water soluble vitamins..

Water Soluble Vitamins –
Vitamin C & B complex – Source,
function & deficiency manifestations.
Dr. Athulya Lakshmanan
Dept of Prosthodontics

VITAMINS
Definition:
Vitamins may be regarded as organic compounds
required in the diet in small amounts to perform specific
biologic functions for normal maintenance of optimum
growth and health of organisms.

CLASSIFICATION:
 FAT-SOLUBLE VITAMINS:
VITAMINS A, D, E, and K
 WATER-SOLUBLE
VITAMINS:
VITAMINS B-COMPLEX and C
Based on solubility, vitamins can be classified in to

CLASSIFICATION OF WATER-SOLUBLE
VITAMINS:
Water-soluble vitamins participate in catalytic
functions or act as control mechanisms in the metabolism,
e.g. as co-enzymes.
Vitamin C

B-COMPLEX VITAMINS CAN BE CLASSIFIED
AS:
ENERGY
RELEASING:
HEAMATOPOIETI
C:

VITAMIN C: ASCORBIC ACID
Anti scorbutic factor, Hexuronic acid.
L
-
It is a hexose derivative and
closely resembles mono
saccharides in structure.
Acidic property is due to enolic
hydroxyl group.
STRONG REDUCING AGENT

BIOLOGICALLY ACTIVE FORMS:
L- ASCORBIC ACID
DEHYDRO L-ASCORBIC ACID
RATIO IN
TISSUES:
15 : 1
 OXIDATION OF VITAMIN C IS REGARDED AS ITS CHEMICAL
INACTIVATION.
 OXIDATION IS RAPID IN PRESENCE OF COPPER. HENCE VITAMIN C
BECOMES INACTIVE IF FOOD IS PREPARED IN COPPER VESSELS.

DIETARY SOURCES:
INDIAN GOOSEBERRY [AMLA]: RICHEST SOURCE OF VIT C
{700mg/100g}
CITRUS FRUITS, GUAVA, STRAWBERRIES, TOMATOES, POTATO
SKIN, CABBAGE,SPINACH.
MILK IS A POOR SOURCE.
RDA: 60- 70mg/day for adults
85 mg for pregnant woman
NORMAL SERUM LEVELS: 0.5- 1.5 mg/dl
ABSORPTION: Rapidly absorbed from intestine.
EXCRETION: Excreted in urine as such or as its metabolites.
.

DEFICIENCY OF VITAMIN C:
MAN CANNOT SYNTHESIZE ASCORBIC ACID DUE TO DEFICIENCY
OF A SINGLE ENZYME viz. L-GULONOLACTONE OXIDASE. SO, THE
REQUIREMENTS MUST BE MET BY DIET.
DEFICIENCY OF VITAMIN C LEADS TO A CONDITION TERMED AS
‘SCURVY’
MOST COMMONLY SEEN IN INFANTS, BETWEEN 6 TO 12
MONTHS OF AGE, WHEN WEANING IS STARTED; AND DIET IS NOT
SUPPLEMENTED WITH VITAMIN C OR ITS SOURCES…….. BARLOW’S
DISEASE

DEFICIENCY MANIFESTATIONS:
SKIN
CHANGES:
PERIFOLLICULAR
HYPERKERATOTIC
PAPULES
• CORK SCREW HAIR

CORKSCREW
HAIR
PERIFOLLICULAR
HYPERKERATOTI
C PAPULES
SPLINTER
HEMORRHAGES
CONJUNCTIVAL
HEMMORHAGE
SCORBUTIC ROSARY:
SEEN IN INFANTS
DEPREESED STERNUM
AND
MORE ANGULAR
COSTOCHONDRAL
JUNCTION

MEGADOSES OF VITAMIN C
• Ascorbic acid, as such has not been found to
be toxic.
• But, dehydro ascorbic acid is toxic.
• Megadoses of vit C are still continued in
common cold, wound healing, trauma etc.
• As an antioxident,, ascorbic acid provides
some health benefits.

THIAMINE [ VITAMIN B1]
Anti-beri beri/ Antinueritic Vitamin
PYRIMIDINE RING
METHYLENE
BRIDGE
THIAZOLE RING
ACTIVE COENZYME:
THIAMINE
PYROPHOSPHATE [TPP]
Or
THIAMINE DIPHOSPHATE
[TDP]
CARBOHYDRAT
E METABOLISM

Dietary sources:
CEREALS, PULSES, OIL SEEDS, NUTS,YEAST, WHOLE WHEAT FLOUR,
UNPOLISHED RICE
Also present in animal foods like pork, liver, egg ,meat, milk etc
RDA: DEPENDS ON THE CARBOHYDRATE/ CALORIE INTAKE
1-1.5 mg/day for adults
0.7-1.2 mg/day for children
PREGNANCY AND LACTATION: 2 mg/day
OLD AGE
ALCOHOLISM
• NORMAL PLASMA CONC.: 1µg/ 100ml
BIOCHEMICAL FUNCTIONS:
• RELEASE OF ENERGY FROM CARBOHYDRATES
• OXIDATIVE DECARBOXYLATION OF KETOACIDS
• TRANSMISSION OF NERVE IMPULSE

OXIDATIVE DECARBOXYLATION
CITRIC ACID CYCLE
IN HMP SHUNT: CONCERNED WITH
PRODUCTION OF RIBOSE AND
NADPH

THIAMINE DEFICIENCY:
Neurological
symptoms,
Edema,
Indigestion,
Constipation
BERI-
BERI

Beri beri
Earliest symptoms:
Anorexia
Dyspepsia
Heaviness and weakness of legs.
Calf tenderness
Easy exhaustion
WET BERI BERI
DRY BERI BERI
INFANTILE BERI
BERI
WERNICKE-KORSAKOFF
SYNDROME
ALCOHOLIC
POLYNUERITIS

Wet beriberi: is characterized by cardiovascular manifestations
including edema of legs, face, trunk and serous cavities, with
breathlessness and palpitations, along with increase in systolic and
decrease in diastolic blood pressure.
Dry beriberi: is associated with neurological manifestations resulting in
peripheral neuritis, with progressive weakening in muscles resulting in
difficulty to walk.
Infantile beriberi: seen in infants born to mothers suffering from
thiamine deficiency, characterized by sleeplessness and restlessness..
Wernicke- Korsakoff syndrome: also called as cerebral beriberi.
Features include encephalopathy plus psychosis.
Polyneuritis: commonly seen in chronic alcoholics. Also associated
with pregnancy and old age.

• Therapeutic Uses –
1. Prophylactic – 2 – 10mg / day
2.Beri beri, Wernicke’s encephalopathy –
100mg/day i.m or iv
Till symptoms subside.
Thamine antagonists-
Pyrithiamine and oxythiamine are two
important antemetabolites of thiamine.

RIBOFLAVIN [VITAMIN B2 ]:
ISOALLOXAZINE
RING
D- RIBITOL
ACTIVE COENZYMES:
FLAVIN MONONUCLEOTIDE
[FMN]
FLAVIN ADENINE
DINUCLEOTIDE [FAD]
REDOX
REACTIONS,
CARBOHYDRATE,
LIPID, PROTEIN,
PURINE
METABOLISM,
ELECTRON
TRANSPORT

Dietary sources:
Milk and milk products, meat, eggs, liver, kidney, crab meat are
rich sources.
Cereals, fruits, vegetables and fish are moderate sources.
RDA:
Adult: 1.2-1.5 mg
PREGNANT AND LACTATING WOMEN:[INCREASED BY 0.2-0.5 mg/day]
PHYSIOLOGICAL ROLE:
Growth, repair, development of body tissues - healthy skin,
eyes and tongue.

RIBOFLAVIN DEFICIENCY:
RIBOFLAVIN
DEFICIENCY

NIACIN/ NICOTINIC ACID:
[PELLAGRA PREVENTING FACTOR OF GOLDBERG]
PYRIDINE-3-
CARBOXYLIC ACID
ACTIVE COENZYMES:
NICOTINAMIDE ADENINE DINUCLEOTIDE
[NAD+
]
NICOTINAMIDE ADENINE DINUCLEOTIDE
PHOSPHATE [NADP+
]
ACCEPTS
ONE
HYDROGE
N ATOM
AND ONE
ELECTRO
N
NADH
NADPH

.
Dietary sources:
The rich natural sources of niacin include liver, yeast, whole grains,
pulses like beans and peanuts.
Milk, fish, eggs and vegetables are moderate sources.
Requirement:
Adults – 15-20 mg
Children-10-15 mg
Pregnancy-+2mg
Lactation-+5mg
• Therapeutic uses –
Prophylactically – 20 – 50 mg/day
Pellagra – 200 – 500 mg / da1y
Sixty milligrams of tryptophan
is equivalent to 1mg of niacin
for the synthesis of niacin
coenzyme.

Deficiency manifestations:
* Niacin deficiency results in a condition called as pellagra.
* The disease pellagra involves skin, gastrointestinal tract and central
nervous system.
* Symptoms are commonly referred to as three D’s. the disease also
progresses in the order Dermatitis, Diarrhea, Dementia, and if not
treated may rarely lead to Death (4th
D).
* The symptoms of dementia include anxiety, irritability, poor memory,
insomnia etc.

Oral manifestations:
* Bald tongue of sandwith.
* Raw beefy tongue.
* The mucosa becomes fiery red and painful.
* Salivation becomes profuse.

Pantothenic acid (Vitamin B5)
Pantothenic acid, also known as chick anti-dermatitis factor or
filtrate factor, is widely distributed in nature.
The functions of pantothenic acid are exerted through coenzyme
A or CoA. CoA is the central molecule involved in all the
metabolisms (carbohydrate, lipid and protein), acting as the carrier of
activated acetyl or acyl groups.
Dietary sources:
Widely distributed in plants and animals.
Rich sources are egg, liver, meat, yeast, milk etc.
Requirement; 5-10 mg for adults

• Burning foot syndrome – pain and numbness
in toes, sleeplessness and fatigue are features.

Pyridoxine (Vitamin B6)
Vitamin B6 is used to collectively represent the three compounds
namely pyridoxine, pyridoxal and pyridoxamine.
The active form of vitamin B6 is the coenzyme pyridoxal phosphate
(PLP).
PLP is closely associated with the metabolism of amino acids.
The synthesis of certain specialized products like serotonin,
histamine, niacin coenzymes from amino acids are dependent on
pyridoxine.
PLP participates in reactions like transamination, decarboxylation,
deamination, transsulfuration, condensation etc.

Dietary sources:
Animal sources such as egg yolk, fish, milk, meat are rich in B6.
Wheat, corn, cabbage, roots and tubers are good vegetable sources.
Requirement
Adult; 2-2.2 mg/day
Pregnancy and lactation:2.5 mg/day
Pyridoxine antagonists: isoniazid, deoxyyridoxine and
methoxypyridoxine

* Pyridoxine deficiency is associated with neurological symptoms such
as depression, irritability, nervousness and mental confusion.
* Convulsions and peripheral neuropathy are observed in severe
deficiency.
* These symptoms are related to the decrease in the synthesis of biogenic
amines like serotonin, nor epinephrine and epinephrine.
* Demyelination of neurons is also observed.
* Decrease in hemoglobin levels, associated with hypochromic
microcytic anemia, is seen in B6 deficiency, this is due to the decrease in
heme production.

Biotin (Vitamin B7)
Biotin, also called as anti-egg white injury factor, vitamin B7 or
vitamin H, is a sulfur containing B-complex vitamin.
Biotin acts as a carrier of CO2 in carboxylation reactions.
Dietary sources:
Biotin is widely distributed in both animal and plant foods.
The rich sources are liver, kidney, egg yolk, milk, tomatoes, grains,
etc.
Requirement: 100-300 mg for adults
This vitamin is abundantly synthesized by the intestinal bacteria.

Deficiency is uncommon.
• symptoms include anemia, loss of appetite, nausea,
dermatitis, glossitis etc.
• Biotin deficiency is not common since it is well
distributed in foods and also supplied by the intestinal
bacteria.

FOLIC ACID:
DERIVED FROM THE LATIN WORD FOLIUM=LEAF; [AS IT IS ABUNDANTLY
FOUND IN GREEN LEAFY VEGETABLES]
• Folic acid consist of pteridine nucleus, p-aminobenzoic acid and
glutamatic acid.
ACTIVE FORM:
TETRAHYDROFOLAT
E[THF or FH4]
ACTIVELY
INVOLVED IN
ONE CARBON
METABOLISM

• DIETARY SOURCES:
GREEN LEAFY VEGETABLES, WHOLE GRAINS, CEREALS, LIVER,
KIDNEY, YEAST AND EGGS.
MILK IS RATHER A POOR SOURCE OF FOLIC ACID.
• RDA:
ADULTS: 100µg/day
PREGNANCY: 300µg/day
LACTATION: 150µg/day
Absorption, transport and storage:
Absorbed in duodenum and jejunum
Stored in liver. Body can store 10-12 mg of folic acid for 2-3
months.

Oral manifestation:
* Glossitis
- The filliform papillae disappears first.
- But in advanced cases the fungiform papillae are lost
and the tongue becomes smooth and fiery red in
colour.

FOLIC ACID ANTAGONISTS:
1. AMINOPTERIN AND METHOTREXATE
Aminopetrin and methotrexate are structural
analogues of folic acid used in treatment of many cancer
including leukemia, these drugs blocks the formation of
THF and hence DNA synthesis is impaired.
2. SULFONAMIDES:
INHIBIT BACTERIAL SYNTHESIS OF FOLIC ACID. HENCE USED
AS ANTIMICROBIALS.

COBALAMIN [VITAMIN B12]:
ANTI-PERNICIOUS ANAEMIA FACTOR/ EXTRINSIC FACTOR OF CASTLE
Chemistry :-
Structure consists of 4 Pyrrole rings with
cobalt atom , called as corrin ring.
4-Pyrroles + Cobalt
CORRIN RING
DIMETHYL BENZIMIDAZOLE
+RIBOSE-5P AMINO ISOPROPANOL
COBALAMIN

• Active Coenzymes:-
• Vitamin B12 exists in two coenzyme forms.
1) Methyl cobalamin 2) 5’-deoxy adenosyl
cobalamin.
Cobalamin + Methyl tetrahydofolate
in Cytoplasm
Methyl-cobalamin + Tetrahydrofolate.

DIETARY SOURCES:
Animal products
– Meat, poultry fish, shellfish.
– Milk, cheese.
– Eggs.
– Not present in the vegetables.
– Intestinal micro organisms synthesize B12 in human colon.
[ ENOUGH TO MEET THE DAILY REQUIREMENTS]
RDA:
ADULTS: 3 µg/day
PHYSIOLOGICAL FUNCTIONS:
Required with folic acid for development of RBCs.
Stimulates appetite and is required for normal health.
Cures neurological symptoms of pernicious anaemia.

BIOCHEMICAL REACTIONS:
 Participates in Methionine biosynthesis
Methionine is a Lipotropic factor which prevents
the fatty liver.
Methionine is an important factor for the
formation of phospholipids, later found in the
structure of myelin sheath.
In some bacteria:-
Cobalamin derivatives useful for Ribose  Deoxyribose
DNA synthesis

DEFICIENCY OF VITAMIN B12:
•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.
•Defective absorption as in Sprue or regional enteritis.
•Drugs induced vitamin B12 deficiency.
Anticonvulsants, Neomycin, Cholestyramine, Para-
amino salycylic acid.

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 improve.
So 100-1000µg of B12 is given intramuscularly.

References
1.Essentials of biochemistry – Satyanarayana.
2. Text book of biochemistry- D M
Vasudevan(6th
edition)
3. Text book of medical biochemistry- M N
Chatterjea(3rd
edition)

water soluble vitamins..

More Related Content

What's hot (20)

Viewers also liked (9)

Similar to water soluble vitamins.. (20)

Recently uploaded (20)

water soluble vitamins..

Editor's Notes