Water Soluble Vitamins

Water Soluble
Vitamins !
C &C & B-complexB-complex
VitaminsVitamins
Tapeshwar Yadav
(Lecturer)
B.M.L.T, D.N.H.E
M.Sc. Medical Biochemistry

Tapeshwar yadav.
(Lecturer)
B.M.L.T, D.N.H.E
M.Sc. Medical Biochemistry
Water soluble
vitamins

VITAMINS
• “VITAMIN” means “vital for life”
• VITAMINS are *Micronutrients*
which are necessary for everyday healthy
functioning of the body.
* Nutrients
required in very
small amounts -
mg or µg
* Nutrients
required in very
small amounts -
mg or µg

VITAMINS -
Two main categories
Water soluble
C
&
B-complex
Fat Soluble
A
D
E
&
K

Water v/s Fat
Soluble Vitamins

WATER SOLUBLE VITAMINS
Vitamins C & B-Complex
• Chemistry & Properties.
• Sources.
•Functions.
• Deficiency.
• RDA .

Water Soluble Vitamins:
Characteristics
• Essential
• Organic Structure
• Non-energy Producing
• Micronutrients
• Stability
• Bioavailability
• Toxicity

ASCORBIC ACID (VITAMIN-C)
 Anti scorbutic factor, Hexuronic acid.
 Chemistry :- White, Crystaline, Odourless with
acid taste.

Highly water soluble in Nature.
Empirical formula=C6H8O6.
Structural formula Resembles that of
Carbohydrate.

 Acidic Properties, due to Enolic Hydroxy groups.
 L-Ascorbic acid undergoes oxidation to form
dehydro ascorbic acid.
 Both are biologically active.

 D-Form is inactive.
 Oxidation of vitamin-c is rapid
in presence of Copper.

Sources :-
Amla(Indian Goose Berry)700mg/100g.
Guava :- 300 mg/100 G.
Green leafy vegetebles.
Absorption :- From intestine not stored in
Body.

 Ratio of Ascorbic/Dehydro Ascorbic acid is 15 :1
in many tissues.
 On hydration Dehydroascorbic acid is converted
to oxalate (via) DiketoGulonic acid.

Functions :-
Metabolisms Enzymes
1) Collagen Hydroxylation of
Lysine/Proline.
(Hydroxylase)
2) Tyrosine a) P-HPP Hydroxylase.
b) Homogentisate oxidase
c) Dopamine βHydroxylase.

3) Bile Acid 7-α-Hydroxylase.
4) Folic Acid Formation of FH4
(Folate reductase)
5) Tryptophan Tryptophan
hydroxylase
6) Biological Oxidation Cytochrome oxidase

7) Bone formation vitamin-C play important role.
8) Iron Absorption Fe3+
Fe2+
9) Meth-hemoglobin Hemoglobin.
10) Antioxidant property spare the
vitamins-A and E.

11) Prevents formation of cataract.
12) Reduces risk of Coronary heart diseases
and cancer.
13) Vitamin-C enhances synthesis of
immunoglobulins and increased Phagocytic
action.

• Deficiency :- Scurvy.
• Infants 6-12 months, due to weaning from milk-
dietary defect.
• Infantile scurvy Barlow’s Disease.

Symptoms :-
Adults :-
• Hypochromic, microcytic anemia.
• Easy fracture of bones.
• Loosing of teeth.
• Poor wound healing.

Deficiency test :-
• Sphygmomanometer cuff is placed on the fore
arm, inflated and pressure kept for 5 minutes.
• Petechiae is observed under skin.
• May be rough and dry, pigmented due to
abnormality of Tyrosine metabolism.

• Load test :-
• Give 500mg of vitamins-C orally.
• Check urinary- vitamin-C level after 5 hours.

• Load test :-
• Normal people 100mgs appear in urine.
• Moderate deficiency <20 mg.
• Severe deficiency <5mg.

• RDA :-
• 70 mg for normal people.
• >100 mg in case of Pregnancy & Lactation.

Thiamin
• Anti Beri-Beri or anti neuritic vitamin.
• Chemistry :- Pyrimidine ring and thiazole ring are
held by a Methylene bridge.

Sources:-
Thiamin mainly concentrated in outer layers of
cereals and breakfast cereals.
Oat meal.
Wheat germ. Fortified white flour.
Unpolished hand pound rice.
Vegetables.
Milk
Eggs, Meat.

• Absorption:
• In duodenum.
• Active transport (low Thiamin levels).
• Passive transport (high B1 levels).

Oxidative Decarboxylation Reactions
1) Pyruvate dehydrogenase
Pyruvate+ CoASH + NAD
+
TPP Acetyl CoA + CO2
+ NADH+H
+
Biochemical FunctionsBiochemical Functions

Oxidative Decarboxyation Reactions
2) α-Keto-Glutarate Dehydrogenase
α KG + CoASH+ NAD
+
TPP Succinyl CoA
+ CO2+NADH+H
+
Important in CHO/energy metabolism.
Biochemical FunctionsBiochemical Functions

2) Transketolase :- (HMP-Pathway)
Ribose-5-(P) Sedoheptulose-7-(P)
+ +
Xylulose-5-(P) Transketolase Glyceraldehyde-3(P)
+ TPP-Mg
+2
+
Erythrose-4-(P) Fructose-6-(P)
RBC transketolase activity is a measure of
Thiamin deficiency.

• Oxidative decarboxylation of branched chain
amino acids by α- keto acid dehydrogenase.
• TPP or Thiamin triphosphate help in nerve
impulse transmission by ion translocation or
synthesis of Acetylcholine.

Deficiency of Thiamin :- Beri-Beri-from dutch
Eastindies.
• Heaviness of legs, Anoxia, Dyspegia, subjects
feel weak.
Beri-Beri
Wet Beri-Beri Dry Beri-Beri Infantile Beri-Beri

Wet Beri Beri
• CVS manifestations.
• Edema of legs, Face,
Trunk..
• Calf muscles are
tender.
• Heart becomes weak
 failure

Dry Beri-Beri
• CNS symptoms.
• Muscles progressively
weak.
• Peripheral neuritis 
paralysis.

• Infantile Beri-Beri :-
• Restlessness.
• Sleeplessness.
• Acute cardiac failure.

• Wernicke-Korsakoff syndrome :-
• Cerebral Beri-Beri-Mainly due to nutrition
deficiency.
• Encephalopathy-Nystagmus, cerebellar ataxia.
• Affinity of TPP towards transketolase.

• Alcoholic Polyneuritis:- Observed in
chronic alcoholics.
Polyneuritis Motor and Sensory defects
Old age and Pregnancy thiamin deficiency.
• RDA:- 1.0-1.5 mg.

• Explanations for deficiency symptoms:-
•
Pyruvate x Acetyl CoA.
Lactate dehydrogenase
Lactate
• Pyruvate, Lactate levels rise in blood, tissues
and urine in BERI-BERI causing vasodilatation
edema.

• Branched- chain α-ketoacids rise in blood and
urine in BERI-BERI as TPP is coenzyme.
• Decline in transketolase activity in BERI-BERI,
elevates Pentose levels in blood, urine .
Estimation of erythrocyte transketolase activity
has a diagnostic value for B1 activity.

• Energy production from glucose is depressed
in nerve tissue and heart in BERI-
BERI,leading to neuronal inflammations,
leisons,lassitude and cardiac failure.
• Neurological symptoms are due to decline in
Beri-Beri may be due to decline direct role of
TPP in nerve impulse transmission.

Riboflavin = B2
• First vitamin among B-complex group to
be isolated in a pure state.
• Vitamin is synthesized by all green plants
and most of the micro-organisms.

• Lactoflavin-Milk, Hepatoflavin-liver, Ovoflavin-
Egg, Verdoflavin-Grass are chemically identical
to Riboflavin.
• Warburg-isolated yellow enzyme is essential for
cellular respiration.
• Coloured heat stable pigment decomposes in
the presence of visible light.

Chemistry
Riboflavin
Isoalloxazine
Ribitol
+

Riboflavin Flavokinase Flavin mono nucleotide(FMN)
ATP ADP ATP
Synthase
PPi
Falvin adenine dinucleotide (FAD)

Chief functions in the body:- Part of
coenzymes-
• FAD (Flavin adenine dinucleotide).
• FMN (Flavin mononucleotide) used in energy
metabolisms.

• FAD dependent reactions :-
1). Succinate dehydrogenase (SDH) :-
Succinate Fumarate.
FAD FADH2
2). Acyl CoA dehydrogenase:-
Acyl CoA α-β Unsaturated Acyl CoA.
FAD FADH2

• FAD dependent reactions :-
3). Xanthine oxidase :-
Xanthine Uric acid
FAD FADH2

• FMN dependent :-
L-Amino acid oxidase
L-Aminoacid α-Keto acid + NH3
FMN FMNH2

Sources :-
• Milk/products
• Enriched grains
• Liver
• Oyster
• Yeast
• Whole grains

• Riboflavin deficiency :-
• Its rare, occur with other vitamin deficiencies.
• Cheilosis A disorder of the lips often due to
riboflavin deficiency and other B-complex
vitamin deficiencies and characterized by
fissures, especially in the corners of the mouth

• Inflammation at angles of mouth – Angular
stomatitis.
• Lingual papillae atrophy and magenta colored
tongue - Glossitis
• Seborrhic dermatitis:- inflammation of
sebaceous glands of skin.

• Assay :-
a) RBC content of Riboflavin.
b) RBC glutathione Reductase activity.
• RDA :- 1.5 mg

Niacin
Other names
1. Vitamin B3.
2. Nicotinic acid.
3. Nicotinamide.
4. Niacinamide.
5. Pellagra preventing factor of
Gold Berger.

COOH
Pyridine Nicotinic acid (Niacin)
CO-NH2
Nicotinamide

Sources :-
• All protein foods.(rich in
Tryptophan)
• 60 mg TRP= 1mg Niacin
• Milk, eggs, meat, fish, poultry.
• Enriched grains and Nuts.

Chief functions:-
– Theraputic uses :- Nicotinic acid for
lowering the plasma cholesterol.
– The main coenzymes are two they are
1) NAD+
and 2) NADP+
.
– NAD
+
(Nicotinamide adenine dinucleotide)
and NADP
+
(its phosphate form) used in
oxidation-reduction reactions of various
metabolisms.

• Primary function of coenzymes is to remove
hydrogen from substrates.
• AH2 + NAD
+
NADH + H
+
+ A
Hydrogen ion

• NAD
+
Reactive site is carbon atom 4 and
NADP
+
nitrogen atom of Nicotinamide ring.
• Rest of the molecule binds to apoenzyme.
• Oxidized form Reduced form
NAD
+
NADH + H
+
NADP
+
NADPH + H
+
• These coenzymes participate in the oxidation
and reduction series of reactions.

• NAD
+
dependent reactions
Glycolysis :-
a) Glyceraldehyde-3-phosphate dehydrogenase.
b) Lactate dehydrogenase.
TCA cycle :-
a) Pyruvate dehydrogenase.
b) Isocitrate dehydrogenase.
c) α-Ketoglutarate dehydrogenase.
d) Malate dehydrogenase.

• NAD
+
dependent reactions
• Aminoacid catabolism :-
a) Branched chain α-Ketoacid dehydrogenase
b) Glutamate dehydrogenase
• Fat metabolism ;-
a) β-Hydroxy acyl CoA dehydrogenase
b) β-Hydroxy butyrate dehydrogenase

NADP
+
dependent
Glucose Dehydrogenase.
Isocitratedehydrogenase.
Glucose-6-Phosphatase.
Malic enzyme.

NADPH dependent
• Dihydro folate reductase.
• Phenylalanine hydroxylase.
• Met Hb reductase.
• Cholesterol -7-a hydrolase.
• Squalene epoxidase.
• HMG- CoA reductase.

• 3-Keto acyl CoA reductase.
• Glutathione reductase.
• Glucose 6-(P) dehydrogenase.
• 6-Phospho gluconate dehydrogenase.

Deficiency
Pellagra(3D’s disease):-
1.Dermatitis.
2.Diarrhea.
3.Dementia.

Dermatitis
• Inflammation of skin.
• Red, itchy, dry thickened, pigmented skin in
hands, feet, axila, wrist, and knees.

Diarrhea: Abnormal, frequent
evacuation of watery feces.
• Intestinal leisons
• Vomiting.

Dementia
• Delerium – Impairement of
memory.
• With cerebral, spinal lesions,
irritability and anxiety.

Cause of deficiency :-
• Maize rich diet where Niacin is in bound,
not useful.
• Sorghum rich diet  Leucine  inhibits
Quinolinate Phoshoribosyl transferase.

RDA :- - 13-19 mg . 13x 60 mg to 19x60 mg .
• Tryptophan (60mg)
Pyridoxal phosphate (PLP).
Niacin (1mg).

Toxicity symptoms
– Painful flush, hives, and rash
(Niacin flush)
– Excessive sweating
– Blurred vision
– Liver damage, impaired glucose tolerance.

Pyridoxine = B6
• Other forms of this vitamin.
– Vitamin B6
.
– Pyridoxal.
– Pyridoxal phosphate.
– Pyridoxamine.

Pyridine
CH2OH
CHO
CH2-NH2
CH2OH
CH2OH
HO CH2OH
H3C
H3C
HO HO
H3C
Pyridoxine
Pyridoxal Pyridoxamine

CHO
CH2O-P
HO
H3C
Pyridoxal phosphate
CHO
OH
CH3
CH2OH
+ ATP +ADP
Pyridoxal

Absorption :- All forms of B6 are absorbed
from intestine.
Pyridoxal + ATP Pyridoxal phosphate+ADP
Kinase (Major)
Pyridoxamine +ATP Pyridoxamine phosphate+ADP
(Minor)
4-Pyridoxic acid
(End product)

Functons :-
Part of coenzymes PLP (pyridoxal phosphate)
and PMP (pyridoxamine phosphate) used in
amino acid and fatty acid metabolism.
Transamination reaction (transaminase).
Aspartate+αKG
AST
Oxaloacetate+Glutamate
Alanine+αKG
ALT
Pyruvate+Glutamate

 Heme biosynthesis (ALA synthase).
 Carbohydrate metabolism .
 PLP is a part of muscle phosphorylase
(Glycogenolysis).
 Lipid metabolism-Formation of sphingo lipids
and myelin sheath.
 Neurotransmitter Synthesis.
5-Hydroxy Tryptophan Serotonin
 Conversion of tryptophan to niacin.

Decarboxylation of amino acid
(decarboxylase).
Glutamate GABA
Histidine Histamine

• Dietary sources
• Rice polishing, Wheat germ,
• Milled Cereals, pulses, oil seeds.
• Milk, Meat, fish, Poultry, Liver.
• Potatoes, Legumes, Soya products
and green leafy vegetables.

• Deficiency :-
 Severe B6 deficiency is characterized by
increased excretion of xanthurenic acid in urine.
 Tryptophan
3- OH Kynurenine
PLP X Xanthurenic acid excreted in urine
3-OH Anthranilate Quinolinate QPRT NMN
NAD
+
and NADP
+

• Deficiency :-
 Neurological symptoms are present since
biological amine synthesis is decreased.
 Mental confusion, Irritability, Nervousness,
Depression.

 Hypochromic Microcytic anemia due to
decreased synthesis of Hb.
 De-myelination of nerves lead to peripheral
neuritis.
 Commonly observed during lactation and
alcoholism.

RDA :- Daily Value set at 2 mg
• 1.3 mg for adults
• 1.7 mg for men over 50
• 1.5 mg for women over 50
• Average intake is more than the RDA

Folate
• Other names
– Folic acid
– Folacin
– Pteroyl glutamic acid (PGA).

Chemistry:-
 Pteridine ring - PABA - glutamate.
9 10

• Stability :-
– Very sensitive to heat.
– Easily oxidized.
– Leached.

Dietary Sources:-
• Fortified Grains
• Leafy Green Vegetables
• Legumes, Seeds
• Liver

Functions
Folic acid
NADPH+H
+
NADP
+
Folate reductase
Dihydrofolate
NADPH+H
+
NADP
+
Dihydrofolatereductase
Tetrahydrofolate

 THF mainly functions as a carrier for one carbon
groups.
 The one carbon group may be carried on N5
or
N
10
or both of tetrahydrofolate.

 They are Methyl(-CH3), Methylene(=CH2)
Methenyl(=CH-), Formyl(-CH=O), Fomimino (-
CH=NH).
 All one carbon groups are inter convertible.
 -CHO +H2 -CH2OH -H2 -CHO

 Sources of one carbon groups :-
Serine is the major source.
Other sources are Glycine, Tryptophan &
Histidine.

• Fate of one carbon groups :-
• N
5
, N
10
methylene THF provides methylene group
to :
a) Uracil to form thymine. Thymine is important for
DNA synthesis.
b) Glycine to form serine.

• N
5
methyl THF provides the methyl group to
Homocysteine to form methionine. This reaction
needs cobalamin.
• N
5
, N
10
methenyl THF provides C8 of Purine ring.
• N
5
formyl THF provides C2 of Purine ring.
• Purines are components of nucleic acids.

• N5
-formyl tetrahydrofolate is also called
Citrovoram factor  folinic acid, is used
as a supplement to folic acid, more
effective than folic acid in anti-cancer
treatment.

Factors causing folate deficiency :-
1) During pregnancy.
2) Defective absorption a) Sprue
b) Coeliac disease
3) Resection of jejunum.
4) Anticonvulsant drugs will inhibit intestinal
enzyme– Folate absorption decreases
5) During excessive hemolytic reaction.

Deficiency manifestations :-
Intracellular concentration of
Tetrahydrofolate.
No conversion dUMP dTMP
No DNA synthesis.
No cell division

• Macrocytic Anemia :-
• Hb accumulates in RBC precursors.
• Reticulosis :- Abnormal RBC trapped in spleen
and destroyed, leads to decreased RBC life
span
• Peripheral smear :- Macrocytic type.
• Daily 300-500 µg of folate will improve the
blood picture in the first condition.

 Pancytopenia all blood cells are affected.
 Leucopenia decreased WBC.
 Thrombocytopenia decreased platelets.
 Impaired growth.

• Neural Tube Defects
– Malformation of the central nervous system that
forms very early in the pregnancy (often even
before woman realizes she is pregnant.
• Spina bifida- Spine develops outside of the
body.
• Anencephaly- Entire brain and skull above
the ears is missing.

Neural tube defects
Spina Bifida Anencephaly

Folacin
• Only known way to prevent these congenital
malformations is adequate Folacin intake prior
to pregnancy
• Adequate folic acid intake can reduce the risk
of Neural tube defects by up to 75%.

• Assessment of Folate deficiency :-
1). Normal serum folate = 20 ng /ml.
2). Histidine load : 2-15g.
(FIGLU excretion) test :-
Histidine -----> Formiminoglutamic acid-
X Excreted in urine
Glutamate
3). Peripheral blood picture.
THF
Formyl THF

Antagonists:-
a) Trimethoprim.
b) Sulphonamides.
c) Aminopterin.
• RDA:- 100 μg

Vitamin B12
• Synonyms :-
 Cobalamin.
 Extrinsic factor of castle.
 Antipernicious anemia factor.

Chemistry :- 4 Pyrrole ring co-ordinated with cobalt
atom is called as corrin ring.
4-Pyrroles substituted + Cobalt
Corrin ring
Dimethyl benzimidazole + Ribose-5 (P)+ Amino
isopropanol
Cobalamin

Absorption
It requires
–HCl
–Pepsin
–Intrinsic factor

Diet
Vitamin B12 attached to proteins
Stomach Proteolytic enzymes
Proteins
B12 intrinsic factor of castle
GP (Molecular weight 50,000)
Complex of Intrinsic factor and B12
NOTE:- GP=Glycoprotein secreted by Gastric perietal
cells

• Intrinsic factor-B12 complex passes on ileum
of gut, where it is absorbed.
• Binding of complex and entry of B12 into
mucosal is mediated by calcium ions .

Plasma10% TC-II
B12 Mucosal cell Methyl B12 90% Trans cobalamin-I TC-I-B12
Other tissues TC-II-B12
Methyl B12 Deoxyadenosyl B12
• TC-I B12 Only water soluble vitamin stored in body about 2 mg in liver
which is useful till 2-3 years

Sources
• Animal products
– Meat, poultry fish, shellfish.
– Milk, cheese.
– Eggs.
– Not present in the vegetables.
– Intestinal micro organisms synthesize B12 in
human colon but it is not absorbed through
the mucosa.

• Coenzymes:-
• Vitamin B12 exists in two coenzyme forms.
1) Methyl cobalamin
2) 5’-deoxy adenosyl cobalamin.

Coenzymes of vitamin B12 :-
Cobalamin + Methyl tetrahydo folate
in Cytoplasm
Methyl-cobalamin + Tetrahydro folate.

Functions :-
Participates in Methionine biosynthesis:-
Homocysteine + N
5
Methyl tetrahydrofolate
Methyl transferase
Methylcobalamin
Methionine + Tetrahydrofolate(important for
haemopoiesis)
 Methionine is a Lipotropic factor which prevents the
fatty liver.

• Methionine is an important factor for the
formation of phospho lipids, later found in the
structure of myelin sheath.
• Isomerism of L-Methyl melonyl coA  Succinyl
coA by methyl melonyl coA mutase with the help
of 5’deoxy adenosylcobalamin in odd chain fatty
acids metabolism.

• In some bacteria :- Cobalamin derivatives useful
for Ribose  Deoxyribose
DNA synthesis

• Deficiency :-
• Decreased vitamin B12 intake, this may occur
among vegetarians.
• Atrophy of gastric mucosa  lack of intrinsic
factor, this give rise to a condition  Pernicious
anemia  above 60 years of age.
• Pernicious anemia :- Low Hb levels, decreased
number of erythrocytes.

• Auto antibodies against gastric parietal cells.
• Anti bodies against intrinsic factors.
• Defctive absorption as in Sprue or regional
enteritis.
• Drugs induced vitamin B12 deficiency.
 Anticonvulsants, Phenformin, Neomycin,
Cholestyramine, Para-aminosalycylic acid.

• Deficiency manifestations :-
• B12 deficiency
N
5
Methyl THF No formation of THF
• This condition is called folate trap or
• Methyl trap  Decreased folate co-enzymes 
Reduced nucleotide and DNA synthesis 
Megaloblastic anemia.
• Megaloblastic anemia is a macrocytic hypochromic
anemia.

Neurological manifestations :- It is
due to lack of myelin sheath due to deficiency of
methionine and disturbance in the metabolism of
odd chain fatty acids.
 It includes sub-acute combined degeneration of
spinal cord :-

 Sensory and Motor tracts are effected.
 Paresthesia of extremities.
 Alterations of reflexes.
 Loss of memory.
 Peripheral neuritis leads numbness, tingling and
weakness of extremities.

Treatment :- Megaloblastic anemia can be
treated with folate alone.
 But lesions cannot improved.
 So 100-1000µg of B12 is given intramuscularly.

• Assessment of B12 deficiency :-
 B12 serum – Radio immuno assay (RIA).
 increased methyl malonic acid excretion in urine
(i.e Methylmalonic aciduria).
 Peripheral blood and bone-marrow morphology.
 Check for Achylia gastrica.

Biotin
• Synonyms :-
 Vitamin-H.
 Vitamin B7.
• Anti egg white injury factor.

Sources
• Widespread in foods both Animal and
Plant origin.
• Liver, Kidney, Fish, Egg yolks, Milk.
• Tomatoes, Soybeans, Whole grains.

• Storage :-
• After absorption, Biotin is stored in liver as
Biocytin (Biotinyl-5-Adenylate)
• Biotin functions as a component of multi-subunit
enzymes that catalyze carboxylation reactions.

Multi-enzyme complex :-
• Biotin carrier protein.
• Biotin carboxylase.
• Biotin acyl transcarboxylase.

Enzyme Pathway Reaction
catalyzed
Propionyl CoA
Carboxylase
Amino acids-
1).Valine, Isoleucine,
Threonine.
2). Odd chain fatty
acid metabolisms.
Propionyl CoA
Methyl melonyl CoA
Acetyl CoA
Carboxylase
Fatty acid
synthesis
Acetyl CoA
Malonyl CoA
β-Methyl
crotonyl CoA
carboxylase
Leucine
catabolism
β-Methyl crotonyl
COA
β-Methyl glutaryl
CoA

Deficiency :-
• The deficiency occurs in sulfonamide treatment
also, causes destruction of intestinal flora.
• Deficiency of holocarboxylase synthetase in
children. The enzyme responsible for
attachment of biotin for carboxylase enzyme.

• Deficiency symptoms :-
1)Retarded growth
2)Dermatitis
3)Alopecia
4)Loss of muscular control.
5)Immuno deficiency disease.

Avidin :-
• Raw egg white – contains Avidin- Glycoprotein
had high affinity to Biotin.
• Intake of raw egg white (un-boiled) may cause
Biotin deficiency-(20 Raw eggs/day for
prolonged time).
• Avidin is heat labile, boiling of egg will neutralize
inhibitory activity.

Leiner’s disease :-
• Occurs in breast fed young infants with
persistent diarrhoea.
• Low Biotin in human milk leads to deficiency.

Antagonist :- Desthiobiotin.
RDA :- 200-300 μg.

Pantothenic Acid
• Greek word “Panto” means everywhere or
Universal.
• It is known as chick anti dermatitis factor.

Chemistry :-
Pantoic acid + β-Alanine
Pantothenic acid

Sources
• Widespread in foods.
• Organ meats.
• Mushrooms.
• Avocado.
• Broccoli.
• Whole grains.

Functions :-
Coenzyme A (CoA SH):- Synthesized from
cysteine, Pantothenic acid, AMP and
phosphate.
Functions of Coenzyme A :- It has a terminal
thiol group (-SH).
• Thiol group act as carrier of acyl or acetyl and
succinate group.

Biochemical Role
Carbohydrates
Pyruvate Acetyl CoA
Alanine Leucine
Glucogenic Ketogenic
aminoacids
Fatty acid
Acetyl Choline
Cholesterol
TCA cycle
Ketone bodies
Detoxification

α-Ketoglutarate Suyccinyl coA Gluconeogenesis
Activation of aceto acetate
ODD chain Fatty acids Porphyrins
Energy
Threonine, Valine, Isoleucine Drug metabolism

Deficiency :-
• Rare in humans. However “burning feet syndrome”
soldiers of second world war- Paresthesia in
lower extremities, staggering gait.
• Sleeplessness :- Linked to this vitamin deficiency.
• This syndrome observed in prison camps,
• Chronic alcoholic famine, renal dialysis patients.

• Non-B Vitamins
• Controversial other dietary compounds
• Still under scientific investigation
• May be “conditionally” essential
• Supplements NOT necessary
• Widespread in foods.

•Choline(Trimethyl hydroxy
ethanolamine):-
• It is needed in relatively big amount.
• Adequate Intake for Men=550 mg/day;
Women=425 mg/day
• Formed from serine.

Functions:-
• Participates in the formation of lecithin and
sphingomylein.
• Lipotropic action (prevents the fatty liver)
• Helps in the formation of acetyl Choline.
• Involved in the one carbon metabolism due to
the presence of three methyl groups.
• By oxidation it is converted into Betaine.

• Inositol(Hexahydroxy cyclohexane):-
• Also called as myoinositol or mesoinositol.
• It is sugar alcohol derived from glucose.
• Lipotropic factor.
• It is a component of phospholipid, phosphatidyl
inositol-Part of cell membrane structure.
• Acts as a second messenger for some hormones.

Lipoic acid(6,8 dithio octanoic acid):-
• Sulphur containing fatty acid.
• Fat as well as water soluble.
• Exist in oxidized and reduced form.
• As an antioxidant it reduces free radicals.
• Reduces the insulin resistance.

Biochemical functions :-
• Decarboxylation reactions
• Pyruvate PDH Acetyl coA
• Keto glutarate SDH Succinyl coA

• Vitamin Imposters
• Ubiquinone (Coenzyme Q10)
• Orotic acid.
• Lipoic acid.
• Vitamin O (oxygenated salt water)
• Vitamin B15 (Pangamic acid)
• Vitamin B17 (Laetrile)

Conclusions
1. Vitamins are derived from a variety of
foods. That is why variety is so important.
2. Vitamin deficiencies rarely occur.
3. If they do, it is usually in conjunction with
severe illness, stress, or trauma that is
superimposed on prolonged inadequate
intake.
4. If there is deficiency, usually several
vitamins (especially in the case of B
vitamins) are involved.

5. Toxicity is also rare but a possibility
– Toxicity is rarely associated with food
– Toxicity results from supplements
6. Vitamin imposters are used

Variety is the Key
Vitamins are
derived from
a variety of
foods.

‘’This life is a hard fact; work your way through it
boldly, though it may be adamantine; no matter, the

WISH U ALL HAPPY NEW YEAR 2068(B.C)

Water Soluble Vitamins

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