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Folic Acid
- indication:For treatment of folic acid deficiency, megaloblastic anemia and in anemias of nutritional supplements, pregnancy, infancy, or childhood.
- pharmacologypharmacology:
- mechanism: Folic acid, as it is biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by dihydrofolate reductase. These folic acid congeners are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids, methylate tRNA, and generate and use formate. Using vitamin B12 as a cofactor, folic acid can normalize high homocysteine levels by remethylation of homocysteine to methionine via methionine synthetase.
- toxicity: IPR-MUS LD<sub>50</sub> 85 mg/kg,IVN-GPG LD<sub>50</sub> 120 mg/kg, IVN-MUS LD<sub>50</sub> 239 mg/kg, IVN-RAT LD<sub>50</sub> 500 mg/kg, IVN-RBT LD<sub>50</sub> 410 mg/kg
- absorprion:
- halflife:
- roouteelimination: Folic Acid is metabolized in the liver to 7, 8-dihydrofolic acid and eventually to 5,6,7,8-tetrahydrofolic acid with the aid of reduced diphosphopyridine nucleotide (DPNH) and folate reductases. A majority of the metabolic products appeared in the urine after 6 hours; excretion was generally complete within 24 hours. Folic Acid is also excreted in the milk of lactating mothers.
- volumedistribution:
- clearance: