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Pharmacology: Pharmacodynamics: Folic acid (pteroylglutamic acid) in its reduced form of tetrahydrofolate serves as an important mediator in many reactions involving one-carbon transfers. Important reaction involves the conversion of homocysteine to methionine and of deoxyuridylate to thymidylate, an important step in DNA synthesis. It is also implicated in the conversion of some amino acids, and in the synthesis and utilization of formate. The deficiency of folic acid can lead to megaloblastic anemia, which develops when dietary intake of folic acid is inadequate, such as megaloblastic changes in the bone marrow of several infants with severe diarrhea, malnutrition and other infections; low birth weight and elevated homocysteine level in conditions such as in infants and children with chronic renal failure and heart disease; in reducing the prevalence and severity of neural tube defects in preconception and periconception.
Pharmacokinetics: It is rapidly absorbed from the gastrointestinal tract, mainly from the duodenum and jejunum. Dietary folates have about half the bioavailability of crystalline folic acid. Naturally occurring folate polyglutamates are largely deconjugated and reduced by dihydrofolate reductase in the intestines to form 5-methyltetrahydrofolate which appears in the portal circulation, where it is extensively bound to plasma proteins. Folic Acid administered therapeutically enters the portal circulation largely unchanged since it is a poor substrate for reduction by dihydrofolate reductase. It is converted to 5-methyltetrahydrofolate in the plasma and liver. Folate undergoes enterohepatic circulation. Folate metabolites are eliminated in the urine and folate in excess of body requirements is excreted unchanged in the urine. Folate is distributed into breast milk. Folic acid is removed through haemodialysis.
