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FOLIC ACID & VITAMIN B12
By-
AMRITA (11)
ANAND(12)
APOORVA(13)
ARMAN(14)
ARSH(15)
Folic acid
INTRODUCTION
• Folium (leaf)
• OCCURRENCE – found in green leafy vegetables
• Animals are unable to synthesize folic acid therefore
required in diet
Structure
• Folic acid consists of three components-
• PABA
• PTERIDINE RING
• GLUTAMIC ACID
•
ACTIVE FORM
• Biologically active form of folic acid is
tetrahydrofolate(TH4 OR FH4)
• It is synthesized fom folic acid in two steps-
a.) reduction of folate in liver by folate reductase
b.) reduction by dihydrofolate reductase
Both these steps are vit c and NADPH dependent
Synthesis of tetrahydrofolate
• Folic acid 7,8 dihydrofolate
5,6,7,8 tetrahydrofolate
Dihydrofolat
e reductase
Folate
reductase
Sources of folic acid
• Rich sources –
Green leafy vegetables
Whole grain
Cereals
Liver ,kidney
Yeast
Egg
MILK IS A POOR
SOURCE OF FOLIC ACID
Dietary requirements ( µgm/day)
Adults
300-400
Adults
300-400
Children
100-300
Children
100-300
Pregnancy
800
Pregnancy
800
Lactation
600
Lactation
600
Absorption , transport & storage
Lumen
diet
muscle cell
Folyl glutamate
Mono glutamate
tetrahydrofolate
methyl
tetrahydofolate
Liver
Folylpolygutamate
tetrahrydrofolate
Methy
tetrahydofolate
circulation
• Inside the cell – found as polyglutamate(potent form)
• Stored in liver - found as polyglutamate to some extent
• Absorbed from intestiune – as monoglutamate
• Transported in blood –as methyl tetrahydrofolate
• in plants, folic acid is found as polyglutamate
functions
• Tetrahydrofolate which is a conenyme of folic acid is
involved in transfer and utilization of 1C group in many
enzymatic reactions
• 1C binds with TH4 at position N5 or N10 or both
Various r groups and TH4 1C DERIVATIVE FORMS
R GROUP TH4 DEIVATIVES
Methyl N5 methyl TH4
methyelene N5,N10 methylene TH4
methenyl N5,m10 methenyl TH4
formyl N5 formyl TH4
formate N10 faormate TH4
formino N5 formino TH4
1C metabolism
• Sources` 1C group carrier of 1C product formed
• formate N10 formyl TH4 purine C2
• formyl methionine
• formino N5N10 methenyl TH4 purine C8
• methylene N5N10 methylene TH4 serine
• dTMP
• methyl N5 methyl TH4 homocystein
Glycine
tryptophan
Histidine
figlu
serine
Choline
betain
Structural analogs
• AMINOPTERIN , AMETHPTERINE
called as methotrexate are structural
analogs of folic acid
• Function-they compitetively
inhibit the enzyme
• dihydrofolate reductase
• synthesis of purines,thymine and
hence DNA is impaired along with
decreased cell division.
• SULPHONAMIDES are structural
analoges of PABA
• Several microorganisms do not
require foloate from outside .they can
synthesize folate as long as PABA is
available in the medium
• Sulphonamides resemble PABA in
microrganisms so inhibit folic acid
synthesis by inhibiting the
incorporation of PABA in the pteridine
rind thus inhibiting the enzyme
• dihydropteridine synthesis
Defeciency
symptoms
• Symtoms-
• Growth and retardation
• Weakness
• Lethargy
• Infertility
Clinical conditions-
• Nutritional macrocytic anemia
• Megaloblastic anemia of pregnancy
• Megaloblastic anemia of infancy
• Macrocytic anemia in liver disease
Causes-
 Poor
absorption
• Inadequate
dietary intake
• Increased
demands as
in pregnancy
& lactation
• Adminstration
of folic acid
antagonists
FOLATE
DEFECIENCY
Macrocytic anemia
• Due to folic acid defeciency,thymine is not formed
.DNA synthesis is delayed but protein synthesis
continue to occur .thus Hb accumulates in RBC
precursors .cell size increases and there is an
increased dissociation of RBCs
FIGLU TEST
OBJECTIVE-
DETECT FOLIC
ACID DEFECIENCY
Generally histidine
metabolizes to figlu
which changes to
glutamate.
In folic acid
defeciency glu not
formed and FIGLU
excreted in urine
FIGLU excretion is
an index of folate
defeciency
Folic acid
therapy
Therapeutic dose of folic
acid is 1 mgm/day
It should not be given
alone to macrocytic
anemia patients .
It is commonly given
with VIT B12
hyperhomo
cystinemia
Folic acid def causes
incresase homoecystein
levels in blood.
Plasma homcystein
level > 15 micromol/L
Cause increased risk of
CORONARY HEART
DISEASE
Spine bifid
If the defeciency of folic
acid occurs in
pregnancy and no
supplements are given it
results in SPINE BIFIDA
in foetus
CANCER AND FOLIC ACID
Folic acid supplements are never given to a cancer
patients since folic acid helps in the synthesis of purine
ring and thymine thud DNA synthesis so abnormal cell
division occurs which increases the risk of cancer

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Folic Acid & Vitamin B12: Functions, Deficiency, Sources

  • 1. FOLIC ACID & VITAMIN B12 By- AMRITA (11) ANAND(12) APOORVA(13) ARMAN(14) ARSH(15)
  • 2.
  • 4. INTRODUCTION • Folium (leaf) • OCCURRENCE – found in green leafy vegetables • Animals are unable to synthesize folic acid therefore required in diet
  • 5. Structure • Folic acid consists of three components- • PABA • PTERIDINE RING • GLUTAMIC ACID •
  • 6. ACTIVE FORM • Biologically active form of folic acid is tetrahydrofolate(TH4 OR FH4) • It is synthesized fom folic acid in two steps- a.) reduction of folate in liver by folate reductase b.) reduction by dihydrofolate reductase Both these steps are vit c and NADPH dependent
  • 7. Synthesis of tetrahydrofolate • Folic acid 7,8 dihydrofolate 5,6,7,8 tetrahydrofolate Dihydrofolat e reductase Folate reductase
  • 8. Sources of folic acid • Rich sources – Green leafy vegetables Whole grain Cereals Liver ,kidney Yeast Egg MILK IS A POOR SOURCE OF FOLIC ACID
  • 9.
  • 10. Dietary requirements ( µgm/day) Adults 300-400 Adults 300-400 Children 100-300 Children 100-300 Pregnancy 800 Pregnancy 800 Lactation 600 Lactation 600
  • 11. Absorption , transport & storage Lumen diet muscle cell Folyl glutamate Mono glutamate tetrahydrofolate methyl tetrahydofolate Liver Folylpolygutamate tetrahrydrofolate Methy tetrahydofolate circulation
  • 12. • Inside the cell – found as polyglutamate(potent form) • Stored in liver - found as polyglutamate to some extent • Absorbed from intestiune – as monoglutamate • Transported in blood –as methyl tetrahydrofolate • in plants, folic acid is found as polyglutamate
  • 13. functions • Tetrahydrofolate which is a conenyme of folic acid is involved in transfer and utilization of 1C group in many enzymatic reactions • 1C binds with TH4 at position N5 or N10 or both Various r groups and TH4 1C DERIVATIVE FORMS R GROUP TH4 DEIVATIVES Methyl N5 methyl TH4 methyelene N5,N10 methylene TH4 methenyl N5,m10 methenyl TH4 formyl N5 formyl TH4 formate N10 faormate TH4 formino N5 formino TH4
  • 14. 1C metabolism • Sources` 1C group carrier of 1C product formed • formate N10 formyl TH4 purine C2 • formyl methionine • formino N5N10 methenyl TH4 purine C8 • methylene N5N10 methylene TH4 serine • dTMP • methyl N5 methyl TH4 homocystein Glycine tryptophan Histidine figlu serine Choline betain
  • 15. Structural analogs • AMINOPTERIN , AMETHPTERINE called as methotrexate are structural analogs of folic acid • Function-they compitetively inhibit the enzyme • dihydrofolate reductase • synthesis of purines,thymine and hence DNA is impaired along with decreased cell division. • SULPHONAMIDES are structural analoges of PABA • Several microorganisms do not require foloate from outside .they can synthesize folate as long as PABA is available in the medium • Sulphonamides resemble PABA in microrganisms so inhibit folic acid synthesis by inhibiting the incorporation of PABA in the pteridine rind thus inhibiting the enzyme • dihydropteridine synthesis
  • 16. Defeciency symptoms • Symtoms- • Growth and retardation • Weakness • Lethargy • Infertility Clinical conditions- • Nutritional macrocytic anemia • Megaloblastic anemia of pregnancy • Megaloblastic anemia of infancy • Macrocytic anemia in liver disease Causes-  Poor absorption • Inadequate dietary intake • Increased demands as in pregnancy & lactation • Adminstration of folic acid antagonists
  • 18. Macrocytic anemia • Due to folic acid defeciency,thymine is not formed .DNA synthesis is delayed but protein synthesis continue to occur .thus Hb accumulates in RBC precursors .cell size increases and there is an increased dissociation of RBCs
  • 19. FIGLU TEST OBJECTIVE- DETECT FOLIC ACID DEFECIENCY Generally histidine metabolizes to figlu which changes to glutamate. In folic acid defeciency glu not formed and FIGLU excreted in urine FIGLU excretion is an index of folate defeciency
  • 20. Folic acid therapy Therapeutic dose of folic acid is 1 mgm/day It should not be given alone to macrocytic anemia patients . It is commonly given with VIT B12
  • 21. hyperhomo cystinemia Folic acid def causes incresase homoecystein levels in blood. Plasma homcystein level > 15 micromol/L Cause increased risk of CORONARY HEART DISEASE
  • 22. Spine bifid If the defeciency of folic acid occurs in pregnancy and no supplements are given it results in SPINE BIFIDA in foetus
  • 23. CANCER AND FOLIC ACID Folic acid supplements are never given to a cancer patients since folic acid helps in the synthesis of purine ring and thymine thud DNA synthesis so abnormal cell division occurs which increases the risk of cancer