Metabolism of folic acid
Last reviewed: 23.04.2024
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Folic acid is important for the normal process of hematopoiesis. With its deficiency, erythro-, granulo- and thrombocytopoiesis are disrupted.
In the child's body, folic acid comes with food. Folate most rich in beef and chicken liver, lettuce, spinach, tomatoes, asparagus, meat, yeast; in female and cow's milk, folate is 6 times more than in goat's milk. The daily requirement for folic acid is 20-50 μg, which is equivalent to 100-200 μg of food folate. Absorption of folate occurs in the duodenum and in the proximal parts of the jejunum. In the cell, folate under the action of dihydrofolate reductase is reduced to 5-methyltetrahydrofolate, which binds to various proteins in the blood plasma (a 2- macroglobulin, albumin, transferrin, a specific folate-carrying protein); 5-methyltetrahydrofolate gives a methyl group to cobalamin during the formation of methionine from cysteine. Compounds of folic acid also play an important role in the synthesis of DNA, being donors of one carbon atom in the conversion of deoxyuridine to deoxythymidine. Tetrahydrofolate is subjected to polyglutamine treatment; apparently, this mechanism ensures the preservation of folic acid in the cell. Most of the folates are transported to the liver, where it is deposited in the form of polyglutamates, or is activated in one of the active cofactors. Folates are also transported to bone marrow cells, as they are necessary for their proliferation. The accumulation of folates in the cell is a vitamin B 12- dependent process. Deficiency of cobalamin leads to blockade of folate metabolism at the stage of formation of methyltetrahydrofolate, as a result of which folate is consumed for the synthesis of deoxyuridine; while polyglutamination is less effective, which causes folic acid to leak out of the cell. A small amount of folate - about 10 ng per day - is excreted in the urine. The total amount of folate in the body is 5-10 mg, half is in the liver.
Pathogenesis of Folic Acid Deficiency
Folate deficiency in a child can be relatively easy, since the daily intake of folate is high, and the intake of resorptable folate with food is limited. Reserves of folate in the body are small. Megaloblastic anemia develops with a deficiency of folic acid after 16-133 days. With a diet without folic acid, there is a rapid and significant decrease in the concentration of folic acid in the blood serum. However, the concentration in erythrocytes at the moment can be still normal and decrease only later, therefore, in order to detect a partial deficit, it is necessary to determine its concentration in erythrocytes.
Lack of folate leads to a decrease in the formation of 5,10-methylenetetrahydrofolic acid, necessary for the synthesis of purine nucleic acid precursors, as a result of which DNA synthesis is disrupted.
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