestation
Clinically, degenerative changes ineyesandskinare
observed commonly in individuals with vitamin A
deficiency.
Vitamindeficiency may beprimary(dietary
insufficiency) orsecondary.

141. Thecauses of secondary deficiency may include:
–Impairedabsorption oflipids
–Failureto synthesize apo B-48 and therefore inability
to form chylomicrons into which vitamin A is
normally incorporated after absorption.
–Lackof lipase, as in pancreatitis.
–Failure in convertingβ-carotene to retinol; because
of an enzyme defect.
Thecauses of secondary deficiency may include:
–Impairedabsorption oflipids
–Failureto synthesize apo B-48 and therefore inability
to form chylomicrons into which vitamin A is
normally incorporated after absorption.
–Lackof lipase, as in pancreatitis.
–Failure in convertingβ-carotene to retinol; because
of an enzyme defect.

142. –Impairedstorage in hepatic cell in liver disease.
–Failureto synthesize retinol binding proteins, thus
affecting transport to target tissues.

143. Effect on Vision
The earliest symptoms of vitamin A deficiencyis:
–Impaired dark adaptation or night blindness
(nyctalopia)
–Poorvision in dim light
–Xerophthalmia.
Effect on Vision
The earliest symptoms of vitamin A deficiencyis:
–Impaired dark adaptation or night blindness
(nyctalopia)
–Poorvision in dim light
–Xerophthalmia.

144. Nightblindness (nyctalopia)
This is characterized by loss of vision in night (in dim or
poor light) sincedark adaptation timeisincreased.
Prolongeddeficiency of vitamin A leads to anirreversible
loss of visual cells.
Severe vitamin A deficiency causes dryness of cornea and
conjunctiva,a clinical condition termed asxerophthalmia
(dry eyes).
Nightblindness (nyctalopia)
This is characterized by loss of vision in night (in dim or
poor light) sincedark adaptation timeisincreased.
Prolongeddeficiency of vitamin A leads to anirreversible
loss of visual cells.
Severe vitamin A deficiency causes dryness of cornea and
conjunctiva,a clinical condition termed asxerophthalmia
(dry eyes).

146. If this situation prolongs,keratinizationandulcerationof
cornea takesplace
Thisresults in destruction of cornea. The cornea becomes
totally opaque resulting in permanent loss of vision
(blindness), a clinical condition termed askeratomalacia.
White opaque spots develop on either side of cornea in
vitamin A deficiency are known asBitot’s spot.
If this situation prolongs,keratinizationandulcerationof
cornea takesplace
Thisresults in destruction of cornea. The cornea becomes
totally opaque resulting in permanent loss of vision
(blindness), a clinical condition termed askeratomalacia.
White opaque spots develop on either side of cornea in
vitamin A deficiency are known asBitot’s spot.

148. Effect on Skin and EpithelialCells
Vitamin A deficiency causeskeratinization of epithelial
cells of skinwhich leads tokeratosisof hair follicles,
and dry, rough and scaly skin.
Keratinization of epithelial cells of respiratory, urinary
tract makes them susceptible to infections.
Effect on Skin and EpithelialCells
Vitamin A deficiency causeskeratinization of epithelial
cells of skinwhich leads tokeratosisof hair follicles,
and dry, rough and scaly skin.
Keratinization of epithelial cells of respiratory, urinary
tract makes them susceptible to infections.

149. Other Symptoms of Vitamin ADeficiency
Failure of growth in children.
Faulty bone modelling producingthick cancellous
(spongy) bonesinstead of thinner and more compact ones.
Abnormalities of reproduction, includingdegenerationof
the testes, abortion or the production of malformed
offspring.
Other Symptoms of Vitamin ADeficiency
Failure of growth in children.
Faulty bone modelling producingthick cancellous
(spongy) bonesinstead of thinner and more compact ones.
Abnormalities of reproduction, includingdegenerationof
the testes, abortion or the production of malformed
offspring.

150. Hypervitaminosis A
Excessive intakesof vitaminAlead to accumulation beyond the
capacity of intracellular binding proteins. Unbound vitamin A
causes membrane lysis and tissue damage. Symptoms of toxicity
affect:
The central nervous system and leads to headache, nausea,
ataxia, and anorexia. These all associated with increased
cerebrospinal fluid pressure.
Theliver: hepatomegaly with histological changes and
hyperlipidemia
Hypervitaminosis A
Excessive intakesof vitaminAlead to accumulation beyond the
capacity of intracellular binding proteins. Unbound vitamin A
causes membrane lysis and tissue damage. Symptoms of toxicity
affect:
The central nervous system and leads to headache, nausea,
ataxia, and anorexia. These all associated with increased
cerebrospinal fluid pressure.
Theliver: hepatomegaly with histological changes and
hyperlipidemia

151. Calciumhomeostasis: thickening of the long bones,
hypercalcemia, and calcification of soft tissues, bone and
jointpain,
Theskin: loss of hair (alopecia), scaly and roughskin.
Inpregnant women, the hypervitaminosis A may cause
congenital malformation in growing fetus (teratogenic
effect).
Calciumhomeostasis: thickening of the long bones,
hypercalcemia, and calcification of soft tissues, bone and
jointpain,
Theskin: loss of hair (alopecia), scaly and roughskin.
Inpregnant women, the hypervitaminosis A may cause
congenital malformation in growing fetus (teratogenic
effect).

152. Why Vitamin A is Considered as a Hormone?
Within cells both retinol and retinoic acid function by binding
to specificreceptorproteins present in the nucleus of target
tissues.
Following binding, thereceptor-vitamin complexinteracts
with severalgenesinvolved in growth and differentiation and
affects expression of these genes.
Why Vitamin A is Considered as a Hormone?
Within cells both retinol and retinoic acid function by binding
to specificreceptorproteins present in the nucleus of target
tissues.
Following binding, thereceptor-vitamin complexinteracts
with severalgenesinvolved in growth and differentiation and
affects expression of these genes.

153. Vitamin D (Cholecalciferol)
Vitamin D is also known ascalciferolbecause of its role
in calciummetabolismandantirachitic factorbecause it
prevents rickets.
Vitamin D (Cholecalciferol)
Vitamin D is also known ascalciferolbecause of its role
in calciummetabolismandantirachitic factorbecause it
prevents rickets.

154. Vitamin D could be thought of as a hormone
ratherthana vitamin
Asit can be synthesized in thebody
Itis released in thecirculation
Hasdistinct targetorgans
Actionof vitamin D is similar tosteroid hormones. It
binds to areceptorin the cytosol. Following binding, the
receptor vitamin complex interacts with DNA to
stimulate the synthesis of calcium binding protein.
Vitamin D could be thought of as a hormone
ratherthana vitamin
Asit can be synthesized in thebody
Itis released in thecirculation
Hasdistinct targetorgans
Actionof vitamin D is similar tosteroid hormones. It
binds to areceptorin the cytosol. Following binding, the
receptor vitamin complex interacts with DNA to
stimulate the synthesis of calcium binding protein.

155. Structure
Vitamin D is asteroidcompound.Thenaturally produced
vitaminD
3orcholecalciferolis obtainedfrom animal
sources in the diet, or made in the skin by the action of
ultraviolet light from sunlighton
Structure
Vitamin D is asteroidcompound.Thenaturally produced
vitaminD
3orcholecalciferolis obtainedfrom animal
sources in the diet, or made in the skin by the action of
ultraviolet light from sunlighton

156. Structureof 1,25-dihydroxycholecalciferol an active
form of vitamin D
3.

157. Theformation of vitamin D
3in the body and
vitamin D
2commercially.

158. Active Form ofVitamin
Cholecalciferolis aninactiveform of vitamin D.
Itneeds further metabolism to produce the active form of
the vitamin.1, 25 dihydroxycholecalciferolalso known
ascalcitriolis the active form of vitamin D.
Active Form ofVitamin
Cholecalciferolis aninactiveform of vitamin D.
Itneeds further metabolism to produce the active form of
the vitamin.1, 25 dihydroxycholecalciferolalso known
ascalcitriolis the active form of vitamin D.

159. Activationof vitamin D.

160. Sources
Bestsources are cod liver oil and often fish oils and
sunlight induced synthesis of vitamin D3 in skin.
Eggyolk and liver are good sources.
NutritionalRequirement
The daily requirements of vitamin D is200–400 IU.
Sources
Bestsources are cod liver oil and often fish oils and
sunlight induced synthesis of vitamin D3 in skin.
Eggyolk and liver are good sources.
NutritionalRequirement
The daily requirements of vitamin D is200–400 IU.

161. Functions
Vitamin D (Calcitriol) plays an essential role as a
hormone in theregulation of calciumandphosphorus
metabolism.
It maintains the normal plasmalevel of calciumand
phosphorusby acting on intestine, kidneys andbones.
Functions
Vitamin D (Calcitriol) plays an essential role as a
hormone in theregulation of calciumandphosphorus
metabolism.
It maintains the normal plasmalevel of calciumand
phosphorusby acting on intestine, kidneys andbones.

162. Action of calcitriol on intestine
Itincreases the plasma calcium and phosphorus
concentrationby stimulating the absorption of
calciumand phosphorus from theintestine.
Action of calcitriol on kidney
Itstimulates the reabsorption of calcium and
phosphorusfrom the kidney and decreases their
excretion.
Action of calcitriol on intestine
Itincreases the plasma calcium and phosphorus
concentrationby stimulating the absorption of
calciumand phosphorus from theintestine.
Action of calcitriol on kidney
Itstimulates the reabsorption of calcium and
phosphorusfrom the kidney and decreases their
excretion.

163. Actionof calcitriol on bone
–Calcitriolpromotes the mineralization of bones by
depositionof calcium and phosphorus.
–Calcitriolalong with PTH stimulates themobilization
of calcium and phosphorus frombone.
Actionof calcitriol on bone
–Calcitriolpromotes the mineralization of bones by
depositionof calcium and phosphorus.
–Calcitriolalong with PTH stimulates themobilization
of calcium and phosphorus frombone.

164. Sitesof formation of vitamin D
3to itsmetabolically
activeform1,25-dihydroxychole-calciferoland its
function.
1,25-DHCC: 1,25-dihydroxycholecalciferol;
PTH: parathyroidhormone
Sitesof formation of vitamin D
3to itsmetabolically
activeform1,25-dihydroxychole-calciferoland its
function.
1,25-DHCC: 1,25-dihydroxycholecalciferol;
PTH: parathyroidhormone

167. DeficiencyManifestation
Deficiency of vitamin Dcauses:
–Rickets(rachitis) in growing childrenand
–Osteomalaciain adults.

168. Rickets
Ricketsis characterized by formation of soft and pliable
bones due topoor mineralizationandcalcium deficiency.
Dueto softness, the weight bearing bones are bent and
deformed.
Themain features of the rickets are, a large head with
protruding forehead,pigeon chest,bow legs, (curved
legs),knock kneesandabnormal curvature of the spine
(kyphosis).
Rickets
Ricketsis characterized by formation of soft and pliable
bones due topoor mineralizationandcalcium deficiency.
Dueto softness, the weight bearing bones are bent and
deformed.
Themain features of the rickets are, a large head with
protruding forehead,pigeon chest,bow legs, (curved
legs),knock kneesandabnormal curvature of the spine
(kyphosis).

169. Bowingof legs in rickets.

170. Rachitic children are usually anemic or prone to
infections. Rickets can be fatal whensevere.
Ricketsis characterized by low plasma levels of calcium
and phosphorus and high alkaline phosphatase activity.
Rachitic children are usually anemic or prone to
infections. Rickets can be fatal whensevere.
Ricketsis characterized by low plasma levels of calcium
and phosphorus and high alkaline phosphatase activity.

171. Osteomalacia(Adult Rickets)
Deficiencyof vitamin D in adults causesosteomalacia.
This is a condition similar to that of rickets.
Osteomalaciacharacterized by demineralization of
previously formed bones, Demineralization of bones
makes them soft and susceptible to fractures.
Osteomalacia especially occurs in women whohave little
exposure to sunlight, and especially afterseveral
pregnancies
Osteomalacia(Adult Rickets)
Deficiencyof vitamin D in adults causesosteomalacia.
This is a condition similar to that of rickets.
Osteomalaciacharacterized by demineralization of
previously formed bones, Demineralization of bones
makes them soft and susceptible to fractures.
Osteomalacia especially occurs in women whohave little
exposure to sunlight, and especially afterseveral
pregnancies

172. RenalRickets (Renal Osteodystrophy)
In chronic renal failure synthesis of calcitriol in kidney is
impaired. As a result, the deficiency of calcitriol occurs
which leads to hypocalcemia and hyperphosphatemia.
Itcan be treated by oral or intravenous administration of
calcitriol (active form of vitamin D).
RenalRickets (Renal Osteodystrophy)
In chronic renal failure synthesis of calcitriol in kidney is
impaired. As a result, the deficiency of calcitriol occurs
which leads to hypocalcemia and hyperphosphatemia.
Itcan be treated by oral or intravenous administration of
calcitriol (active form of vitamin D).

173. Vitamin D Resistant Rickets
As the name implies, this is a disease which does not
respond to treatment with vitamin D.
Thereare various possible causes of this condition and
all involve a defect in the metabolism or mechanism of
action of 1,25dihydroxycholecalciferol.
Vitamin D Resistant Rickets
As the name implies, this is a disease which does not
respond to treatment with vitamin D.
Thereare various possible causes of this condition and
all involve a defect in the metabolism or mechanism of
action of 1,25dihydroxycholecalciferol.

174. –Duetodefective vitamin D receptor
–Dueto adefective 1,α-hydroxylaseactivity in kidney
–Dueto liver disease and kidney failure as the
production of25-hydroxycholecalciferoland 1,25
dihydroxycholecalciferolrespectivelywill be
inefficient in the damaged tissue
–Duetodefective vitamin D receptor
–Dueto adefective 1,α-hydroxylaseactivity in kidney
–Dueto liver disease and kidney failure as the
production of25-hydroxycholecalciferoland 1,25
dihydroxycholecalciferolrespectivelywill be
inefficient in the damaged tissue

175. Hypervitaminosis D
High doses of vitamin D over a long period are toxic.
Theearly symptoms of hypervitaminosis D include nausea,
vomiting, anorexia, increased thirst, loss of weight, etc.
Hypercalcemiais seen due to increased bone resorption and
intestinal absorption of calcium.
Theprolonged hypercalcemia causes calcification of soft
tissues and organs such as kidney and may lead to formation
of stones in the kidneys.
Hypervitaminosis D
High doses of vitamin D over a long period are toxic.
Theearly symptoms of hypervitaminosis D include nausea,
vomiting, anorexia, increased thirst, loss of weight, etc.
Hypercalcemiais seen due to increased bone resorption and
intestinal absorption of calcium.
Theprolonged hypercalcemia causes calcification of soft
tissues and organs such as kidney and may lead to formation
of stones in the kidneys.

176. Vitamin E (Tocopherol)
Structure
Vitamin E consists of eight naturally occurring tocopherols,
of whichα-tocopherolis the most active form

177. Sources
The major dietary sources of vitamin E are fats and oils.
The richest sources are germ oil, corn oil, fish oil, eggs,
lettuce and alfalfa.
NutritionalRequirements
A daily consumption of about:
10 mg (15 IU) ofα-tocopherolfor a man
8 mg (12 IU) forα-woman is recommended.
Onemg ofα-tocopherolis equal to 1.5 IU.
Sources
The major dietary sources of vitamin E are fats and oils.
The richest sources are germ oil, corn oil, fish oil, eggs,
lettuce and alfalfa.
NutritionalRequirements
A daily consumption of about:
10 mg (15 IU) ofα-tocopherolfor a man
8 mg (12 IU) forα-woman is recommended.
Onemg ofα-tocopherolis equal to 1.5 IU.

178. Functions
VitaminE acts as a naturalantioxidantby scavenging
free radicals and molecular oxygen.
VitaminE is important for preventing peroxidation of
polyunsaturated fatty acids in cell membranes.
Protectionof erythrocyte membrane from oxidant is the
major role of vitamin E in humans. It protects the RBCs
from hemolysis.
Functions
VitaminE acts as a naturalantioxidantby scavenging
free radicals and molecular oxygen.
VitaminE is important for preventing peroxidation of
polyunsaturated fatty acids in cell membranes.
Protectionof erythrocyte membrane from oxidant is the
major role of vitamin E in humans. It protects the RBCs
from hemolysis.

179. Vitamin E also helps to prevent oxidation of LDL.
Oxidized LDL may be more atherogenic than native LDL
and thus vitamin E may protect against athreo­matous
coronary heart disease.
Whether vitamin E affects human fertility is unknown.
In animals, vitamin E is required for normal reproduction
and prevents sterility.
Vitamin E also helps to prevent oxidation of LDL.
Oxidized LDL may be more atherogenic than native LDL
and thus vitamin E may protect against athreo­matous
coronary heart disease.
Whether vitamin E affects human fertility is unknown.
In animals, vitamin E is required for normal reproduction
and prevents sterility.

180. Deficiency Manifestation
Themajor symptom of vitamin E deficiency in human is
hemolytic anemiadue to an increased red blood cell fragility.
Anothersymptom of vitamin E deficiency isretrolental
fibroplasia (RLF)observed in some premature infants of low
birth weight. Children with this defect showneuropathy.
Hypervitaminosis E
Unlike other fat soluble vitamins such as A and D, vitamin E
does not seem to have toxic effects.
Deficiency Manifestation
Themajor symptom of vitamin E deficiency in human is
hemolytic anemiadue to an increased red blood cell fragility.
Anothersymptom of vitamin E deficiency isretrolental
fibroplasia (RLF)observed in some premature infants of low
birth weight. Children with this defect showneuropathy.
Hypervitaminosis E
Unlike other fat soluble vitamins such as A and D, vitamin E
does not seem to have toxic effects.

181. Vitamin K
This vitamin is called ananti-hemorrhagic factoras its
deficiency produced uncontrolled hemorrhages due to
defect in blood coagulation.
In1929, H Dam gave the name koagulation vitamin from
the Danish wordkoagulation. It is now called vitamin K.
Vitamin K
This vitamin is called ananti-hemorrhagic factoras its
deficiency produced uncontrolled hemorrhages due to
defect in blood coagulation.
In1929, H Dam gave the name koagulation vitamin from
the Danish wordkoagulation. It is now called vitamin K.

182. Structure
VitaminK1 or phylloquinonederived from plant.
VitaminK2 or menaquinones, produced by
microorganisms.
VitaminK3 or menadioneis a syntheticproduct
Structure
VitaminK1 or phylloquinonederived from plant.
VitaminK2 or menaquinones, produced by
microorganisms.
VitaminK3 or menadioneis a syntheticproduct

183. Structureof vitamin K.

184. Sources
Excellentsources are cabbage, cauliflower, spinach and
other green vegetables.
Goodsources include tomatoes, cheese, dairy products,
meat, egg yolk, etc.
Thevitamin is also synthesized by microorganisms in the
intestinal tract.
NutritionalRequirements
The suggested intake for adults is70–140 mg/day.
Sources
Excellentsources are cabbage, cauliflower, spinach and
other green vegetables.
Goodsources include tomatoes, cheese, dairy products,
meat, egg yolk, etc.
Thevitamin is also synthesized by microorganisms in the
intestinal tract.
NutritionalRequirements
The suggested intake for adults is70–140 mg/day.

185. Functions of Vitamin K
VitaminK plays an important role inblood coagulation.
Vitamin K is required for theactivationof bloodclotting
factors, prothrombin (II), factor VII, IX and X.
Theseblood clotting proteins are synthesized in liver in
inactive form, and are converted to active form by
vitamin K dependent carboxylationreaction.
In this, vitamin K dependent carboxylase enzyme adds
the extra carboxyl group at-carbon of glutamic acid
residues of inactive blood clotting factors.
Functions of Vitamin K
VitaminK plays an important role inblood coagulation.
Vitamin K is required for theactivationof bloodclotting
factors, prothrombin (II), factor VII, IX and X.
Theseblood clotting proteins are synthesized in liver in
inactive form, and are converted to active form by
vitamin K dependent carboxylationreaction.
In this, vitamin K dependent carboxylase enzyme adds
the extra carboxyl group at-carbon of glutamic acid
residues of inactive blood clotting factors.

186. Roleof vitamin K in the gamma-carboxylation of glutamyl residues of inactive
proteins of blood-clotting factors.

187. VitaminK is also required for the carboxylation of
glutamic acid residues ofosteocalcin, a Ca2+ binding
protein present in bone.
Anticoagulants,Dicumarolandwarfarinarestructurally
similar to vitamin K and inhibit the action of vitamin K.
VitaminK is also required for the carboxylation of
glutamic acid residues ofosteocalcin, a Ca2+ binding
protein present in bone.
Anticoagulants,Dicumarolandwarfarinarestructurally
similar to vitamin K and inhibit the action of vitamin K.

188. DeficiencyManifestation
Vitamin K is widely distributed in nature and its production
by the intestinal micro flora ensures that dietary deficiency
does not occur.
VitaminK deficiency is associated withhemorrhagic
disease.
In vitamin K deficiency,clotting timeof blood is
increased. Uncontrolled hemorrhages occur on minor
injuries as a result of reduction in prothrombin and other
clotting factors.
DeficiencyManifestation
Vitamin K is widely distributed in nature and its production
by the intestinal micro flora ensures that dietary deficiency
does not occur.
VitaminK deficiency is associated withhemorrhagic
disease.
In vitamin K deficiency,clotting timeof blood is
increased. Uncontrolled hemorrhages occur on minor
injuries as a result of reduction in prothrombin and other
clotting factors.

189. Vitamin K deficiency, however, is found in:
Patientswith liver diseaseandbiliaryobstruction.Biliary
obstruction inhibits the entry of bile salts to the intestine.
In new-borninfants, because the placenta does not pass
the vitamin to the fetus efficiently, and the gut is sterile
immediately after birth.
Followingantibiotic therapythat sterilizes the gut.
Infat malabsorption, that impairs absorption of vitamin
K.
Vitamin K deficiency, however, is found in:
Patientswith liver diseaseandbiliaryobstruction.Biliary
obstruction inhibits the entry of bile salts to the intestine.
In new-borninfants, because the placenta does not pass
the vitamin to the fetus efficiently, and the gut is sterile
immediately after birth.
Followingantibiotic therapythat sterilizes the gut.
Infat malabsorption, that impairs absorption of vitamin
K.

190. HypervitaminosisK
Excessive doses of vitamin K produce a hemolytic anemia
(due to increased breakdown of RBCs) and jaundice (in
infants).
HypervitaminosisK
Excessive doses of vitamin K produce a hemolytic anemia
(due to increased breakdown of RBCs) and jaundice (in
infants).

191. Thank you