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
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
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