2. INTRODUCTION
• Folic acid or folacin (Latin :folium-leaf) is abundantly foundin green leafy
vegetables.
• It is important for one carbon the metabolism and is required for the
synthesis of certain amino acids purines and the pyrimidine-thymine.
3. CHEMISTRY
• Folic acid consists of three components–
pteridine ring, p-amino benzoic acid (PABA) and
glutamic acid (1 to 7 residues).
• Folic acid mostly has one glutamic acid residue and is known as pteroyl-glutamic acid
(PGA)
• The active form of folic acid is tetrahydrofolate (THF or FH4). It is synthesized
from folic acid by the enzyme dihydrofolate reductase.
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5. RECOMMENDED DIETARY TO ALLOWANCE (RDA)
• The daily requirement of folic acid is around 200 microgram/day
• pregnancy (400 microgram/day)
• lactation (300 microgram/day).
6. DIETARY SOURCES
• The rich sources are green leafy vegetables, whole grains, cereals, liver,
kidney, yeast and eggs.
• Milk is rather a poor source of folic acid.
• Folic acid is not synthesized in human body and supplied through the
diet.
7. BIOCHEMICAL FUNCTIONS
• Tetrahydrofolate (THF or FH4), the coenzyme of folic acid, is actively involved in the
one carbon metabolism.
• Many important compounds are synthesized in one carbon metabolism.
1. Purines (carbon 2, 8) which are incorporated into DNA and RNA.
2.Glycine, serine, ethanolamine and choline are produced.
3.Tetrahydrofolate is mostly trapped as N5-methyl THF in which form it is present in
thecirculation.Vitamin B12 is needed for the conversion of N5-methyl THF to THF, in a
reaction wherein homocysteine is converted to methionine.
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11. DEFICIENCY SYMPTOMS
• Folic acid deficiency is probably the most common vitamin deficiency,
observed primarily in the pregnant women, in both developed
(including USA) anddeveloping countries (including India).
• The folic acid deficiency may be due to (one or more causes)
inadequate dietaryintake, defective absorption, use of anticonvulsant
drugs (phenobarbitone, dilantin,phenyltoin), and increased demand.
12. • In folic acid deficiency, decreased production of purines and dTMP is observed which
impairs DNA synthesis.
• Due to a block in DNA synthesis, the maturation of erythrocytes is slowed down
leading to macrocytic RBC. The rapidly dividing cells of bone marrow are seriously
affected.
• The macrocytic anemia (abnormally large RBC) associated with megaloblastic changes
in bone marrow is a characteristic feature of folate deficiency.
• In case of folic acid deficiency, FIGLU (Formiminoglutamate)accumulates and is
excreted in urine.
13. FOLIC ACID ANTAGONISTS
• Aminopterin and amethopterin (also called as methotrexate) are structural
analogues of folicacid.
• Aminopterin and methotrexate are successfully used in the treatment of many
cancers, including leukemia.
• Trimethoprim (a component of the drug septran or bactrim) and
pyrimethamine (antimalarial drug) are structurally related to folic acid. They
inhibit dihydrofolate reductase, and the formation of THF.
• Trimethoprim is used to treat bacterial infections of sore throat, urinary tract,
gastrointestinal tract etc