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Metabolism of folic acid

 
, medical expert
Last reviewed: 04.07.2025
 
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Folic acid is important for normal hematopoiesis. Its deficiency disrupts erythropoiesis, granulopoiesis, and thrombopoiesis.

Folic acid enters the child's body with food. Folates are most abundant in beef and chicken liver, lettuce, spinach, tomatoes, asparagus, meat, yeast; human and cow's milk contain 6 times more folates than goat's milk. The daily requirement for folic acid is 20-50 mcg, which is equivalent to 100-200 mcg of dietary folates. Folates are absorbed in the duodenum and in the proximal jejunum. In the cell, folate is reduced to 5-methyltetrahydrofolate by the action of dihydrofolate reductase, which binds to various proteins in the blood plasma (a 2 -macroglobulin, albumin, transferrin, a specific protein - a folate carrier); 5-Methyltetrahydrofolate donates a methyl group to cobalamin during the formation of methionine from cysteine. Folate compounds also play an important role in DNA synthesis, donating one carbon atom in the conversion of deoxyuridine to deoxythymidine. Tetrahydrofolate undergoes polyglutamination; this mechanism apparently ensures the retention of folate in the cell. Most folates are transported to the liver, where they are deposited as polyglutamates or activated into one of the active cofactors. Folates are also transported to bone marrow cells, since they are necessary for their proliferation. The accumulation of folates in the cell is a vitamin B 12 -dependent process. Cobalamin deficiency leads to a blockade of folate metabolism at the stage of methyltetrahydrofolate formation, as a result of which folate is spent on the synthesis of deoxyuridine; polyglutamination occurs less efficiently, causing folate to leak out of the cell. A small amount of folate - about 10 ng per day - is excreted in the urine. The total folate content in the body is 5-10 mg, half of which is found in the liver.

Pathogenesis of folate deficiency

Folate deficiency in a child can occur relatively easily, since the daily folate intake is high and the intake of resorbable folates with food is limited. Folate reserves in the body are small. Megaloblastic anemia develops with folate deficiency after 16-133 days. With a diet without folate, there is a rapid and significant decrease in the concentration of folate in the blood serum. However, the concentration in erythrocytes at this point may still be normal and decrease only later, so to detect partial deficiency, it is necessary to determine its concentration in erythrocytes.

Folate deficiency results in decreased formation of 5,10-methylenetetrahydrofolic acid, which is necessary for the synthesis of purine precursors of nucleic acids, resulting in impaired DNA synthesis.

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