this presentation shows different watre soluble vitamins and their role in our daily life and what happens if they become deficient in our body and how we can overcome this deficiency of these vitamins.

1. WATER SOLUBLE
WATER SOLUBLE
VITAMINS
VITAMINS
DR MEENAL ATHARKAR
MDS
DEPT OF ENDODONTICS AND
CONSERVATIVE DENTISTRY

4. SYNONYM- ANTI SCORBUTIC VITAMIN

7. METABOLISM,ABSORPTION,DISTRIBUTION &
EXCRETION
• Absorbed readily from small intestine,peritonium &
subcutaneous tissue.
• From maternal blood,it can cross placental barrier &
supplies the foetus.
• Normal blood plasma contains aprox 0.6-1.5mg of ascorbic
acid /100ml.
acid /100ml.
• It is also secreted in milk.
• Under normal dietary intake 75-100 mg
• Converted to inactive form
50-75%
• Excreted in urine
25-50%

8. GOOSEBERRY(AMALA),ORANGE,LEMON GUAVA

9. • 60-70mg/day – ADULTS
• 30 mg/day – INFANTS
• 100mg/day –PREGNANT WOMEN
• 100mg/day –PREGNANT WOMEN
• 150mg/day – LACTATING WOMEN

10. METABOLIC ROLE & FUNCTION
1) Role in collagen synthesis - hydroxyproline &
hydroxylysine are important constituent of mature
collagen, vit C is necessary for maintenance of normal
connective tissue & wound healing process.

11. 2. Bone formation- bone tissues possess an organic
matrix, collagen & inorganic calcium, phosphate, etc.
Vit C is required for bone formation.
3. Activity of fibroblast/osteoblast- ascrobic acid is
required for formation of MPS of connective tissue,
osteoid tissue, dentine & intercellular cement substance
of capillary.
of capillary.

16. DETECTION OF DEFICIENCY IN MAN
1. URINE ASCORBIC ACID SATURATION TEST- Administer test dose -
5mg/lb body wt . If 50% or more is excreted in next 24 hr, the
individual has no defect of vitamin.
2. INTRADERMAL TEST – Consists of Intradermal inj of 2,6-
dicholorophenol indophenol & determine time required for
decolorization . Abnormally long persistence of blue color in
cutaneous wheal indicates subsaturation of ascorbic acid.
cutaneous wheal indicates subsaturation of ascorbic acid.
3. TORNIQUENT TEST – a sphygmomanometer cuff is applied
around the arm & inflated so that it compresses the venous
flow. In short time , appearance of several petechial
hemorrhages on the skin indicates deficiency.

18. “CORK-SCREW” Hair pattern seen.
“WOODY LEGS. ” Seen.

19.  Pathognomic sign- swollen,spongy gums ,
particularly interdental papilla-scurvy bud
appearance.
 In sever cases -hemorrages to periodontal
ORAL MANIFESTATION
 In sever cases -hemorrages to periodontal
membrane, loss of bone , loosening of teeth.
 Poor dentine formation-in children leading to poor
teeth formation.

20. i
 In treatment & control of infectious disease.
Vit C helps in wound healing,in ulcer , trauma ,
burn.
During labour- vit C given in doses of 150-
200mg produces an oxytoxic action,increasing
200mg produces an oxytoxic action,increasing
both in frequency & intensity of uterine
contraction, in methaemoglobinaemia may be
used for its reducing property.

22. • SYNONYMS- anti beri beri, anti neuritic
vitamin, aneurin.
• Water soluble
• Has specific enzyme TPP –associated with
CARBOHYDRATE MEATBOLISM.
CARBOHYDRATE MEATBOLISM.

23. is

27. • ADULTS- 1-1.5 mg/day
• INFANTS-0.4mg/day
• PREADOLESCENT-1.3mg/day
• PREGNANCY- 2mg/day
• PREGNANCY- 2mg/day

28. Requirement increases in-
• Anoxia –shock, haemorrage ,serious illness
&injury during prolonged administration of
broad spectrum oral antibiotics.
• Increased carbohydrate intake.
• Increased calorie expenditure like fever.
• Increased calorie expenditure like fever.
• Increased alcohol intake &pregnancy& in
lactation.

29. LIVER, MEAT,EGG,PORK/HAM –RICH SOURCE.
IN CEREALS CONCENTRATED IN OUTER GERM. PEA,BEAN, WHOLE CEREAL GRAIN,NUTS ..ETC….

34. Breathlessness
Hheart failure

36. ccolic

38. THIAMINE ANTAGONIST
• Pyrithiamine-thiazole ring is replaced by a
pyridine ring,it is a potent antagonist to
thiamine.
• Oxy-thiamine & 2-n-butyl thiamine are milder
• Oxy-thiamine & 2-n-butyl thiamine are milder
antagonists.

40. • Synonyms- lactoflavin,ovoflavin,hepatoflavin
CHEMISTRY-
• It is an orange-yellow compound containing
* a ribose alcohol-D-Ribitol
* a hetrocyclic parent ring structure
“isoallaxone”
• Riboflavin contains 6,7-dimethyl isoallaxazine
• Riboflavin contains 6,7-dimethyl isoallaxazine
attached to D-ribitol by a nitrogen atom.
• Ribitol is open chain form of sugar ribose with
aldehyde group reduced to alcohol.

41. COENZYME OF RIBOFLAVIN

43. chain.

44. • Absorption-flavin nucleotide readily absorbed
in small intestine ,free riboflavin under goes
phosphorylation, a prerequisite for
absorption.
• Riboflavin present in all tissues as nucleotide
• Riboflavin present in all tissues as nucleotide
bound to protein highest concentration in liver
& kidney.
• Excretion- upto 50% as nucleotide in urine.
Daily urinary excretion 0.1 to 0.4 mg.

45. • Adult- 1.2 -1.7 mg
• Woman –pregnancy-2.0 mg
lactation-2.5 mg
• Infants-0.6 mg
• Infants-0.6 mg
• Children-1.0-1.8 mg
• Adolescence- 2.0 -2.5 mg

46. PLANT-YEAST,WHOLE GRAIN, DRY BEAN,PEA NUTS,DAL.
ANIMAL- LIVER,KIDNEY,MILK EGG,CRAB MEAT.

47. • Lession of mouth,tongue,nose,skin &eyes with
weakness & lassitude is reported.
• Lips-redness & shiny appearance.
• Cheilosis- angle of mouth leading to painful
fissures.
Tongue – painful glossitis,tongue becomes red-
• Tongue – painful glossitis,tongue becomes red-
purple colour.
• Eyes- corneal vascularization & inflamation with
cloudiness of cornea, watering , burning of eye.

48. ORAL MANIFESTATION
-
riboflavin deficiency.

49. ANTIMETABOLITE
• GALACTOFLAVIN IS ANTI METABOLITE OF
RIBOFLAVIN.

50. • Nasolabial seborrhea
• Vascularisation of cornea
• Scrotal dermatitis

51. VITAMIN

53. CHEMISTRY & SYNTHESIS OF
COENZYME

55. • Coenzymes NAD+ &NADP+ are involved in variety of
oxidation-reduction reaction.
• They accept hydride ion & undergo reduction in pyridine
ring. This results in neturalization of positive charge.
• Nitrogen atom at 4th carbon atom of nicotinamide ring
participate in reaction. While one atom of hydrogen is
accepted by coenzyme ; the other hydrogen ion is
accepted by coenzyme ; the other hydrogen ion is
released into surrounding.
• This reaction is reversed when NADH is oxidized to
NAD+,NADP+ also functions like NAD+ in oxidation-
reduction reaction.

56. • ADULT- 17 -21 mg/day
• Adolescence- 17mg/day
• Infant – 6 mg /day

57. RICH SOURCE-LIVER,YEAST,WHOLE GRAIN,CERIALS,PULSES.
MODERATE SOURCE-MILK,EGG,FISH.

58. • PELLAGRA- nicotinic acid deficiency causes pellagra.
• Cardinal features are – 3 D’s
DERMATITIS
DIARRHOEA
DEMENTIA
A) Skin lessions- skin exposed to sunlight & subjected to
A) Skin lessions- skin exposed to sunlight & subjected to
pressure, heat or other trauma.
B) GI manifestation-
anorexia,nausea,vomitting,abdominal pain.
C) Cerebral manifestation-headache, insomnia,
depression & other mental symptoms.

59. • BALD TONGUE OF SANDWITH
• PROFUSED SALIVATION
• RED BEEFY TONGUE
• Gingivitis & Stomatitis with reddening
• Gingivitis & Stomatitis with reddening
of tip & margin of tongue, which
becomes swollen & cracked.

61. • In Greek- Pantos-everywhere.
• It is also k/n chick anti-dermatitis
factor,filtrate factor.
• Its metabolic role as co-enzyme A is
wide spread.
wide spread.

65. For human – not clearly known.
ADULTS- 5-10 mg/day

66. • Rich sources are – egg , liver ,
meat , yeast , milk , etc …

68. n

69. b6
PYRIDO
PYRIDO
XIN

71. • Vitamin b6 compounds are pyridine derivatives.
• They differ from each other in structure of functional
group attached to 4th carbon in pyridine ring.
• Pyridoxine is primary alcohol, pyridoxal is aldehyde
form while pyridoxamine is an amine.
form while pyridoxamine is an amine.

72. • active form of vit B₆ is coenzyme pyridoxal
phosphate (PLP)
• PLP can be synthesized from 3 compounds
pyridoxine, pyridoxal & pyridoxamine.
• B₆ is excreted in urine as 4-pyridoxic acid.
• B₆ is excreted in urine as 4-pyridoxic acid.

76. • ABSORPTION- Dietary vit B₆ gets absorbed by
intestine.
• EXCRETION- Pyridoxal & pyridoxamine –
excreted in urine. (0.5 to 0.7mg/day )
excreted in urine. (0.5 to 0.7mg/day )

77.  ADULT- 2mg/day
INFANT -0.3 -0.4 mg/day
PREGNANCY - 2.5 mg/day
PREGNANCY - 2.5 mg/day

78. DIETARY SOURCE
RICH SOURCE- YEAST, GERMINAL PORTION OF VARIOUS SEEDS & CEREAL GRAIN,EGG YOLK.
MODERATE SOURCE-LIVER,KIDNEY,MUSCLE,FISH

80. • Decrease in hb level,associated with
hypochromic microcytic anemia-seen in vit b₆
deficiency.
• Dietary deficiency of pyridoxine is rare & is
observed in women consuming oral
contraceptives, alcoholics .
contraceptives, alcoholics .

81. • ISONIAZID is a drug used for treatment of Tb.
patients on long term use of isoniazid ,develop
peripheral neuropathy ,which responds to B₆
therapy.
• Penicillamine is a drug used for treatment of
• Penicillamine is a drug used for treatment of
Rheumatoid Arthritis ,Wilson’s disease & cystinuria .
This drug reacts with PLP to form inactive
thiazolidine derivatives. Therefore pyridoxine
supplementation should be taken to avoid B₆
DEFICIENCY.

82. Pyridoxine antagonist
Isoniazid
Deoxypyridoxine
 Methoxy pyridoxine

83. Toxic effect of overdose of B₆
• More than 200mg/day of B₆ MAY cause
neurological damage.

84. biotin

89. biotin
biotin
Propionyl Co A Methylmalonyl CoA
propionyl CoA carboxylase

90. ADULTS – 100-300 mg/day
To what extent the synthesized
biotin contributes to body
requirement is not known clearly.
requirement is not known clearly.

91.  Plant Source – tomatoes , grains
 Animal Source liver , kidney, egg yolk,milk.

92. Causes of defeciency- a) destruction of intestinal flora
due to prolonged use of drugs such as
sulfonamides.
b) High consumption of raw eggs .about 20 raw eggs
per day is needed to cause deficiency.
per day is needed to cause deficiency.
Blocks absorption from intestine
Raw egg white
Glycoprotein avidin biotin

94. ANTAGONIST
• Desthiobiotin
• Biotin sulphonic acid

95. FOLIC ACID
9

101.  ADULT – 400-500 mg/day
INFANT – 50mg/day
CHILD – 100-300 mg/day
PREGNANT WOMAN – 800 mg/day
PREGNANT WOMAN – 800 mg/day
 LACTATING WOMAN – 600 mg/day

102. MILK IS POOR SOURCE…

103. absorption

105. • Other manifestation include- growth
retardation,weakness, lethargy, reproduction
difficulties , inadequate lactation.
• Bone marrow – shows arrested development
of all elements- erythroid, myeloid &
thrombocytes.
thrombocytes.
• Megaloblast & myeloblast accumulate at the
expence of more mature cells viz. erythroblast
, myeloblast. The number of megakaryocytes
decresses.

106. GLOSSITIS -
The filliform papillae disappear first , but in
advance cases the fungiform papillae are lost &
tongue becomes smooth & fiery red in colour.

110. C
Y
N
O
C
O
B
A
A
L
A
M
I
N
E

111. • SYNONYM - anti pernious vitamin , extrensic factor of
castle .
• CHEMISTRY-
o Structure of vit B₁₂ consists of a corrin ring with a central
cobalt atom.
o Corrin ring is similar to tetrapyrole ring structure found in
other prophyrin compounds eg : heme & chlorophyll.
There are 2 coenzyme of vit B ₁₂
o There are 2 coenzyme of vit B ₁₂
a) Methyl cobalamine- in which cyanide isreplaced by
methyl group.
b)5’deoxyadenosyl cobalamin – cynide is replaced by
5’deoxyadenosin forming an unusual carbon cobalt bond.

112. • ABSORPTION –
1)VIT B₁₂ is absorbed from ileum. It requires
presence of Hcl & intrensic factor of castle , a
constituent of normal gastric juice.
2) INTRENSIC FACTOR –secreted by parietal cell, its
a glycoprotein ,constituent of gastric muco
protein.
protein.
It is destroyed by heat at 70 -80 degree C for half
an hour.
Inactivated by prolonged digestion with
pepsin/trypsin
Found in cardiac end & fundus of stomach but not
in pylorus.

113. • EXCRETION –practically there is no urinary
excretion, but following parenteral
adminstration there is excretion upto 0.3
mg/day.
• STORAGE – mainly in liver .

114. Adult – 3mg/day
Infants – 0.3mg/day
Children – 1-2 mg/day
Pregnancy/lactation -4 mg/day
Pregnancy/lactation -4 mg/day

116. • 1) ADULT PERNIOUS ANEMIA – vit B ₁₂
deficiency produces macrocytic anemia. In
addition to haematological manifestation, it is
combined with neurological features.
• Degenerative changes of posterior lateral
• Degenerative changes of posterior lateral
column of spinal cord, resulting in peripheral
sensory disturbance,hyperactive
reflexes,ataxia,paralysis.

117. • 3) BONE MARROW –shows evidence of
arrested development of all the elements-
erythroid,myeloid,thrombocytes.
• Number of megakaryocytes decreses.
• 4) DNA SYNTHESIS- in pernious anemia,DNA
synthesis in maturing RBC is depressed.
• Failure in conversion of RNA to DNA.
• Failure in conversion of RNA to DNA.
Prolonged resting phase b/w successive mitosis
of maturing RBC.
5)Congenital pernious anemia
6) Juvenile pernious anemia.

118. Beefy red tongue with glossopyrosis ,glossitis
& glossodynia.
Hunter’s glossitis which is similar to bald
tongue of sand with seen in pellagra.

119. REFERENCES
 HARPER’S BIOCHEMISTRY
 VASUDEVEN
 U. SATAYANARAYANA-ESSENTIAL OF BIOCHEM.
 M.N. CHATTERJEE- MEDICAL BIOCHEMISTRY
 M.N. CHATTERJEE- MEDICAL BIOCHEMISTRY
 HARSH MOHAN-ESSENTIAL OF PATHOLOGY
 PICTURES FROM INTERNET