Water Soluble Vitamins - Chemistry, Sources, RDA, Deficiency,Symptoms.

1. WATER SOLUBLE
VITAMINS
PREPARED BY:
NEHA SHETH
TUTOR
DEPT. OF BIOCHEMISTRY
PARUL INSTITUTE OF MEDICAL SCIENCES & RESEARCH

3. ASCORBIC ACID (VITAMIN C)
• Water soluble vitamin
• Easily destroyed by heat , alkali and
storage.
• In process of cooking, 70% of Vitamin
C is lost.
Carbohydrat
es
Hexose
derivative

4. CHEMISTRY
The strong reducing
property of Vitamin C
depends on the double-
bonded (enediol)
carbon.
Enediols: the two hydroxyl groups are attached to
the double-bonded carbon.

5. Possess
Antiscorbutic
activity
Possess
Antiscorbutic
activity
NO Antiscorbutic
activity

6. OXIDATION OXIDATION
Inactive
Oxidation of ascorbic acid is rapid in the presence of
copper. Hence Vitamin C become inactive if the foods are

7. The plasma and tissues contain ascorbic acid in
the reduced form.
Ratio
15:1

8. BIOSYNTHESIS OF ASCORBIC ACID IN ANIMALS
• MOST ANIMALS AND PLANTS CAN SYNTHESIS ASCORBIC ACID FROM
GLUCOSE.
• HIGHER PRIMATES, HUMAN AND GUINEAPIGS AND BATS ARE THE ONLY
SPECIES WHICH CANNOT SYNTHESIS ASCORBIC ACID.
• REASON:
THEY LACK IN SINGLE ENZYME L-GULONOLACTONE OXIDASE.
THE VITAMIN, THERE FORE SHOULD BE SUPPLIED IN THE DIET OF
THESE SPECIES.
STAPLE DIET SHOULD CONTAIN FRUITS AND VEGETABLES RICH
IN ASCORBIC ACID.

10. METABOLISM OF ASCORBIC ACID
• READILY ABSORBS FROM THE GASTROINTESTINAL TRACT.
• VITAMIN IS EXCRETED IN THE URINE.
• VITAMIN C IS STRONG REDUCING AGENT, THE
BENEDICT'S TEST WILL BE POSITIVE IN THE URINE SAMPLE
AFTER THE VITAMIN ADMINISTRATION.

11. OXIDATION OXIDATION
Ascorbic acid is partly excreted unchanged and
partly as oxalic acid. Most of the oxalates in urine
are derived from ascorbic acid, and the rest from
glycine metabolism.

12. REFERENCE VALUE OF VITAMIN C
• ASCORBIC ACID (VITAMIN C) – 0.7 – 1.2 mg/dL OF PLASMA
• LOW LEVELS IN BLOOD IS NOTED IN :
WOMEN TAKING CONTRACEPTIVE PILLS
CHRONIC ALCOHOLICS
• VERY HIGH CONCENTRATION IS OBSERVED LOCALLY IN HEALING
WOUNDS.
THUS, VITAMIN C IS IMPORTANT FOR WOUND HEALING.

13. REVERSIBLE OXIDATION-REDUCTION
Biochemical functions of
Vitamin C

14. 1. COLLEGEN FORMATION
• ESSENTIAL FOR THE
FORMATION OF
CROSS LINKS IN THE
COLLAGEN, WHICH
GIVES THE TENSILE
STRENGTH TO THE
FIBRES.
2. BONE
FORMATION

15. 3. TRYPTOPHAN METABOLISM
• REQUIRED FOR
THE FORMATION
OF SEROTONIN
• ENZYME:
HYDROXYLASE
Ascorbic Acid

16. 4. TYROSINE METABOLISM
• REQUIRED TO FORM
HOMOGENTISIC ACID
• ALSO INVOLVED IN SYNTHESIS
OF CATECHOLAMINES FROM
TYROSINE

17. • ENZYME :
DOPAMINE- BETA-
HYDROXYLASE

18. 5. IRON METABOLISM
ASCORBIC ACID ENHANCES THE IRON ABSORPTION FROM THE INTESTINE BY
KEEPING IT IN THE FERROUS STATE
THIS IS DUE TO REDUCING PROPERTY OF VITAMIN.
IT HELPS IN THE FORMATION OF FERRITIN (STORAGE FORM OF IRON)
AND MOBILIZATION OF IRON FROM FERRITIN.
It is useful for re-conversion of met-hemoglobin to
hemoglobin.

19. 7. FOLIC ACID METABOLISM
ASCORBIC ACID IS HELPING THE ENZYME FOLATE REDUCTASE TO REDUCE
FOLIC ACID TO TETRAHYDROFOLIC ACID (FH4) ( ACTIVE FORM OF FOLIC ACID).
THUS IT HELPS IN THE MATURATION OF RBC.
8. SYNTHESIS OF CORTICOSTEROID HORMONES
ADRENAL GLAND POSSESSES HIGH LEVELS OF ASCORBIC ACID,
PARTICULARLY DURING STRESS. IT IS NECESSARY FOR HYDROXYLATION
REACTIONS IN THE SYNTHESIS OF HORMONES.
VITAMIN C HELPS IN THE SYNTHESIS OF BILE ACIDS FROM
CHOLESTEROL.

20. 9. IMMUNOLOGICAL FUNCTION
ENHANCES THE SYNTHESIS OF IMMUNOGLOBINS (ANTIBODIES) AND INCREASE
THE PHAGOCYTIC ACTION OF LEUKOCYTES.
10. ANTI-OXIDANT PROPERTY / SPARING ACTION
SPARES VITAMIN A, VITAMIN E AND SOME B-COMPLEX VITAMINS FROM
OXIDATION.
11. PREVENTIVE ACTION ON CATARACT
REDUCES THE RISK OF CATARACT FORMATION.
11. PREVENTIVE ACTION ON CHRONIC DISEASES

21. DEFICIENCY SYMPTOMS OF VITAMIN
C
DEFICIENCY OF VITAMIN C RESULTS IN SCURVY.
CHARACTERIZED BY:
• SPONGY AND SORE GUMS
• LOOSE TEETH
• ANEMIA
• SWOLLEN JOINTS
• FRAGILE BLOOD VESSELS
• DELAYED WOUND HEALING
• SLUGGISH HORMONAL FUNCTION OF ADRENAL CORTEX AND GONADS
• OSTEOPOROSIS
• HEMORRHAGE

23. INFANTILE SCURVY (BARLOW'S
DISEASE):
OCCURS IN INFANTS BETWEEN 6 TO 12 MONTHS OF AGE,
(PERIOD IN WHICH WEANING FROM BREAST MILK), THE
DIET SHOULD BE SUPPLEMENTED WITH VITAMIN C
SOURCES. OTHERWISE, DEFICIENCY OF VITAMIN C IS SEEN.

24. DIETARY SOURCES OF VITAMIN C
REQUIREMENT OF VITAMIN C
RECOMMENDED DAILY ALLOWANCE : 75 MG/DAY
(EQUAL TO 50 ML ORANGE JUICE).
DURING PREGNANCY, LACTATION, AND IN AGED PEOPLE REQUIREMENT MAY BE 100 MG/
DAY

25. THERAPEUTIC USE OF VITAMIN C
• VITAMIN C IS USED AS AN ADJUVANT IN INFECTIONS.
• BENEFICIAL EFFECT OF ASCORBIC ACID IS REPORTED IN THE TREATMENT OF
TUBERCULOSIS
• VITAMIN C HAS BEEN RECOMMENDED FOR TREATMENT OF ULCER, TRAUMA
AND BURNS.
• EXCEPT IN SCURVY AND SUB-SCORBUTIC
CONDITIONS THE THERAPEUTIC USE OF VITAMIN IS
NOT SPECIFIC.

26. TOXICITY OF VITAMIN C
• SINCE IT IS A WATER SOLUBLE SUBSTANCE, EXCESS VITAMIN C IS
EXCRETED, AND NOT ACCUMULATED IN THE BODY.
• HOWEVER, MORE THAN 2000 MG OF VITAMIN C DAILY FOR A LONG
TIME CAN CAUSE IRON OVERLOAD, BECAUSE VITAMIN C HELPS IN
ABSORPTION OF IRON.
• OXALATE IS A MAJOR METABOLITE OF VITAMIN C AND IT IS BEEN
IMPLICATED IN THE FORMATION OF KIDNEY STONE.

27. CHOOSE THE ODD ONE OUT..
A. VITAMIN A
B. VITAMIN D
C. VITAMIN C
D. VITAMIN E
E. VITAMIN K

28. ASCORBIC ACID IS REQUIRED IN THE
EFFECTIVE UTILIZATION OF ALL OF THE
FOLLOWING AMINO ACID EXCEPT ..
A. METHIONINE
B. TRYPTOPHAN
C. TYROSINE
D. PROLINE
E. LYSINE

29. SCURVY IS DUE TO IMPAIRED ……
SYNTHESIS
A. COLLAGEN
B. PROTHROMBIN
C. HAEMOGLOBIN
D. ELASTIN
E. ALBUMIN
S

30. A 20-YEAR-OLD MALE PRESENTS WITH
HYPERTENSION. HE HAS BEEN PRESCRIBED A
DRUG THAT WORK BY INHIBITING THE
SYNTHESIS OF CATECHOLAMINES. WHICH OF
THE FOLLOWING VITAMINS PARTICIPATES IN
THE SYNTHESIS OF CATECHOLAMINES?
A. VITAMIN B12
B. VITAMIN C
C. NIACIN
D. FOLIC ACID

31. THESE VITAMINS ARE CHEMICALLY NOT RELATED
TO ONE ANOTHER. THEY ARE GROUPED TOGETHER
BECAUSE ALL OF THEM FUNCTION IN THE CELLS AS
COENZYMES.
THIAMINE
RIBOFLAVIN
NIACIN
PYRIDOXINE
PANTOTHENIC ACID
BIOTIN
FOLIC ACID
CYANOCOBALAMIN
B-COMPLEX GROUP OF VITAMINS

33. Vitamin Function
Vitamin
B1
• Biological active form of TPP
• principally involved in carbohydrate metabolism
Vitamin
B2
• Serve as coenzyme (FAD and FMN)
Vitamin
B3
• Serve as coenzyme (NAD+ and NADH)
Vitamin
B5
• Active form of Coenzyme A
Vitamin
B6
• Serve as coenzyme ( PLP)
• Principally involved in amino acid metabolism
Vitamin
B7
• serves as carrier of C02 in carboxylation reaction.
Vitamin • active form is THF or FH4

34. THIAMINE (VITAMIN B1)/
ALSO, called as Aneurine ( it can relieve neuritis) or antiberiberi factors.
STRUCTURE OF THIAMINE:
Active coenzyme
• Water soluble
vitamin
• Coenzyme form:
TPP
• Partially destroyed
by the heat

35. SOURCES
• Rich Source: Aleurone layer of cereals (food grains).
• Therefore, whole wheat flour and unpolished rice have better
nutritive value than completely polished fined foods.
• Good Source: Yeast.
Aleuron
e layer

36. PHYSIOLOGICAL ROLE OF THIAMINE
Pyruvate
dehydrogenase
Alpha-
ketoglutarate
dehydrogenase
Trans ketolase
Main role of thiamine (TPP) is in Carbohydrate
Metabolism. So, the requirement of thiamine is
increased along with higher intake of
carbohydrates.

37. HMP SHUNT PATHWAY CITRIC ACID CYCLE

39. • THE OXIDATIVE DECARBOXYLATION OF BRANCHED CHAIN AMINO
ACIDS TO THE RESPECTIVE KETO ACIDS. (ENZYME -
DEHYDROGENASE) REQUIRES TPP.
• TPP PLAYS IMPORTANT ROLE IN THE TRANSMISSION OF NERVE
IMPULSE.
( REQUIRED FOR ACETYLCHOLINE SYNTHESIS)

40. DEFICIENCY MANIFESTATION OF
THIAMINE
Beriberi
•Singhalese Meaning
“Weakness” / I
cannot
•Symptoms:
 anorexia
Dyspepsia
Heaviness
Weakness
Types: WET beriberi
Wet Beriberi
•Cardiovascular
manifestation are
prominent.
•Main features
 Edema of legs, face,
trunk and serous
cavities.
Observation: of
palpitation,
breathlessness,
Dry beriberi
• CNS manifestation
are prominent.
•Main features:
 walking become
difficult
Peripheral neuritis
with sensory
disturbances lead to
complete paralysis.

42. Infantile Beriberi
• Occurs in infants born
to mothers suffering
from thiamine
deficiency
• Observation:
restlessness,
sleeplessness
Wernicke-Korsakoff
syndrome
• Also called as cerebral
beriberi
Seen only when the
nutritional status is
severely affected.
Polyneuritis
• Common in chronic
alcoholics.
• Alcohol utilization
requires large doses
of thiamine.
• Alcohol inhibit
intestinal absorption
of thiamine.
• May also be associated
with pregnancy and
old age.

43. WERNICKE-KORSAKOFF SYNDROME
• ALSO CALLED AS CEREBRAL BERIBERI
• MOSTLY SEEN IN CHRONIC ALCOHOLICS.
• THE BODY DEMANDS OF THIAMINE INCREASE IN ALCOHOLISM.
• CAUSES:
INSUFFICIENT INTAKE
IMPAIRED INTESTINAL ABSORPTION OF THIAMINE
• CLINICAL FEATURES:
LACK OF INTEREST (APATHY)
 LACK OF CONTROL ON FINE VOLUNTARY MOVEMENT (CEREBELLAR ATAXIA)
RHYTHMICAL TO AND FRO MOTION OF THE EYE BALLS (NYSTAGMUS)
SEVERE MENTAL DISORDER IN WHICH THOUGHT AND EMOTIONS ARE SO IMPAIRED

44. VITAMIN B1 DEFICIENCY (IN ALCOHOLISM)
LEADS TO LACTIC ACIDOSIS

45. BIOCHEMICAL PARAMETERS
• Blood thiamine is reduced.
• But pyruvate, alpha-ketoglutarate and lactate are
increased.
• Erythrocyte transketolase activity is reduced; this
is the earliest symptoms seen even before clinical
disturbances.
( comatose patients, alcoholics, CRF, malnutrition
as well as in elderly patients).

46. • A LIPID SOLUBLE ACYLATED DERIVATIVE (
BENFOTIAMINE) IS NOW BEING RECOMMENDED
FOR DIABETIC PATIENTS TO DECREASE
GLYCATION OF PROTEIN (AGE) AND TO IMPROVE
DIABETIC NEUROPATHY.

47. THIAMINE DEFICIENCY DUE TO
THIAMINASE
THIAMINASE IS PRESENT IN CERTAIN SEAFOODS.
THEIR INCLUSION IN DIET WILL DESTROY VITAMIN
THIAMINE BY CLEAVAGE ACTION (PYRIMIDINE AND
THIAZOLE RING SPLIT)
INCIDENT : BERI BERI IN SOME PART OF JAPAN IS
ATTRIBUTED TO THE CONSUMPTION OF FISH ( RICH
IN THIAMINASE).

48. THIAMINE ANTAGONISTS
• PYRITHIAMINE
• OXYTHAIMINE

49. RDA
• It depends on calories intake (0.5mg/1000
calories)
• Requirement is 1 – 1.5 mg/day.
• Thiamine is useful in the treatment of beriberi,
alcoholic polyneuritis, neuritis of pregnancy and

50. RIBOFLAVIN/ VITAMIN B2
• STRUCTURE
6,7-Dimethyl
Isoalloxazine
ring
D-Ribitol
Heat Stable but sensitive to
light.

51. ACTIVE/ COENZYME FORM OF RIBOFLAVIN

52. RIBOFLAVIN EXISTS IN TISSUES TIGHTLY BOUND (NOT COVALENTLY) WITH ENZYMES.
ENZYMES CONTAINING RIBOFLAVIN ARE CALLED FLAVOPROTEINS.
MANY FLAVOPROTEINS CONTAINS METAL ATOMS (IRON, MOLYBDENUM, ETC ) WHICH IS
KNOWN AS METALLOFLAVOPROTEINS.

53. BIOCHEMICAL FUNCTIONS
PARTICIPATES IN MANY REDOX REACTIONS RESPONSIBLE
FOR ENERGY PRODUCTION.
FAD ACCEPTS HYDROGEN

54. FMN DEPENDENT ENZYME

55. FAD- DEPENDENT ENZYME
Reaction Enzymes location
Succinate to fumarate Succinate
dehydrogenase
Krebs cycle
Acyl-CoA to alpha-
beta unsaturated acyl-
CoA
Acyl-CoA
dehydrogenase
Beta Oxidation
Xanthine to Uric Acid Xanthine Oxidase Purine metabolism
Pyruvate to Acetyl-
CoA
Pyruvate
dehydrogenase
Glycolysis – Krebs cycle
Alpha-Ketoglutarate
to succinyl Co-A
Alpha ketoglutarate
dehydrogenase
Krebs cycle

58. RIBOFLAVIN DEFICIENCY
CAUSE: NATURAL
DEFICIENCY OF
RIBOFLAVIN IN MAN
IS UNCOMMON.
BECAUSE IT IS
SYNTHESIZED BY THE
INTESTINAL FLORA.

59. MANIFESTATIONS
SYMPTOMS ARE CONFINED TO SKIN AND MUCOUS
MEMBRANES.
i. GLOSSITIS (GLOSSA= TONGUE)
ii. MAGENTA COLORED TONGUE
iii. CHELOSIS (CHEILOS = LIP)
iv. ANGULAR STOMATITIS (INFLAMMATION AT THE
CORNERS OF THE MOUTH)
v. CIRCUMCORNEAL VASCULARIZATION
vi. PROLIFERATION OF THE BULBAR CONJUNCTIVAL
CAPILLARIES IS THE EARLIEST SIGN OF RIBOFLAVIN
DEFICIENCY.

61. SOURCES & DAILY REQUIREMENTS
• DIETARY SOURCES OF RIBOFLAVIN
RICH SOURCES:
LIVER, EGG AND WHOLE MILK
GOOD SOURCES:
FISH, WHOLE CEREALS, LEGUMES AND
GREEN LEAFY VEGETABLES.
DAILY REQUIREMENT
Biochemical
Functions:
mainly concerned with the
metabolism of carbohydrates. &
requirement is related to calorie
Adult on
sedentary work:
1.5
mg/day
Additional( pregnancy,
lactation& old age):
0.2-0.4
mg/day

62. ANTIMETABOLITE
• GALACTOFLAVIN

63. NIACIN
• ALSO CALLED AS NICOTINIC ACID OR PELLAGRA PREVENTING
FACTOR OF GOLDBERGER.
• IN NAD+ OR NADP+, THE REACTIVE SITE IS THE CARBON ATOM 4
AND THE NITROGEN ATOM OF THE NICOTINAMIDE RING.
Active Form of
vitamin present
in tissues.
Pyridine-3-
carboxylic acid

64. Coenzyme for of niacin (NAD+ AND
NADP+)

65. ONE HYDROGEN AND ONE
ELECTRON

66. NAD+ DEPENDENT ENZYMES

70. NADPH GENERATING REACTIONS
Enzyme Locations
Glucose-6-phosphate
dehydrogenase
HMP Shunt pathway
6- phospho-gluconate
dehydrogenase
HMP Shunt pathway
Cytoplasmic isocitrate
dehydrogenase
Krebs cycle
Malic enzyme Malate to pyruvate

71. NADPH UTILIZING REACTIONS
Enzyme Location
Keto acyl ACP reductase De-novo synthesis of fatty acid
(Lynen Cycle) step -4
Alpha, beta unsaturated acyl
ACP / Enoyl ACP reductase
De-novo synthesis of fatty acid
(Lynen Cycle) step -6
HMG CoA reductase Cholesterol Synthesis
Met-hemoglobin →
hemoglobin
Folate reductase Folic acid to THF
Phenyl alanine hydroxylase Catabolism of phenylalanine to

72. NAD+ AND NADP+ ARE INVOLVED
IN ALMOST ALL THE METABOLISMS.
( CARBOHYDRATE, LIPIDS, PROTEIN
ETC.)

73. NADH PRODUCED IS OXIDIZED IN
THE ELECTRON TRANSPORT CHAIN
TO GENERATE ATP.
NADPH IS ALSO IMPORTANT FOR
MANY BIOSYNTHETIC REACTIONS AS
IT DONATES REDUCING

74. •NAD+ IS THE SOURCE OF ADP-RIBOSE
FOR THE ADP-RIBOSYLATION OF
PROTEINS AND POLY-ADP-
RIBOSYLATION OF NUCLEOPROTEINS.

75. NIACIN DEFICIENCY
• DEFICIENCY OF NIACIN LEADS TO THE CLINICAL
CONDITION CALLED PELLAGRA.
• PELLAGRA IS AN ITALIAN WORD, MEANING "ROUGH
SKIN".
• PELLAGRA IS CAUSED BY THE DEFICIENCY OF
TRYPTOPHAN AS WELL AS NIACIN.
• PELLAGRA IS SEEN MORE IN WOMEN.
REASON: THIS MAY BE BECAUSE TRYPTOPHAN METABOLISM IS

76. SYMPTOMS OF PELLAGRA
1. DERMATITIS:
• IN EARLY STAGES- BRIGHT RED ERYTHEMA OCCURS,
ESPECIALLY IN THE FEET, ANKLES AND FACE .
• INCREASED PIGMENTATION AROUND THE NECK IS KNOWN
AS CASAL'S NECKLACE.
• THE DERMATITIS IS PRECIPITATED BY EXPOSURE TO
SUNLIGHT

78. 2. DIARRHOEA:
• MAY BE MILD OR SEVERE WITH BLOOD AND MUCUS.
• THIS MAY LEAD TO WEIGHT LOSS.
• NAUSEA AND VOMITING MAY ALSO BE PRESENT.
3. DEMENTIA:
• IT IS FREQUENTLY SEEN IN CHRONIC CASES.
• ASSOCIATED WITH DEGENERATION OF NERVOUS TISSUE.
• SYMPTOMS: ANXIETY, IRRITABILY, POOR MEMORY LOSS,
INSOMNIA ETC

79. PELLEGRA ARE COMMONLY REFERRED
TO AS THREE DS.
DISEASES PROGRESSES IN THE ORDER
1. DERMATITIS
2. DIARRHEA
3. DEMENTIA
4. DEATH (4TH D).

80. NIACIN IS SYNTHESIZED FROM TRYPTOPHAN
• QUINOLINATE PHOSPHORIBOSYL TRANSFERASE IS THE RATE
LIMITING ENZYME IN THE CONVERSION OF NIACIN TO NAD.

81. • ABOUT 60 MG OF
TRYPTOPHAN IS
EQUIVALENT TO 1
MG OF NIACIN
• TRYPTOPHAN
CANNOT TOTALLY
REPLACED NIACIN.

82. EXCRETION
•NAD+ AND NADP+ IS MOSTLY
EXCRETED IN THE URINE AS N-
METHYLNICOTINAMIDE.

83. CAUSES FOR NIACIN DEFICIENCY
I. DIETARY DEFICIENCY OF TRYPTOPHAN
II. DEFICIENT SYNTHESIS: KYNURENINASE
III.ISONIAZID (INH)
IV.HARTNUP DISEASE
V. CARCINOID SYNDROME

84. I. DIETARY DEFICIENCY OF TRYPTOPHAN:
PELLAGRA IS SEEN AMONG PEOPLE WHOSE STAPLE DIET IS MAIZE
(SOUTH AND CENTRAL AMERICA). IN MAIZE, NIACIN IS
PRESENT; BUT IT IS IN A BOUND FORM, AND IS
UNAVAILABLE. TRYPTHOPHAN CONTENT IS LOW.
PELLAGRA IS ALSO SEEN WHEN STAPLE DIET IS SORGHUM (JOWAR OR
GUINEA CORN) AS IN CENTRAL AND WESTERN INDIA. SORGHUM,
CONTAINS LEUCINE IN HIGH QUANTITIES. LEUCINE INHIBITS THE
QPRT ENZYME, AND SO NIACIN CANNOT BE CONVERTED
TO NAD+ (LEUCINE PELLAGRA).

85. II. DEFICIENT SYNTHESIS OF
KYNURENINASE:
• KYNURENINASE, AN IMPORTANT ENZYME IN THE PATHWAY OF
TRYPTOPHAN, IS PYRIDOXAL PHOSPHATE DEPENDENT. SO
CONVERSION OF TRYPTOPHAN TO NIACIN IS NOT
POSSIBLE IN PYRIDOXAL DEFICIENCY.
III. ISONIAZID (INH):
• IT IS AN ANTI-TUBERCULOUS DRUG, WHICH INHIBITS

86. IV. HARTNUP DISEASE
TRYPTOPHAN ABSORPTION FROM INTESTINE IS DEFECTIVE IN THIS
CONGENITAL DISEASE. MOREOVER, TRYPTOPHAN IS EXCRETED IN
URINE IN LARGE QUANTITIES. THIS LEADS TO LACK OF
TRYPTOPHAN AND CONSEQUENTLY DEFICIENCY OF
NICOTINAMIDE.
V. CARCINOID SYNDROME:
THE TUMOR UTILIZES MAJOR PORTION OF AVAILABLE TRYPTOPHAN
FOR SYNTHESIS OF SEROTONIN; SO TRYPTOPHAN IS UNAVAILABLE.

87. DIETARY SOURCES OF NIACIN
RICHEST NATURAL SOURCES OF NIACIN : DRIED YEAST, RICE
POLISHING, LIVER, PEANUT, WHOLE CEREALS, LEGUMES, MEAT AND
FISH.
ABOUT HALF OF THE REQUIREMENT IS MET BY THE
CONVERSION OF TRYPTOPHAN TO NIACIN. ABOUT 60 MG OF
TRYPTOPHAN WILL YIELD 1 MG OF NIACIN.
•RECOMMENDED DAILY ALLOWANCE (RDA):
NORMAL REQUIREMENT IS 20 MG/DAY. DURING LACTATION,

88. THERAPEUTIC USE OF NIACIN
• INHIBITS LIPOLYSIS IN THE ADIPOSE TISSUE AND
DECREASE THE CIRCULATORY FREE FATTY ACID.
• LDL, VLDL , TG AND CHOLESTEROL ARE LOWERED.
HENCE USED IN TREATEMENT OF
HYPERLIPOPROTEINEMIA TYPE II B ( ELEVATION OF LDL
AND VLDL).

89. TOXICITY OF NIACIN
MEGADOSE OF NIACIN ARE USEFUL FOR THE
TREATMENT OF HYPERLIPIDAEMIA BUT THERE ARE
CERTAIN SIDE EFFECT ALSO.
• GLYCOGEN AND FAT RESERVES OF SKELETAL AND CARDIAC MUSCLE ARE
DEPLETED.
• TENDENCY TO INCREASE THE LEVELS OF GLUCOSE AND URIC ACID IN THE
CIRCULATION.
• PROLONGED USE RESULTS IN ELEVATED SERUM LEVELS OF CERTAIN
ENZYMES, SUGGESTING LIVER DAMAGE.
• VASODILATION OF THE CUTANEOUS VESSELS AND RELEASE OF
HISTAMINE OCCURS.

90. QUESTION:
IS NIACIN A
VITAMIN????

91. VITAMIN B5
PANTOTHENIC ACID
(“PANTOS” MEANS EVERYWHERE)

92. STRUCTURE

93. SYNTHESIS
OF COENZYME
A
COA

94. STRUCTURE OF COENZYME
A

95. • IT IS THE ACTIVE SITE WHERE ACYL GROUPS ARE CARRIED.
THEREFORE, CO-ENZYME A IS SOMETIMES ABBREVIATED AS
COA-SH TO DENOTE THIS ACTIVE SITE.
(THIOL OR SULFHYDRYL GROUP)

96. BIOCHEMICAL FUNCTIONS
• FUNCTIONS OF B5 ARE EXERTED THROUGH COENZYME A
OR CO A (A FOR ACETYLATION).
• COENZYME A IS A CENTRAL MOLECULE INVOLVED IN ALL
THE METABOLISMS. (CARBOHYDRATE, LIPID AND
PROTEIN)
• INVOLVED IN INTEGRATED METABOLISM.
• MORE THAN 70 ENZYMES DEPENDS ON COENZYME A.

97. • ACETYL CO A
• SUCCINYL CO A
• HMG CO A
• ACYL CO A
Co A serves as a carrier of
activated acetyl or acyl groups (as
thiol esters).

98. COENZYME A
MAY BE
REGARDED AS A
COENZYME OF
METABOLIC
INTEGRATION.

99. CO-ENZYME A IS AN IMPORTANT COMPONENT OF FATTY ACID
SYNTHASE COMPLEX. THE ACP (ACYL CARRIER PROTEIN) ALSO
CONTAINS PANTOTHENIC ACID.

100. RDA: 5-10 MG IS ADVISED FOR ADULTS.
DIETARY SOURCES: MOST WIDELY
DISTRIBUTED.
ALSO SYNTHESIS BY
INTESTINAL FLORA.

101. BURNING FEET SYNDROME, ALSO KNOWN
AS GRIERSON-GOPALAN SYNDROME, IS A MEDICAL
CONDITION THAT CAUSES SEVERE BURNING AND
ACHING OF THE FEET.
• PAIN
• NUMBNESS IN TOES
• SLEEPLESSNESS
• FATIGUE
• ETC.
Deficiency
Symptoms

102. VITAMIN B6
PYRIDOXINE / PYRIDOXAL / PYRIDOAMINE
(VITAMERS OF B6)
4-pyridoxic
acid excreted
form in urine.

104. BIOCHEMICAL FUNCTIONS
Transamination Decarboxylation
Deamination Transsulfuration
Condensatio
n
PLP acts as co-enzyme for many
reactions in

105. TRANSAMINIATION
THUS, VITAMIN B6 IS AN ENERGY RELEASING
VITAMIN. IT INTEGRATES CARBOHYDRATE AND
AMINO ACID METABOLISM.

107. DECARBOXYLATION
SOME OF ΑLPHA - AMINO ACIDS UNDERGOES
DECARBOXYLATION TO FORM THE RESPECTIVE
AMINES.
Serotoni
n
Tryptopha
n
Catechola
mines
Catecholamin
es

108. HEME SYNTHESIS

109. PRODUCTION OF NIACIN

110. TRANSSULFURATION

111. DEAMINATION
PLP
PLP

113. GLYCOGENOLYSIS
PLP

114. DEFICIENCY MANIFESTATION OF
PYRIDOXINE
1. NEUROLOGICAL MANIFESTATIONS:
IN VITAMIN B6 DEFICIENCY, PLP DEPENDENT ENZYMES FUNCTION
POORLY. SO, SEROTONIN, EPINEPHRINE, NORADRENALIN AND GABA ARE
NOT PRODUCED PROPERLY.
NEUROLOGICAL SYMPTOMS ARE THEREFORE QUITE COMMON IN B6
DEFICIENCY.
2. DERMATOLOGICAL MANIFESTATIONS:
DEFICIENCY OF B6 WILL AFFECT TRYPTOPHAN METABOLISM. SINCE
NIACIN IS PRODUCED FROM TRYPTOPHAN, B6 DEFICIENCY IN TURN LEADS

115. 3. HEMATOLOGICAL MANIFESTATIONS:
IN ADULTS HYPOCHROMIC MICROCYTIC ANEMIA MAY OCCUR DUE TO THE
INHIBITION OF HEME BIOSYNTHESIS.
• THE METABOLIC DISORDERS WHICH RESPOND TO VITAMIN B6
THERAPY ARE XANTHURENIC ACIDURIA AND HOMOCYSTINURIA.
ASSAY OF VITAMIN B6 VITAMIN
B6 STATUS IS ASSAYED BY THE ACTIVATION OF
ERYTHROCYTE TRANSAMINASES BY ADDITION OF
PYRIDOXAL PHOSPHATE IN THE REACTION MIXTURE.

116. EFFECT OF DRUGS ON VITAMIN
B6
i. INH: ISONICOTINIC ACID HYDRAZIDE (ISONIAZID) IS AN
ANTITUBERCULOSIS DRUG. IT INHIBITS PYRIDOXAL
KINASE; REDUCES THE FORMATION OF PLP AND CAUSES
VITAMIN B6 DEFICIENCY.
ii. CYCLOSERINE: IT ACTS AS B6 ANTAGONIST.
iii. ORAL CONTRACEPTIVES: MILD VITAMIN B6 DEFICIENCY
MAY BE SEEN IN WOMEN TAKING ORAL CONTRACEPTIVE
PILLS.
iv. ETHANOL: IT IS CONVERTED TO ACETALDEHYDE,
WHICH INACTIVATES PLP. HENCE B6 DEFICIENCY

117. DIETARY SOURCES OF VITAMIN B6 :
RICH SOURCES ARE YEAST, RICE POLISHING, WHEAT
GERMS, CEREALS, LEGUMES (PULSES), OIL SEEDS, EGG,
MILK, MEAT, FISH AND GREEN LEAFY VEGETABLES.
REQUIREMENT OF VITAMIN B6 :
REQUIREMENTS ARE RELATED TO PROTEIN INTAKE AND NOT TO
CALORIE INTAKE . IT IS RECOMMENDED THAT ADULTS NEED 1 TO 2
MG/DAY.
DURING PREGNANCY AND LACTATION, THE REQUIREMENT IS
INCREASED TO 2.5 MG/DAY.

118. VITAMIN B7
(BIOTIN)
ANTI-EGG WHITE INJURY FACTOR OR
VITAMIN H
• SULFUR CONTAING B-COMPLEX VITAMIN
• PARTICIPATES AS COENZYME IN THE CARBOXYLATION

119. STRUCTURE
Biocyti
n

120. BIOTIN REQUIRING CO2
FIXATION REACTIONS
1. ACETYL COA CARBOXYLASE
2. PROPIONYL COA CARBOXYLASE
3. PYRUVATE CARBOXYLASE

121. BIOTIN-INDEPENDENT
CARBOXYLATION REACTIONS
I. CARBAMOYL PHOSPHATE SYNTHETASE,
II. ADDITION OF CO2 TO FORM C6 IN PURINE
RING.
III. MALIC ENZYME, CONVERTING PYRUVATE TO
MALATE

122. BIOTIN ANTAGONISTS
•AVIDIN, A PROTEIN PRESENT IN EGG WHITE HAS GREAT
AFFINITY TO BIOTIN.
• HENCE INTAKE OF RAW (UNBOILED) EGG MAY CAUSE BIOTIN
DEFICIENCY. BIOTIN WAS ORIGINALLY NAMED AS ANTI-EGG-
WHITE INJURY-FACTOR.
• AVIDIN IS HEAT LABILE, AND BOILING OF EGG WILL
NEUTRALIZE THE INHIBITORY ACTIVITY.
• ONE MOLECULE OF AVIDIN CAN COMBINE WITH FOUR
MOLECULES OF BIOTIN
• EGG WHITE CONTAINS AVIDIN AND EGG YOLK CONTAINS

123. APPLICATION
• THE AFFINITY OF AVIDIN TO BIOTIN IS GREATER THAN MOST OF
THE USUAL ANTIGEN-ANTIBODY REACTIONS. THEREFORE
AVIDIN-BIOTIN SYSTEM IS COMMONLY UTILIZED FOR DETECTION
OF PATHOGENS IN THE ELISA TEST.
• BIOTIN LABELLING OF DNA IS BECOMING MORE POPULAR.
• BIOTIN IS ADDED TO NUCLEOTIDES, WHICH WILL BE
INCORPORATED INTO THE NEWLY SYNTHESIZED DNA. THE FIXED
BIOTIN CAN BE IDENTIFIED BY REACTION WITH AVIDIN.
• STREPTAVIDIN PURIFIED FROM STREPTOMYCES AVIDINII, CAN
BIND 4 MOLECULES OF BIOTIN.

124. DEFICIENCY OF BIOTIN
• I. PROLONGED USE OF ANTIBACTERIAL DRUGS
• II. BIOTIN DEFICIENCY SYMPTOMS INCLUDE DERMATITIS,
ATROPHIC GLOSSITIS, HYPERESTHESIA, MUSCLE PAIN,
ANOREXIA AND HALLUCINATIONS.
• INJECTION OF BIOTIN 100-300 MG WILL BRING ABOUT RAPID CURE OF THESE
SYMPTOMS.

125. •REQUIREMENT OF BIOTIN:
ABOUT 200-300 MG WILL MEET THE DAILY
REQUIREMENTS.
•SOURCES OF BIOTIN:
NORMAL BACTERIAL FLORA OF THE GUT WILL PROVIDE
ADEQUATE QUANTITIES OF BIOTIN.
MOREOVER, IT IS DISTRIBUTED UBIQUITOUSLY IN PLANT
AND ANIMAL TISSUES. LIVER, YEAST, PEANUT, SOYBEAN,
MILK AND EGG YOLK ARE RICH SOURCES.

126. VITAMIN B12
(COBALAMIN / EXTRINSIC FACTOR (EF) OF CASTLE /
ANTI-PERNICIOUS ANEMIA VITAMIN )
INTRODUCTION:
• WATER SOLUBLE
• HEAT STABLE
• RED IN COLOUR
• CONTAINS 4.35% COBALT BY WEIGHT.
• UNIQUE VITAMIN : SYNTHESIS ONLY BY MICROORGANISMS.

127. CHEMISTRY
• ONLY VITAMIN WITH COMPLEX STRUCTURE.
• EMPIRICAL FORMULA OF VITAMIN B12 : C63H90N14014PCO
• STRUCTURE:
CONSIST OF A CORRIN RING WITH A CENTRAL COBALT
ATOM. THE CORRIN RING IS ALMOST SIMILAR TO THE
TETRAPYRROLE RING STRUCTURE FOUND IN OTHER
PORPHYRIN COMPOUNDS. EG. HEME (WITH FE) AND
CHLOROPHYLL ( WITH MAGNESIUM)

128. STRUCTURE OF
VITAMIN B12

129. FORMS OF VITAMIN B12
Forms of Vitamin B12 Functions
Cyanocobalamin (-CN)
(No physiological function)
• Cyanide is added to get stable
crystals
• Oral preparations are in this
form.
Hydroxy Cobalamin (-OH) or
Vitamin B12a
• Injectable preparations are in this
forms.
Adenosyl Cobalamin (Ado-B12)
• Functional coenzyme in body
• When taken up by cells, all
groups are removed and
converted into deoxy adenosyl
cobalamin.
• Major storage form seen in liver.
Methyl Cobalamin (-CH3) or • When methyl group replaces

130. BIOC
Absorption of
Vitamin B12
• Intrinsic Factor (IF) of
Castle
• Cobalophilin
• One IF
combines with
2 molecules of
B12

131. TRANSPORT
AND STORAGE
• METHYL COBALAMIN
(METHYL B12) :
PREDOMINANT FORM IN
BLOOD
• ADENOSYL COBALAMIN
(ADO-B12): MAJOR
STORAGE FORM IN LIVER
• 2 MG OF B12 STORED IN
LIVER

132. BIOCHEMICAL FUNCTIONS OF
VITAMIN B12
1. SYNTHESIS OF METHIONINE
FROM HOMOCYSTEINE
( METHIONINE SYNTHASE OR
HOMOCYSTEINE METHYL TRANSFERASE)
2. METHYL FOLATE TRAP AND
FOLATE DEFICIENCY.
( FORMATION OF METHYL-THFA IS
IRREVERSIBLE.)
Folate
Trap

133. 3. ISOMERIZATION OF METHYL
MALONYL COA TO SUCCINYL
COA
DEGRADATION OF:
• ODD CHAIN FA
• A. A (VALINE , ISOLEUICINE,
METHIOININE,
THREONINE)
• PYRIMIDINE ( THYMINE AND URACIL)
IN B12 DEFICINECY – METHYL MALONYL
COA ACCUMULATES AND IS EXCRETED IN

134. CAUSES OF B12 DEFICIENCY
1. NUTRITIONAL (VERY COMMON IN INDIA)
2. DECREASE IN ABSORPTION (GASTRECTOMY, RESECTION OF ILIUM,
MALABSORPTION) – INTRINSIC FACTOR DEFICIENT
3. AUTOIMMUNE DESTRUCTION - ( ANTIBODY ARE GENERATED
AGAINST IF)ADDISONIAN PERNICIOUS ANEMIA
4. INSUFFICIENT PRODUCTION OF IF AND / OR GASTRIC HCL –
OCCASIONALLY SEEN IN OLDER PEOPLE.
5. PREGNANCY
6. FISH TAPEWORM – DIPHILLOBOTHRIUM LACTUM HAS AFFINITY TO
B12 CAUSING REDUCTION IN AVAILABLE VITAMIN.

135. DEFICIENCY MANIFESTATIONS
1. FOLATE TRAP:
VITAMIN B12 DEFICIENCY CAUSES SIMULTANEOUS FOLATE
DEFICIENCY DUE TO THE FOLATE TRAP. THEREFORE ALL THE
MANIFESTATIONS OF FOLATE DEFICIENCY ARE ALSO SEEN.
2. PERNICIOUS ANEMIA:
MEGALOBLASTIC ANEMIA: IN THE PERIPHERAL BLOOD,
MEGALOBLASTS AND IMMATURE RBCS ARE OBSERVED.
3. ABNORMAL HOMOCYSTEINE LEVEL:
IN VITAMIN B12 DEFICIENCY, STEP NO. 2 IS BLOCKED, SO THAT
HOMOCYSTEINE IS ACCUMULATED, LEADING TO
HOMOCYSTINURIA

136. 4. DEMYELINATION:
IN VITAMIN B12 DEFICIENCY, STEP 3 IS ALSO SUPPRESSED DUE TO THE
NON-AVAILABILITY OF ACTIVE METHIONINE.
THEREFORE, METHYLATION OF PHOSPHATIDYL ETHANOLAMINE TO
PHOSPHATIDYL CHOLINE IS NOT ADEQUATE.
THIS LEADS TO DEFICIENT FORMATION OF MYELIN SHEATHS OF
NERVES, DEMYELINATION AND NEUROLOGICAL LESIONS.
SYMPTOMS:
• PARESTHESIA (NUMBNESS AND TINGLING) OF FINGERS AND TOES.
• CONFUSION, LOSS OF MEMORY
• POSITIVE ROMBERG’S SIGN (FALLING WHEN EYES ARE CLOSED)
• POSITIVE BABINSKI’S SIGN (EXTENSOR PLANTAR REFLEX)

138. ASSESSMENT OF B12
DEFICIENCY
• SERUM B12: IT IS QUANTITATED BY RADIO-IMMUNO-ASSAY OR BY
ELISA.
• SCHILLING TEST
• METHYL MALONIC ACID: IT IS SEEN IN URINE.
• FIGLU EXCRETION TEST
• PERIPHERAL SMEAR: PERIPHERAL BLOOD AND BONE MARROW
MORPHOLOGY SHOWS MEGALOBLASTIC ANEMIA
• HOMOCYSTINURIA

139. TREATMENT
• ALL THE MACROCYTIC ANAEMIAS ARE GENERALLY
TREATED WITH FOLATE AND VITAMIN B12.
• THERAPEUTIC DOES OF VITAMIN B12 IS 100 - 1000
MICROGRAM BY INTRAMUSCULAR INJECTIONS.

140. RDA OF VITAMIN B12
NORMAL DAILY ADULT : 1- 2 MICROGRAM/ DAY
DURING PREGNANCY AND LACTATION, INCREASES BY 2
MICROGRAM/DAY
THOSE WHO TAKE FOLIC ACID SHOULD ALSO TAKE VITAMIN B12
DIETARY SOURCES
• NOT PRESENT IN VEGETABLES
• LIVER IS THE RICHEST SOURCE
• CURD IS THE GOOD SOURCE.

141. FOLIC ACID
FOLACIN ( LATIN : FOLIUM – LEAF)
• FOLIC ACID IS ABUNDANT IN VEGETABLES.
• IMPORTANT FOR ONE CARBON METABOLISM
• FOLIC ACID IS SOLUBLE IN WATER.
• WHEN EXPOSED TO LIGHT, IT IS RAPIDLY DESTROYED.
• COMPOSED OF THREE CONSTITUENTS. ( PTERIDINE RING,
P-AMINO BENZOIC ACID AND GLUTAMIC ACID [1-7] )

142. CHEMISTRY OF FOLIC ACID

143. ACTIVE FORM
OF FOLIC ACID

144. ABSORPTION, TRANSPORT AND
STORAGE OF FOLIC ACID
• FOLIC ACID IS READILY ABSORBED BY THE UPPER PART OF
JEJUNUM.
• IN THE BLOOD, IT IS TRANSPORTED BY BETA GLOBULINS.
• IT IS TAKEN UP BY THE LIVER WHERE THE COENZYMES ARE
PRODUCED.
• FOLIC ACID IS NOT STORED IN TISSUES.

145. BIOCHEMICAL
FUNCTIONS OF FOLIC
ACID

146. THFA IS THE CARRIER
OF ONE- CARBON
GROUPS.
• FORMYL (-CHO)
• FORMIMINO (-
CH=NH)
• METHENYL (-CH=)
• METHYLENE (-CH2–)
• HYDROXYMETHYL (-
CH2OH)
• METHYL (-CH3).

147. THE ATTACHMENT OF FORMYL (-CHO) AT POSITION 5 OF THF GIVES N5-
FORMLY TETRAHYDROFOLATE WHICH IS COMMONLY KNOWN AS FOLINIC
ACID OR CITROVORUM FACTOR.

149. CAUSES FOR FOLATE
DEFICIENCYFOLIC ACID DEFICIENCY IS VERY COMMON IN INDIA.
1. PREGNANCY: REQUIREMENT IS INCREASED.
2. DEFECTIVE ABSORPTION: RESECTION AND SHORT-CIRCUITING OF
JEJUNUM
3. DRUGS: IN THE DIET, FOLACIN ARE MAINLY IN POLYGLUTAMATE FORM. GI
ENZYMES IN THE GUT REMOVE THE GLUTAMATE RESIDUES AND ONLY THE
MONO-GLUTAMATE FORM OF FOLIC ACID IS ABSORBED. (HYDANTOIN,
PHENYTOIN, PHENOBARBITONE) WILL INHIBIT THE INTESTINAL ENZYME, SO
THAT FOLATE ABSORPTION IS REDUCED.
4. HAEMOLYTIC ANEMIAS: AS REQUIREMENT OF FOLIC ACID BECOMES MORE
INCREASES
5. DIETARY DEFICIENCY: ABSENCE OF VEGETABLES IN FOOD FOR

150. DEFICIENCY
MANIFESTATIONS
1.REDUCED DNA SYNTHESIS
IN FOLATE DEFICIENCY, THFA IS REDUCED AND
THYMIDYLATE SYNTHASE ENZYME IS INHIBITED.
THUS CELL DIVISION IS ARRESTED.

152. 2. MACROCYTIC ANEMIA
(ABNORMALLY LARGE RBCS WITH LOW
CONCENTRATION OF HB)
• IMMATURE LOOKING NUCLEUS ( DNA SYNTHESIS IS DELAYED.
PROTEIN SYNTHESIS CONTINUOUS) ASSOCIATED WITH
MEGALOBLASTIC CHANGES IN BONE MARROW.
• RETICULOCYTOSIS IS OFTEN SEEN.
• HEMOLYSIS (LEADS TO ANEMIA)
• LEUKOPENIA AND THROMBOCYTOPENIA.

155. 3. HYPERHOMOCYSTEINEMIA :
• INCREASED HOMOCYSTEINE LEVELS IN BLOOD.
• PLASMA HOMOCYSTEINE LEVELS ABOVE 15 MICROMOLES / L
(KNOWN TO INCREASE THE RISK OF (CAD).
• PROVIDING ADEQUATE DOSES OF B6 , B12 AND FOLIC ACID MAY LOWER
THE HOMOCYSTEINE LEVELS.
4. BIRTH DEFECTS:
DURING PREGNANCY MAY LEAD TO NEURAL TUBE DEFECTS IN THE FETUS.
(SPINA BIFIDA, ANENCEPHALY)
SO, SUPPLEMENTATION OF FOLIC ACID FROM EARLY PREGNANCY IS A MUST TO PREVENT
NEURAL TUBE DEFECTS IN THE CHILD.
5. PREVENTION OF CANCER.

156. Anencephaly Spina Bifida

157. ASSESSMENT OF FOLATE
DEFICIENCY
• SERUM FOLIC ACID - 20 NANOGRAM/ML (MEASURED BY
RADIO-IMMUNO-ASSAY).
• HISTIDINE LOAD TEST OR FIGLU EXCRETION TEST:
HISTIDINE IS NORMALLY METABOLISED TO FORMIMINO GLUTAMIC ACID (FIGLU) FROM
WHICH FORMIMINO GROUP IS REMOVED BY THFA. THEREFORE IN FOLATE DEFICIENCY,
FIGLU IS EXCRETED IN URINE.
• AICAR EXCRETION:
(AICAR) ACCUMULATES AND IS EXCRETED IN URINE.
• PERIPHERAL BLOOD PICTURE.

159. SOURCES OF FOLIC ACID :
RICH SOURCES OF FOLATE ARE YEAST, GREEN LEAFY VEGETABLES.
MODERATE SOURCES ARE CEREALS, PULSES, OIL SEEDS AND EGG.
MILK IS A POOR SOURCE FOR FOLIC ACID.
RECOMMENDED DAILY ALLOWANCE
(RDA):
THE REQUIREMENT OF FREE FOLATE IS 200 MICROGRAM/ DAY.
IN PREGNANCY THE REQUIREMENT IS INCREASED TO 400 MICROGRAM/DAY

160. FOLIC ACID THERAPY
• THERAPEUTIC DOSE IS 1 MG OF FOLIC ACID PER DAY
ORALLY.
• FOLIC ACID ALONE SHOULD NOT BE GIVEN IN
MACROCYTIC ANEMIA BECAUSE IT MAY AGGRAVATE THE
NEUROLOGICAL MANIFESTATION OF B12 DEFICIENCY.
SO, FOLIC ACID AND VITAMIN B12 ARE GIVEN IN
COMBINATION TO PATIENTS.
• REGULAR SUPPLEMENTATION OF FOLIC ACID MAY
REDUCE THE INCIDENCE OF BIRTH DEFECTS,
CARDIOVASCULAR DISEASES AND CANCERS

161. TOXICITY OF FOLIC ACID
• DOSES OVER 1 MG MAY CAUSE AGGRAVATION OF
VITAMIN B12 DEFICIENCY.
• SINCE SOLUBILITY OF FOLIC ACID IS LOW, LARGE DOSES
SHOULD NOT BE GIVEN PARENTERALLY.
• DANGER OF CRYSTALLIZATION IN KIDNEY TUBULES
LEADING TO RENAL DAMAGE.

162. FOLATE ANTAGONISTS
1. AMINOPTERIN AND AMETHOPTERIN
AMINOPTERIN (4-AMINO FOLIC ACID) AND AMETHOPTERIN
(METHOTREXATE) (4-AMINO, 10-METHYL FOLIC ACID) ARE POWERFUL
INHIBITORS OF FOLATE REDUCTASE AND THFA GENERATION.
THUS THESE DRUGS DECREASE THE DNA FORMATION AND CELL DIVISION.
THEY ARE WIDELY USED AS ANTICANCER DRUGS.
ESPECIALLY FOR LEUKAEMIA'S AND CHORIOCARCINOMAS.
METHOTREXATE IS ALSO USED IN TREATMENT OF RHEUMATOID ARTHRITIS
AS AN IMMUNOSUPPRESSANT.

163. 2. PYRIMETHAMINE :
• THIS ANTIFOLATE AGENT IS USED AGAINST PLASMODIAL
INFECTIONS (ANTIMALARIAL DRUG).
• INHIBITORS OF FOLATE REDUCTASE AND THFA GENERATION.
3. SULPHONAMIDES
• STRUCTURAL ANALOG OF PABA.
• THEY COMPETITIVELY INHIBIT THE ENZYME RESPONSIBLE FOR THE
INCORPORATION OF PABA INTO DIHYDRO PTEROIC ACID, THE
IMMEDIATE PRECURSOR OF FOLIC ACID.
• BECAUSE OF THIS REASON THEY ARE USED AS ANTIBACTERIAL
DRUGS.

164. VITAMINOIDS
• COMPOUNDS WITH ‘VITAMIN‐LIKE’ ACTIVITY
• CONSIDERED BY SOME TO BE VITAMINS OR
PARTIALLY TO REPLACE VITAMINS.
• INCLUDES FLAVONOIDS, INOSITOL, CARNITINE,
CHOLINE, LIPOIC ACID, ETC..

165. CHOLINE
• CHOLINE IS SYNTHESIZED IN THE BODY (FROM
SERINE) AND THEREFORE IT IS NOT A VITAMIN.
• IT IS INCLUDED AS A MEMBER OF VITAMIN B
COMPLEX.
• RICE POLISHING'S, VEGETABLES, MILK, EGG AND
LIVER ARE GOOD SOURCES.

166. CHEMISTRY
• IT IS HYDROXY ETHYL TRIMETHYL AMINE, OR
TRIMETHYL ETHANOL AMINE. IT IS WATER
SOLUBLE.

167. • COMPONENT OF PHOSPHOLIPIDS (LECITHINS)
• PREVENTS THE ACCUMULATION OF FAT IN LIVER (AS LIPOTROPIC
FACTOR).
• IT PROMOTES THE SYNTHESIS OF PHOSPHOLIPIDS AND LIPOPROTEINS
AND THE DISPOSAL OF TRIACYLGLYCEROLS FROM LIVER.
• ACTIVELY INVOLVED IN ONE CARBON METABOLISM.
• A PRECURSOR FOR THE SYNTHESIS OF ACETYLCHOLINE WHICH IS
REQUIRED FOR TRANSMISSION OF NERVE IMPULSE.
BIOCHEMICAL FUNCTIONS

168. INOSITIOL
• INOSITOL IS HEXAHYDROXY-CYCLOHEXANE.
• IT IS ALSO FOUND AS MYO-INOSITOL OR MESO-
INOSITOL
• IT IS SEEN IN YEAST, CEREALS AND MILK.

169. BIOCHEMICAL FUNCTIONS
• SYNTHESIS OF PHOSPHATIDYLINOSITOL (LIPOSITOL)
• ACTS AS A LIPOTROPIC FACTOR (ALONG WITH CHOLINE) AND
PREVENTS THE ACCUMULATION OF FAT IN LIVER.
• SOME HORMONES, INOSITOL ACTS AS A SECOND MESSENGER AT
THE MEMBRANE LEVEL FOR THE RELEASE OF CA2+ IONS.
• INOSITOL CONCENTRATION IN THE HEART MUSCLE IN HIGH.
• PHYTIN IS HEXAPHOSPHATE OF INOSITOL FOUND IS PLANTS. IT
PREVENTS THE ABSORPTION OF IRON AND CALCIUM FROM THE
INTESTINE.

170. LIPOIC ACID
• LIPOIC ACID (THIOCTIC ACID) IS A SULPHUR CONTAINING
FATTY ACID (6,8-DITHIOOCTANOIC ACID).
• IT EXISTS IN AN OXIDIZED AND REDUCED FORM.
• LIPOIC ACID IS FAT AS WELL AS WATER SOLUBLE.

171. BIOCHEMICAL FUNCTIONS
• LIPOIC ACID IS INVOLVED IN THE DECARBOXYLATION
REACTIONS ALONG WITH OTHER VITAMINS (THIAMINE,
NIACIN, RIBOFLAVIN AND PANTOTHENIC ACID).
• THE CONVERSION OF PYRUVATE TO ACETYL COA (BY
PYRUVATE DEHYDROGENASE) AND A-KETOGLUTARATE TO
SUCCINYL COA (BY CX,-KETOGLUTARATE
DEHYDROGENASE) REQUIRES LIPOIC ACID.

172. THERAPEUTIC USES
• BEING FAT AND WATER SOLUBLE, IT CAN COMFORTABLY REACH
VARIOUS TISSUES.
THE THERAPEUTIC APPLICATIONS OF LIPOIC ACID ARE RELATED TO ITS
ANTIOXIDANT PROPERTY (REGARDED AS UNIVERSAL ANTIOXIDANT),
SOME OF THEM ARE LISTED
• REDUCES THE FREE RADICALS IN BRAIN THAT OTHERWISE CONTRIBUTE
TO ALZHEIMER'S DISEASE AND MULTIPLE SCLEROSIS.
• LIPOIC ACID STIMULATES PRODUCTION OF GLUTATHIONE (GSH),
BESIDES HELPING IN THE RECYCLE OF VITAMINS E AND C.
• MAY BE USEFUL IN THE PREVENTION OF STROKE AND MYOCARDIAL
INFARCTION.

173. PABA
• PARA AMINOBENZOIC ACID (PABA) IS A STRUCTURAL
CONSTITUENT OF FOLIC ACID.
• PABA MAY BE REGARDED AS A VITAMIN IN ANOTHER
VITAMIN (FOLIC ACID)

174. • PABA IS SYNTHESIZED BY THE BACTERIA AND IS ESSENTIAL FOR
THEIR GROWTH.
• THE SULFA DRUG SULFONILAMIDE (P-AMINO BENZENE
SULFANILAMIDE) IS A STRUCTURAL ANALOGUE OF PABA.

175. BIOFLAVONOIDS
• FLAVONOIDS, ISOLATED FROM LEMON PEEL (KNOWN AS CITRIN)
WERE RESPONSIBLE FOR MAINTENANCE OF NORMAL CAPILLARY
PERMEABILITY.
• THE TERM VITAMIN P (P FOR PERMEABILITY) WAS USED TO THIS
GROUP OF SUBSTANCES.
• HOWEVER, THEY ARE COMMONLY KNOWN AS BIOFLAVONOIDS.
• BIOFLAVONOIDS ACT AS ANTIOXIDANTS AND PROTECT ASCORBIC
ACID FROM BEING DESTROYED

176. TAURINE
• TAURINE IS AN AMINO ACID TAKING PART IN IN A VARIETY OF
PHYSIOLOGICAL ACTIVITIES, INCLUDING NEUROMODULATION, OSMOTIC
REGULATION AND THE STABILIZATION OF CELL MEMBRANES.
• IT IS ESSENTIAL FOR THE METABOLISM OF BILE ACIDS SALTS.
• FROM THE OXIDATION OF CYSTEINE, MOST ANIMALS CAN SYNTHESIZE
SUFFICIENT AMOUNTS OF TAURINE ENDOGENOUSLY. HOWEVER, SOME
ANIMALS, ESPECIALLY DOMESTICATED AND WILD FELIDS AND HUMAN
INFANTS FAIL TO SYNTHESIZE ENOUGH AMOUNTS OF TAURINE.
CURRENTLY, TAURINE IS REGULARLY ADDED TO ALL INFANT FORMULAS
TO PROMOTE INFANT DEVELOPMENT.

177. CARNITINE
• CARNITINE PLAYS AN IMPORTANT ROLE IN ACCEPTING
ACTIVATED FATTY ACIDS AT THE OUTER MITOCHONDRIAL
MEMBRANE AND MAKING THEM READY FOR Β-OXIDATION.
• ADULTS CAN SYNTHESIZE SUFFICIENT CARNITINE, IT IS
DIFFICULT FOR INFANTS TO SYNTHESIZE ENOUGH AMOUNTS
OF CARNITINE.
• CARNITINE IS RELATIVELY ABUNDANT IN MEATS AND DAIRY
PRODUCTS, WHILE CEREAL GRAINS IS NOT ONLY LOW IN
CARNITINE BUT ALSO LOW IN LYSINE AND METHIONINE- THE
PRECURSORS OF CARNITINE.

178. COENZYME Q
• COENZYME Q IS DEFINED AS A GROUP OF LIPID-LIKE
COMPOUNDS WITH STRUCTURE SIMILAR TO VITAMIN E.
• COENZYME Q PLAYS A KEY ROLE IN MITOCHONDRIAL
ELECTRON TRANSPORT.

179. QUESTIONS
1. ANTI-TUBERCULOSIS DRUG, INH LEAD TO THE DEFICIENCY
OF VITAMIN …..
2. THE EGG INJURY FACTOR PRESENT IN RAW EGG WHITE …..
3. THE ‘BURNING FEET SYNDROME’ IN MAN IS ASSOCIATED
WITH THE DEFICIENCY OF …..
4. THE VITAMIN THAT IS SYNTHESIS BY ONLY
MICROORGANISMS …..
5. THE THREE DS IN PELLAGRA STANDS FOR …… , …… AND
…… .

180. 6. THE FIGLU IS EXCRETED IN URINE IN THE DEFICIENCY OF
VITAMIN …..
7. THE METABOLITE EXCRETED IN URINE IN THIAMINE
DEFICIENCY ……
8. THE COENZYME DIRECTLY CONCERNED WITH THE
SYNTHESIS OF BIOGENIC AMINES ….. .
9. FOLIC ACID ANTAGONISTS USED IN THE TREATMENT OF
CANCER ….
10. STORAGE FORM OF B12. ….

181. 11. ….. IS CARRIER OF ONE CARBON METABOLISM.
12. WHAT IS THE CHEMICAL NAME OF VITAMIN C?
13. WHAT IS THE CHEMICAL NAME OF VITAMINE B6?
14. THE CHEMICAL NAME OF VITAMIN B7 IS –
15. WHICH VITAMIN PROTECTS HUMAN BODY
FROM BERIBERI DESEASE?

182. 16. WHICH VITAMIN PROTECTS HUMAN BODY
FROM PELLAGRA DISEASE?
17. WHICH VITAMIN PROTECTS HUMAN BODY
FROM PARAESTHESIA?
18. SCIENTIFICALLY WHICH VITAMIN PROTECTS
HUMAN BODY FROM SCURVY DISEASE?
19. WHICH ARE THE WATER SOLUBLE
VITAMINS?

183. 20. WHICH VITAMIN PRODUCES COLLAGEN?
21. WHAT ARE THE BRAIN VITAMINS?
22. PART OF A CO-ENZYME NEEDED FOR NEW CELL
SYNTHESIS.
23. NIACIN – VITAMIN B3 …OTHER 2 NAMES??
24.WERNICKE KORSAKOFF SYNDROME CAUSE DUE TO
…
25. METHY MALONIC ACIDURIA IS ASSOCIATED WITH
VITAMIN …..
26. GLYCOGEN DEGRADATION REQUIRES VITAMIN …..

184. 27. ……. REACTION REQUIRES BIOTIN
28. ACTIVE FORM OF ASCORBIC ACID
29. METHOTREXATE COMPETITIVELY INHIBITS
SYNTHESIS OF REDUCED FORM OF …..
30. FIGLU TEST IS FOR THE ASSESSEMENT OF …..
DEFICIENCY.
31. COENZYME FORM OF PYRIDOXINE …..
32. SULFUR CONTAINING VITAMIN …