vitamins biochemistry mbbs md dr darshna.ppt

Vitamins mbbs biochemistry first prof

1. Presented by
Dr. Darshna Jain
M.B.B.S , M.D
ASSISTANT PROFESSOR
DEPT. OF BIOCHEMISTRY
G.M.C RATLAM(M.P)

2. 2
Vitamins may be defined as organic compounds occurring in small quantities
in different natural foods and necessary for growth and maintenance of good
health In human beings and in other living organisms.
Vitamins are classified into Two types
I.Fat soluble vitamins
II.Water soluble vitamins
Comparison of Fat and Water soluble vitamins
Type Fat soluble vitamins Water soluble vitamins
Solubilit
y
Soluble in fat Soluble in water
Absorpti
on
Along with lipids Requires
bile salts and phospholipids
Absorption simple
Carrier
proteins
Present No Carrier protein required
StorageStored in liver No Storage Excretion in urine and
faeces
Deficien
cy
disorder
Manifests only when stores
are depleted
Manifests rapidly as there is no
storage
Toxicity Hypervitaminosis may
result
Unlikely, since excess is excreted
Major
vitamins
Vitamin - A,D, E and K Vitamin B complex group, e.g. B1,
B2, B3, B6, B12, Niacin etc. and
Vitamin - C

3. B Complex group of Vitamins
I.Thiamine (Vitamin B
1
)
II.Riboflavin (Vitamin B
2
) and FAD
III.Niacin, NAD
+
and NADP
+
IV.Pyridoxine (Vitamin B
6)
V.Pantothenic acid and Coenzyme A
VI.Biotin
VII.Folic acid
VIII.Vitamin B
12 (Cyanocobalamine)
IX.And Ascorbic acid (Vitamin - C) etc.

4. •Thiamine is synthesized by plants not synthesized by
human being. It is synthesized by intestinal bacterial
flora.
•Sources:
•Plant: Peas, Beans, cereals, nuts, yeast etc.
•Animal : Liver, Meat, egg, Milk, etc.
•Absorption and excretion:
•Free Thiamine is readily absorbed from small
intestine.
•Thiamine is excreted by urine faeces

Thiamine (Vitamin B
1
)

5. RDA (Recommended daily allowance)
•1 to 1.5 mg/day
•Requirement is increased in :-
»Pregnancy and lactation
»Beri – Beri
»Alcoholic Poly neuritis
»It is also Increased in old age

6. Metabolic role of Thiamine
•Coenzyme form of Thiamine is TPP
•This Coenzyme TPP is used in following biochemical reactions as a co factor / Co
enzyme
PDH
1. Pyruvate Acetyl CoA
TPP
Alfa -Oxoglutarate
degydrogenase
2. Alfa -Oxoglutarate Succinyl Co A
TPP
Transketolase
3. Ribose – 5-p + xylulose -5-p
TPP Sedoheptulose – 7-p +Glyceraldegyde–3-p

7. Deficiency manifestations (Disorder)
•Beriberi: Deficiency of thiamine leads to beriberi. The early
symptoms are anorexia and weakness.
•Wet Beriberi: Here cardiovascular manifestations are prominent.
Edema of legs, face, and serous cavities are the main features.
Death occurs due to heart failure.
•Dry Beriberi: in this condition, CNS manifestations are the major
features. Peripheral neuritis with sensory disturbance leads to
complete paralysis.
•Wernicke-Korsakoff’s syndrome: it is also called as cerebral
beriberi. Clinical features are those of encephalopathy plus
psychosis. It is seen only when the nutrition is severely affected.
•Polyneuritis: It is common in chronic alcoholics. Alcohol utilization
needs large doses of thiamine. Polyneuritis may also be associated
with pregnancy and old age.

8. Riboflavin (Vitamin B
2
)
•Riboflavin is synthesized by plants in man
considerable amount can be synthesized by
intestinal bacterial flora but is not adequate for
nutrition
•Source:
–Plant: Yeast, whole grains, dry beans peas, nuts,
green vegetables
–Animals: Liver, Kidney, milk, egg.
•Absorption & Excretion:
–Flavin nucleotides are readily absorbed in small
intestine. Free riboflavin undergoes phosphorylation,
a prequisite for absorption
–It is excreted in urine, & faeces

9. RDA (Recommended daily allowance)
•Adults -1.5 – 1.8 mg/day
•Pregnancy & lactation – 2 – 2.5mg/day
•Adolescence – 2.0 – 2.5 mg/day
•Requirement increases:
–Severe injury /burns
–Acute illness
–During oral broad spectrum antibiotic therapy.

10. Metabolic role of Riboflavin
•Riboflavin is converted to its active coenzyme forms
FMN & FAD with the help of ATP .
•During the oxidation process FAD accepts two hydrogen
atoms from substrate. in turn, FAD is reduced to FADH
2
•FAD-dependent enzymes:
Succinate dehydrogenase
1. Succinate Fumarate (TCA cycle )
Xanthine oxidase
2. Xanthine Uric Acid
PDH
3. Pyruvate Acetyl CoA

11. Deficiency manifestations (Disorder)
•Deficiency is usually associated with deficiencies
in other B-Vitamins
•Symptoms are confined to skin and mucous
membranes
I.Glossitis (Greek, glossa = tongue).
II.Magenta-colored tongue
III.Cheilosis (Greek, Cheilos = lip)
IV.Angular stomatitis (inflammation at the corners of
mouth).
V.Circumcorneal vascularization.

12. Niacin (Nicotinic acid / pellagra preventing factor
of Gold berger)
•Biosynthesis:
•Amino acid Tryptophan is a precursor of
Nicotinic acid in many plants, and animal
species including human beings. 60 mg of
tryptophan can give rise to 1 mg of niacin.
•It can be synthesized also by intestinal
bacteria.
•Absorption & Excretion:
•Nicotinic acid and its amide are absorbed from
small intestine.
•It is excreted in urine.

13. Source:
•Plant:- Legumes such as peas, beans, nuts,
coffee, tea, in germ in cereal grains, yeast
•Animals:- Liver, Kidney, Meat, Fish,
RDA:-
–Adult :- 17-21 mg /day
–Increased in:- Pregnancy and lactation
High corn /Maize diet
Injury / infection, acute illness.

14. Metabolic Role:
•The Coenzymes forms are Nicotinamide
adenine dinucleotide (NAD
+
) & Nicotinamide
adenine dinucleotide phosphate (NADP
+
)
•In oxidised form nitrogen of the nicotine amide
residue has a positive charge. Eg. NAD
+
•In reduction process
2H
NAD
+
NADH+H
+
Oxidised H+ reduced

15. •NAD dependent enzymes.
LDH
1.Lactate Pyruvate
PDH
2.Pyruvate Acetyl coA
Glyceraldehyde 3-P
3.Glyceraldehyde 3-P 1,3- bisophospho glycerate
dehydrogenase

16. •NADP depedent enzymes.
Phenylalanine hydroxylase
1.Phenylalanine Tyrosine
Met-Hb
2.Met hemoglobin hemoglobin
Reductase

17. Niacin Deficiency
•Dietary deficiency of Tryptophan: Pellagra is seen among people
whose staple diet is maize. Pellagra is also seen when staple diet is
sorghum as in Central and Western India. Sorghum, contains leucine in
high quantities. Leucine inhibits conversion of niacin to NAD
+
Niacin Deficiency leads to a disease called as Pellagra” \
(Pelle = skin ; agra = rough)
Cardinal features described as “3 D’s” are
Dermatitis :- skin becomes reddened, later brown, thickened and scaly.
Diarrhoea :- nausea, vomitting , abdominal pain, with alternating
constipation/diarrhoea.
Dementia :- headache, insomnia, depression and other mental
symptoms
•Lack of synthesis of vitamin B
6: 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.

18. •Isoniazid (INH): It is an anti-tuberculous
drug, which inhibits pyridoxal phosphate
formation. Hence there is block in
conversion of tryptophan to NAD
+
•Carcinoid syndrome: The tumor utilizes
major portion of availabel tryptophan for
synthesis of serotonin; so tryptophan is
unavailable.

19. Pyridoxine (Vit. B
6)
•Biosynthesis:-
Pyridoxine can formed by plants and
microorganism. In human beings
intestinal bacterial flora can synthesize
vitamin but is not adequate for nutrition.
•Absorption & Excretion:
Dietary vit B
6 is readily absorbed by the
intestinal bacterial flora.
It is excreted in urine.

20. Source:
•Plant:- Ricepolishings, Cereal grain,
Germinal portion of seeds, Yeast
•Animals:- Liver, Kidney, Egg yolk, Fish,
RDA:-
–Adult :- 1-2 mg/day
–Pregnancy and lactation:- 2.5mg/day

21. Metabolic role
•Pyridoxal phosphate is involved in protein metabolism
•PLP Depedent reaction
1.Transamination:-
Transaminase
Alanine+ keto glutarate Pyruvate +Glutamic acid
PLP
2.Decarboxylation:-
PLP
Histidine Histamine
3. Cysteine metabolism:-
Cystathionine synthase
Homocysteine + serine Cystathionine
PLP

22. 4. Production of Niacin:-
Tryptophan Niacin
PLP
5. Glycogenolysis:-
Phosphorylase
Glycogen Glucose – 1 – p
PLP
6. Heme synthesis

23. Pyridoxine Deficiency Manifestations
•Neurological: Neurological symptoms are common in B
6

deficiency in children, B
6 deficiency leads to convulsions due to
decreased formation of GABA. PLP is involved in the synthesis of
sphingolipids; so B
6 deficiency leads to demyelination of nerves
and consequent peripheral neuritis.
•Dermatological: Deficiency of B
6 will also affect tryptophan
metabolism. Since niacin is produced from tryptophan, B
6
deficiency in turn leads to niacin deficiency which is manifested
as pellagra.
•Hematological: Hypochromic microcytic anemia may occur due
to the inhibition of heme biosynthesis. Impaired antibody
formation is also reported.

24. Pantothenic acid
•pantos means everywhere
•Is composed of pantoic acid and beta alanine
•Biosynthesis:- It is formed by plants and
microorganisms.
•In human beings it is synthesized by intestinal
bacterial flora.
•Pantothenic acid and beta – mercapto ethanol
amine are part of co-enzyme A (CoA)
•Absorption and excretion :-
•It is excreted in urine

25. Source:
•Plant:- Sweet potatoes, Yeast.
•Animals:- Liver, Eggs.
RDA:-
–Adult :- 5-12 mg/day
–Increased in :-
–Pregnancy and lactation
–Oral antibiotic therapy for prolonged Period.
–Acute illness, Infection

26. Metabolic Role
•Pantothenic acid dependent reaction
PDH
1.Pyruvate + CoA + NAD Acetyl CoA+ NADH
2.Acetyl CoA + Choline Acetyl choline + CoA

27. Pantothenic acid Deficiency
•No serious disorder associated with its Deficiency
has been identified till date. This may be because of
its wide spread occurance in natural foods.
•Burning feet syndrome reported by Dr C Gopalan is
manifestation of pantothenic acid deficiency
characterized by numbness and tingling in hands and
feet , hyperactive deep tendon reflex and weekness
of extensor muscle associated with anaemia .

28. Biotin
•Biotin is a sulphur containing vitamin.
•Participates in carboxylation reactions.
•It plays an important role in gluconeogenesis and
fatty acid synthesis.
•Role in metabolism of odd chain AA and branched
chain AA .
•More popularly known as anti egg white injury
factor. Avidin a protein present in egg white has a
strong affinity for biotin.

29. Biotin
•It is found in :-
–Free form:- Biocytin, oxybiotin, besthiobiotin.
–Bound form.
•Biosynthesis:-
–It is synthesis by bacteria, yeast, fungi and plants.
–In human beings normal bacterial flora of gut
provide adequate amount of biotin.
•Absorption and excretion :-
–It is absorbed by small intestine and stored in liver
and kidney.
–It is excreted in urine faeces and milk.

30. Source:
•Plant:- Soyabean, peanut, Yeast.
•Animals:- Liver, Egg yolk.
RDA:-
–Adult :- 200-300 µ gm/day
–Increased in :- Pregnancy and lactation
Oral antibiotic therapy For
prolong period

31. Metabolic Role
•Biotin is prosthetic group of certain enzymes.
1.In Co
2 fixation reaction:-
Acetyl CoA carboxylase
1. Acetyl CoA Malonyl CoA
Pyruvate carboxylase
2. Pyruvic acid
Oxaloacetate
2.Leucine metabolism:-
β methyl crotonyl
β methyl crotonyl CoA β methyl gluta conyl CoA
CoA Carboxylase

32. Biotin Deficiency Manifestations
•Biotin Deficiency may be due to.
•Inclusion of large amounts of raw egg white in the diet
•By using sulphonamide drugs or broad spectrum oral antibiotic for
prolong period
•Biotin deficiency features are
•Dermatitis
•“Spectacle – eyed” appearance
•Circumocular alopecia
•Thinning of hairs
•Pallor of skin and mucous membrane
•Anorexia and nausea
•Muscle pains
•Depression