VITAMINS

 HISTORICAL BACKGROUND
THIAMIN, ASCORBIC ACID, (VIT-A)
(NIGHT BLINDNESS)
[BERI – BERI] (SCURVY)
 DEFINITION:
ESSENTIAL ORGANIC MICRONUTRIENTS
MUST BE PROVIDED REGULARLY IN THE
DIET
 FAT SOLUBLE, WATER SOLUBLE VITAMINS
 WATER SOLUBLE VITAMINS
(FEATURES)
 NOT STORED EXCEPT VIT B12
 NO TOXICITY BUT EXCESS EXCRETED
IN URINE
 CO-ENZYMES IN METABOLIC
PROCESSES OF CARBOHYDRATES,
PROTEIN AND LIPID METABOLISM
 RESPIRATORY CHAIN
WATER SOLUBLE VITAMINS
1. THIAMINE (B-1) [BERI BERI]
2. RIBOFLAVIN (B-2) [CHEILOSIS,
GLOSSITIS, SEBHORRHOEA]
3. NIACIN (B-3) [PELLEGRA PREVENTING
FACTOR]
4. PANTOTHENIC ACID (B-5) [Co-A - SH] &
[ACP]
5. PYRIDOXINE (B-6) [PERIPHERAL
NEURITIS)
6. BIOTIN (CO2 FIXATION)
7. COBALAMINES (B-12) [MEGALOBLASTIC
AND PERNICIOUS ANAEMIA,
METHYLMALONYL ACIDURIA
HOMOCYSTEINMIA]
8. FOLIC ACID (MEGALOBLASTIC
ANAEMIA)
9. ASCORBIC ACID (VIT C) [SCURVY]
 THIAMINE( B – 1)
 ACTIVE THIAMINE IS THIAMINE
DIPHOSPHATE
 ACTIVATION IN BRAIN & LIVER
1. BIOCHEMICAL ROLL OF THIAMINE (VIT – B1)
a. AN OXIDATIVE DECARBOXYLATION OF α-
KETO ACIDS
 PYRUVATE ACETYL COA
o ENZYME PYRUVATE DEHYDROGENASE
b. -KETOGLUTARATE SUCCINYL COA
o ENZYME -KG DEHYDROGENASE
c. -KETOANALOGS OF BRANCHED CHAIN A ACIDS
d. TRANSKETOLASE REACTION (HMP)
o ACTIVITY OF TRANSKETOLASE IS DECREASED IN VIT
B1 DEFICIENCY
 RIBOSE-5P + XYLULOSE-5P SEDUHEPTULOSE +
GLYCER ALDEYDE-3P
 XYLULOSE-5P + ERYTHROSE-4P FRUCTOSE-
6P + GYCERALDEHYDE -3P
 GLYCERALDEHYDE – 3P + SEDUHEPTULOSE-7P
FRUCTOSE – 6P + ERYTHROSE – 4P
 THIAMINE DEFICIENCY [BERI BERI]
 HIGH CHO DIET, HEAVY ALCOHOL, I-V GLUCOSE
 AEROBIC METABOLISM OF GLUCOSE IS
DISTURBED AND CELLS CAN NOT UTILIZE
GLUCOSE (BRAIN)
 ACCUMULATION OF PYRUVIC AND LACTIC ACID
 CARDIAC FAILURE, PERIPHERAL NEUROPATHY &
ENCEPHLOPATHY
TYPES OF BERI BERI
(SEVERE WEAKNESS EVEN PARALYSIS)
1. WET AND DRY BERI BERI PREGNANCY,
2. INFANTILE BERI BERI LACTATIN
3. WERNICK’S ENCAPHELOPATHY INFANTS, AND
4. KORSAKOFF’S PSYCHOSIS DIALYSIS
PRECIPITATE
 WET BERI BERI
1. MECHANISM
 ACCUMULATION OF PYRUVIC ACID AND LACTIC
ACID, PERIPHERAL VASO DILATATION, Na+
RETENTION
 HYPOPROTEINEMIA
2. CLINICAL FEATURES
 HIGH CARDIAC OUTPUT FAILURE, OEDEMA
 ECG CHANGES (INVERTED T WAVE , CONDUCTION
DEFECTS), TACHYCARDIA, PRECARDIAL PAIN
 SKIN FIRST WARM THEN LATER COLD
3. LAB TEST
 PYRUVIC ACID AND LACTIC ACID INCREASED
 LOW TRANSKETOLASE ACTIVITY IN RBCs
 PLASMA AND URINARY THIAMIN LOW
 DRY BERI BERI
 LONG STANDING DEFICIENCY OF VIT B1
 DEGENERATION AND DEMYELINATION OF
SENSORY AND MOTOR NERVES
 MUSCLE WASTING, CALF MUSCLE
 BLOOD PYRUVIC ACID AND LACTATE ARE
NORMAL
 PERIPHERAL NEUROPATHY (DUE TO
COMBINED DEFICIENCYOF B GROUP e.g. B6,
NIACIN & B12
 REFLEXES ARE LOW (KNEE JERK)
 WERNICK’S ENCAPHALOPATHY
 OCCURS IN ALCOHALICS WITH
DEFICIENCY OF VIT B1 IN DIET. PURELY
INVOLVE CEREBRAL CORTEX
 CLINICAL FEATURES
[IN ALCOHALICS, DIET DEF IN B1]
 CONFUSION, BILATERAL
OPHTHALMOPLEGIA, ATAXIA, APATHY,
DROWSINESS
 TRANSKETOLASE ACTIVITY IS LOW
 KORSAKOFF’S PSYCHOSIS
 UNTREATED WERNICK’S
ENCAPHALOPATHY LEADS TO
PERMANENT DAMAGE OF THE BRAIN
 PROFOUND IMPAIRMENT OF
MEMORY, OTHERWISE CONSCOIUS
 INDIVIDUAL INCAPABLE OF LIVING
INDEPENDENTLY
 REQUIRES INSTITUTIONAL CARE
RIBOFLAVIN (VIT B2)
 RIBOFLAVIN (VIT B2)
1. SOURCE: YEAST, LIVER, KIDNEY, MILK.
YELLOW FLORESCENT PIGMENT.
DECOMPOSES IN LIGHT, HEAT STABLE IN
LEAFY VEG. [MILK EXPOSED TO LIGHT]
2. BIOCHEMICAL ROLE
ACTIVE FORM IS FLAVIN
MONONEUCLEOTIDE (FMN) AND FLAVIN
ADENINE DINEUCLEOTIDE (FAD). THESE ARE
CALLED FLAVO PROTEINS [CONTAIN Mb & Fe]
FLAVIN + ATP FMN FAD
 SERVES AS CO-ENZYME OF OXIDO
REDUCTASES ENZYMES
1. -AMINO OXIDASE (DEAMINATION)
2. XANTHINEOXIDASE (PURINE CATABOLISM)
3. ALDEHYDE DH (ALDEHYDE DEGRADATION)
4. GLYCEROL-3-P DH [TPT OF REDUCING
EQUIVALENT]
5. SUCCINATE DH (TCA)
6. ACYL-COA DH AND ELECTRON TRANSFER
PROTEIN (FATTY ACID OXIDATION)
7. OXIDATIVE DECARBOXYLATION
(PYRUVATE AND -KETOGLUTARATE)
8. ELECTRON TRANSPORT CHAIN
9. FAD AS COENZYME TO GLUTATHIONE
REDUCTASE
 DEFICIENCY
 CAUSES:
 SENSITIVE TO BOILING IN ALKALINE MEDIUM
 SENSITIVE TO UV LIGHT (VIT IS STORED IN
BROWN BOTTLE)
 NEONATES WITH INCREASED SERUM
BILIRUBIN TREATED BY PHOTOTHERAPY
1. ANGULAR STOMATITIS
 NOT SPECIFIC. RESULT DUE TO COMBINED
DEFICIENCY OF NIACIN, PYRIDOXIN & IRON.\
CAN FOLLOW HERPES FIBRILIS AT THE
ANGLES OF MOUTH
2. CHEILOSIS IS ZONE OF RED DENUDED
EPITHELIUM AT THE LINE OF CLOSURE
OF LIPS. COMBINED WITH NIACIN i.e. ALSO
IN PELLAGRA
3. NASOLABIAL DYSSEBACEA (SCALINESS
/ GREASINESS)
 CAN ALSO OCCUR IN PELLAGRA
4. VASCULARIZATOIN OF CORNEA
5. MAGENTAL COLOUR TONGUE AND
ANAEMIA
 DEFICIENCY IN EXPERIMENTAL
ANIMALS INDUCE BIRTH DEFECTS
DURING PREGNANCY
 DIAGNOSIS
 LOW ERYTHROCYTE GLUTATHIONE
REDUCTASE ACTIVITY
NIACIN (VIT- B-3)
 NIACIN (VIT- B-3)
 SOURCE: WIDELY DISTRIBUTED PLANTS
AND ANIMALS, COFFEE GOOD SOURCE,
LIVER, MEAT, FISH
 TRYPTOPHAN (60 mg) CONVERTED TO VIT B6
(1mg)
 RESISTANT TO HEAT. DIFFERENT NAMES AS
 NIACIN, NICOTINAMIDE AND NICOTINIC
ACID
 60 GRAMS PROTEIN = 10 mg NIACIN
BIOCHEMICAL ROLE
 ACTIVE NIACIN IS NICOTINAMIDE ADENINE
DINUCLEOTIDE (NAD) AND NICOTINAMIDE ADENINE
DINUCLEOTIDE PHOSPHATE (NADP)
 NAD AND NADP ARE CO-ENZYMES OF ENZYMES
OXIDOREDUCTASES [ADDITI OF H+ ION H+]
1. THEY ARE KEY COMPONENTS OF METABOLIC
PATHWAYS FOR CARBOHYDRATES, LIPIDS
AND AMINO ACID METABOLISM (TCA, HMP)
2. CO-ENZYME FOR DEHYDROGENASES
ENZYMES
 LACTATE DEHYROGENASE IN CYTOSOL
 MALATE DEHYDROGENASE IN
MITOCHONDRIA
3. NADP LINKED DH OR REDUCTASES IN
CYTOSOL FOR REDUCTIVE SYNTHESIS OF CHO
AND LIPIDS
4. PART OF RESPIRATORY CHAIN
5. PYRUVATE DEHYDROGENASE
6. α-KETOGLUTARATE DEHYDROGENASE
7. DECREASES CHOLESTEROL
 NIACIN DEFICIENCY
(PELLAGRA SYNDROME)
1. CAUSES:
 WHEN STAPLE DIET IS MAIZE (NIACIN IS IN BOUND
FROM i.e. NIACYTIN IN MAIZE) MAIZE IS ALSO
DEFICIENT IN TRYPTOPHAN. HIGHLY LEUCIN DIET
 ALCOHOLICS WITH POOR DIET. VIT B6 LOW DIET
 HEARTNUP’S DISEASE, INH, CARCINOID SYNDROME
2. CLINICAL FEATURES, DISEASE OF THREE Ds
 DERMATITIS, DIARRHEA, DEMENTIA, WEIGHT LOSS,
DEPRESSION
a. SKIN (DERMATITIS)
 ERYTHEMA AROUND THE NECK IN CHILD LEADING
TO VESICULAION, EXUDATION AND ULCERS
 VULVA, PERINIAL AREA ALSO INVOLVED
b. ALIMENTARY TRACT [NON INFECTIVE
INFLAMATION]
 ANNOREXIA, NAUSIA, DYSPHAGIA
 GLOSSITIS, ANGULAR STOMATITIS LEADING
TO INFLAMMATION OF GIT AND DIARRHEA
c. NERVOUS SYSTEM (DELIRIUM AND
DEMENTIA)
 URINARY METHYL NICOTINAMIDE OR RBC
NAD IS THE BIOCHEMICAL TEST FOR
DIAGNOSIS
d. MANAGEMENT:
1.HIGH PROTEIN DIET 2. VIT B COMPLEX
3. ALCOHOL SHOULD BE AVOIDED
PYRIDOXINE (VIT B6)
 PYRIDOXINE (VIT B6)
 SOURCE: WIDELY DISTRIBUTED IN PLANTS, LIVER,
EGG, FRUIT [BANANA] WHOLE GRAIN CEREALS
 FORMS: PYRIDOXINE, PYRIDOXAL, PYRIDOXAMINE,
 ALL HAVE EQUAL VIT ACTIVITY

BIOCHEMICAL ROLE
 PYRIDOXAL PHOSPHATE IS THE COENZYME OF
SEVERAL ENZYMES OF AMINO ACID METABOLISM
 ACTIVATED TO PYRIDOXAL PHOSPHATE IN BODY
PYRIDOXAL
 PYRIDOXAL PYRIDOXAL PO4 (PLP)
+ ATP KINASE
1. CO-ENZYME OF AMINO ACID METABOLISM
i. TRANSAMINATION (SGOT, SGPT)
ii. DECARBOXYLATION OF DOPA TO DOPAMINE
ALDOLASE
iii. THREONINE GLYCINE +
ACETALDEHYDE
iv. TRYPTOPHANE DEGRADATION
2. CO-ENZYME FOR GLYGENOLYSIS
 INTEGRAL PART OF PHOSPHORELASE: 70-80%
VIT B6 IS WITH MUSCLE PHOSPHORELASE
3. CO-ENZYME FOR SYNTHESIS OF DELTA
AMINO LEVULINIC ACID (PORPHYRIN
SYNTHESIS)
 DEFICIENCY
 SOLITARY DEFICIENCY IS RARE
 SOLITARY DEFICIENCY CAN OCCUR IN LACTATION,
ALCOHOLICS AND ISONIAZID THERAPY OF
TUBERCULOSIS
LACTATION
 MOTHER ARE DEPLETED OF VIT B6 DUE TO ORAL
CONTRACEPTIVES
ALCOHALICS
 ETHANOL CONVERTED TO ACETALDEHYDE WHICH
HYDROLYZE PYRIDOXAL PHOSPHATE TO
PYRIDOXINE
ISONIAZID (INH)
[CHEMICAL ANTAGONIST]
 PYRIDOXINE PYRIDOXAL HYDRAZINE
TOXICITY
 NEUROLOGICAL INVOLVEMENT IF >.2 gm / Day
BIOTIN
 BIOTIN
COLOURLESS, HEAT STABLE, MONOCARBOXYLIC
ACID
SOURCE
 INTESTINAL BACTERIAS
 NATURAL FOODS, LIVER, KIDNEY, YEAST, ROYAL JELLY,
EGG YOLK
BIOCHEMICAL ROLE
 ACTIVE FORM AS BIOTNYL CARBOXYLASE
 CO-ENZYME OF CARBOXYLASE ENZYMES FOR FIXATION OF
CO2 IN THE FORM OF ACTIVATED COOH GROUP
1. PYRUVATE CARBOXYLASE (PYRUVATE TO GLUCOSE,
REPLENISH OXALOACITATE FOR TCA)
2. ACETYL CoA CARBOXYLASE (FATTY ACIDS SYNTHESIS)
ACETYL CoA TO MALONYL - CoA
3. PROPIONYL COA CARBOXYLASE (PROPIONATE TO
SUCCINATE)
4. B-METHYLE CROTONYL COA CARBOXYLASE (CATABOLIZE
LEUCINE AND ISOPRENOID UNITS)
5. FIXATION OF CO2 AS CARBAMYOL PO4
 DEFICIENCY (RARE)
CAUSE: (RAW EGGS (BIOTIN ANTAGONIST AVIDIN)
LONG TERM PARENTRAL NUTRITION
 SCALY DERMATITIS
 ALOPECIA
 PARAESTHESIA
 SEBORRHIC TYPE OF DERMATITIS
CLINICAL FEATURES OF BIOTIN
 DERMATITIS, ALOPECIA, PARAESTHESIA,
DEPRESSION, HALLUCINATIONS, MUSCLE PAIN
 IMMUNODEFICIENCY DISEASE RELATED TO
ACCUMULATION OF LACTATE, β-
METHYLCROTONATE, β-HYDROXYISOVALERATE, β-
HYDROXYPROAONATE
PANTOTHENIC ACID
STRUCTURE: (PANTOIC ACID + B-ALANINE)
SOURCE: WIDELY DISTRIBUTED [PANTOS MEANS
EVERY WHERE]
BIOCHEMICAL ROLE: (-SH IS REACTIVE THIOL GP)
 ACTIVE IN THE FORM OF CO-ENZYME-A (CoA-SH)
 ACYLE CARRIER PROTEIN (ACP)
1. REQUIRED IN THE FOLLOWING AS CoA
 TCA, FATTY ACID OXIDATION, ACETYLATION OF
DRUGS, CHOLESTEROL SYNTHESIS
2. REQUIRED AS ACP IN FATTY ACID SYNTHESIS
DEFICIENCY
 NOT SPECIFIC
 BURNING FEET SYNDROME CAN BE ASSIGNED TO ITS
DEFICIENCY [DUE TO DECREASED ACETYLATION
REACTION]
 RESTLESSNESS, FATIGUE, GIT DISTURBANCES
 ASCORBIC ACID (VIT C)
(RESEMBLE GLUCOSE)
SOURCE:
 FRESH FRUITS (GAUVA, LEMON, ORANGE), GREEN
LEAFY VEGETABLES, MILK IS DEFICIENT
 ANIMALS WITH GULONOLACTONE OXIDASE CAN
SYNTHESIZE
BIOCHEMICAL ROLE
 ACTIVE VIT C IS ASCORBIC ACID WHICH IS DONOR
OF REDUCING EQUIVALENTS IN CERTAIN
REACTIONS
 ASCORBIC ACIDS DEHYDRO ASCROBIC
ACID
 CAN REDUCE, MOLECULAR OXYGEN, NITRATES,
CYTOCHROMES a&c
FOLLOWING ARE THE ROLES
1. HYDROXYLATION OF PROLINE TO HYDROXY PROLINE
(POSTTRANSLATIONAL MODIFICAITON OF COLLAGEN) +
HYDROXYLATION OF LYSINE
2. TYROSINE METABOLISM
CU++
 P-OH PHENYLE ALANINE HOMOGENSTITATE
 HOMOGENSTITATE MALEYL ACETOACETATE
Fe++
3. SYNTHESIS OF EPINEPHRINE
 DOPAMINE-β-HYDROXYLASE STEP TO FORM NOR
EPINEPHRINE
4. BILE ACIDS FORMATION-7 α - HYDROXYLASE
5. STEROIDOGENESIS IN ADRENAL CORTEX
6. ABSORPTION OF IRON
7. ASCORBIC ACID ACTS AS ANTIOXIDANT AND INHIBIT
NITROSAMINE FORMATION IN GUT
8. PREVENT LIPID PEROXIDATION INDIRECTLY TO REDUCE VIT-
E REQUIREMENT
PREVENTION
 DIET SHOULD CONTAIN CITRUS FRUITS AND FRESH
VEGETABLES
 BREAST FEEDING, MOTHER’S DIET WITH JUICES
 INFANT SHOULD BE GIVEN JUICES
 DIFFERENT FRUITS HAVE FOLLOWING CONCENT
RATIONS OF VIT C.
 LEMON 50 mg/g
 ORANGE 49 mg/g
 GUAVA 300 mg/dl

BLOOD LEVEL OF VIT C IS 1 mg/dl

 LESS THAN 0.4 mg/dl DEFICIENCY OCCUR
 LESS THAN 0.2 mg/dl SCURVY APPEARS
 NORMAL STORES OF VIT-C ARE SUFFICIET FOR 3-4
MONTHS BEFORE SCURVY APPEARS
 DEFICIENCY (SCURVY)
 ABNORMAL FORMATION OF CONNECTIVE TISSUE DUE TO
ABNORMAL COLLAGEN RESULT INTO:
 DELAYED WOUND HEELING
 SUBCUTANEOUS & CAPILLARY HEMORRHAGES
 SUBNORMAL PLATELET ADHESIVENESS
ADULT SCURVY
 CLASSICAL SYNDROME OF VIT C DEFICIENCY
1. SWOLLEN AND SPONGY GUMS (SCURVY BUDS)
2. PERIFOLLICULAR AND PETICHIAL HEMORRHAGES,
ECHYMOSIS
3. DELAYED WOUND HEELING
LAB DIAGNOSIS
 PLASMA LEVEL OF ASCORBIC ACID LOW
INFANTILE SCURVY
 LASSITIDE, SUBPERIOSTEAL HEMORRHAGES, ANOREXIA,
GINGIVITIS
 PAINFUL LIMBS
 ENLARGEMENT OF COSTROCHONDRAL JUNCTIONS
COBALAMINES (VIT B12)
 COBALAMINES (VIT B12)
 EXTRINSIC FACTOR
 ANTI-PERNICIOUS ANAEMIC FACTOR
CHEMICAL STRUCTURE [CORRIN RING +
COBALT ]
SOURCE: ANIMAL ORIGIN (LIVER),
MICROORGANISMS
RDA = 3 MICROGRAM/DAY
ABSORPTION, TRANSPORT AND STORAGE
 INTRINSIC FACTOR (IF) MANDATORY FOR
ABSORPTION, STORED IN LIVER [UNIQUE
SITUATION]
 ABSORPTION AND TRANSPORT OF
VITAMIN B12
 ENTEROHEPATIC CIRCULATION OF VIT B12
 THIS SYSTEM IS DISTURBED IN
FOLLOWING CONDITIONS
[INTESTINAL LOOP SYNDROME – SPRUE
AND CROHN’S DISEASE]
ALL THESE LEAD TO MALABSORPTION
AND REQUIREMNET OF EXOGENOUS VIT
B12 IS INCREASED
BIOCHEMICAL ROLE
 THE ACTIVE VIT B12 ACTS AS CO-
ENZYMES IN THE FOL FORMS:
1. METHYL COBALAMINE
(CYTOSOLE) 3% IN PLASMA
2. DEOXYADENOSYL COBALAMINE
(MITOCHONDRIA) 70%
3. HYDROXYCOBALAMINE (PLASMA)
 ACTS AS A CO-ENZYME IN FOLLOWING REACTIONS
MUTASE
1. METHYL MALONYL COA SUCCINYL COA
(DEOXYADENOSYL FORM)
2. HOMOCYSTEINE
METHIONIEN
METHIONINE SYNTHASE
+ +
N5 -METHYL H4 FA H4 FOLATE
METHYL COBALAMIN

PURINES, PYRIMIDINE &

DNA SYNTHESIS
NUCLEIC ACID
SYNTHESIS
DECREASED VIT B12 [FOLATE TRAP]
[FOLATE SINK]
 DEFICIENCY
(PERNICIOUS ANEMIA)
CAUSES:
 DIETARY (VEGANS)
 INTRINSIC FACTOR DEFICIENCY
GASTRIC ATROPHY
CONGENITAL DEFICIENCY
TOTAL GASTRECTOMY
 DISEASE OF TERMINAL ILLEUM
 PARASITIC INFESTATION (TAPE WORM)
 DRUGS
LABORATORY DIAGNOSIS:
 LEVEL IN RBCs, SHAPE OF RBCs
(MEGALOBLASTIS)
 SERUM VIT B12
 SCHILLING TEST
 ANTIBODY TO INTRINSIC FACTOR
 METHYL MALONYL ACIDURIA
 HOMOCYSTINURIA
 RBC-COUNT IS DRASTICALLY
DECREASED IN PERNICIOUS
ANAEMIA
 SCHILLING TEST
o ORAL VIT B12 RADIOACTIVE
o PARENTRAL NON RADIOACTIVE
o % EXCRETION OF RADIOACTIVE VIT
B12
 CLINICAL FEATURES
 PERNICIOUS ANAEMIA (DEFICIENCY OF
INTRINSIC FACTOR)
 MEGALOBLASTIC ANAEMIA
THERE IS DELAYED DIVISION OF DNA
AND THE TIME BETWEEN DIVISION
INCREASES WHICH GIVE TIME TO CELL
FOR GROWING INTO MEGALOBLAST
 GIT PROBLEMS
INTERMITTENT SORNESS OF TONGUE
PERIODIC DIARRHEA
 NEUROLOGICAL PROBLEMS
o PARAESTHESIA OF FINGER AND TOES
o DEMENTIA MAY OCCUR
o UNSTEADINESS OF GAIT
o SPINAL CORD AND PERIPHERAL
NERVES ARE CLEARLY INVOLVED
FOLATE OR FOLACIN
(FOLIC ACID)
FOLIUM (LEAF)
 FOLATE OR FOLACIN (FOLIC
ACID)
 FOLIUM (LEAF)
CHEMICAL STRUCTURE
 PTERIDINE + PABA + GLUTAMATE ACID
 SOURCE
 PLANT ORIGIN, LEAFY VEGETABLES
(POLYGLUTAMATE CONGUGATES)
SYNTHESIZED IN GIT
 ABSORPTION AND TRANSPORT IN BLOOD
 IN GIT EXISTS AS POLYGLUTAMATES
MONOGLUTAMATE
 IN BLOOD 2/3 OF FOLATE IS BOUND WITH
PROTEIN
 IN LIVER MAJOR FOLATE IS STORED AS
PENTAGLUT-AMATE CONGUGATE
 BIOCHEMICAL ROLE
 ACTIVE FOLATE IS TETRAHYDROFOLIC ACID
 (H4 FOLATE)
 1. H4 FOLATE IS CARRIER OF ACTIVATED ONE
CARBON UNIT IN DIFFERENT OXIDATION STATES
 METHYL -CH3 ALL ARE
 METHYLENE -CH2-
METABOLICALLY
 METHENYL -CH=
INTERCONVERTABLE

 FORMYL C
O H
 FORMIMINO HN=CH-
 SERINE IS A THE MAJOR SOURCE OF ONE CARBON UNIT
(METHYLENE – CH2 –)
2. FOR SYNTHESIS OF PURINES i.e. THYMIDYLATE FOR DNA
SYNTHSIS
 N5 , N10 METHYLENE-H4 FOLATE PROVIDES METHYL GROUP IN
THE FORMATION OF THYMIDYLATE FROM URIDYLATE, A
NECESSARY PRECURSOR OF DNA SYNTHESIS &
ERYTHROPOISIS
TRIMETHOPRIM
FOLIC ACID DIHYDRO FOLIC ACID

METHOTREXATE

FOLATE REDUCTASE

TETRA HYDRO FOLATE

(H4 FOALTE)
 TRIMETHOPRIM (ANTIBACTERIAL) AND METHOTRAXATE
(ANTICANCER) ACT AS FOLATE ANTAGONISTS
 DEFICIENCY
CAUSES
 INADEQUATE DIET
 UPPER GIT DISEASE (COELIAC AND SPRUE)
 INCREASED BODY DEMAND THAN INTAKE
 PREGNANCY (COMMON)
 ACTIVE CELL PROLIFERATION
 HEMOLYTIC ANAEMIAS
 LEUKEMIAS
 EXTENSIVE PSORIASIS
 DRUGS, METHOTREXATE DECREASED
DEHYDRO FOLATE REDUCTASE
 ALCOHOL, PHENYTOIN AND PRIMIDONE
CLINICAL FEATURES
 MEGALOBLASTIC ANAEMIA IN TROPICAL
COUNTR-IES DUE TO MALNUTRITION,
PREGNANCY:
 ANAEMIA IS DIFFERENTIATED FROM VIT B12
DEFICIENCY BY FOLLOWING
 GLOSSITIS IS LESS APPARENT,NEUROLOGICAL
SYMPTOMS ARE NOT THERE SPERMATOGENESIS
AND OOGENESIS FAILURE
 LAB DIAGNOSIS
 FIGLU TEST
 SERUM & ERYTHROCYTE CONCENTRATION OF
FOLIC ACID
 THERAPEUTIC DOSE RESPONSE 300-500 mg / DAY