FOLIC ACID DEFICIENCY. THE MECHANISM OF THE BACTERIOSTATIC ACTION OF SULFONAMIDE DRUGS

Folic acid (vitamin B9) is an essential water-soluble vitamin involved in DNA synthesis, cell division, and amino acid metabolism. Deficiency of folic acid leads to impaired nucleotide synthesis, resulting in megaloblastic anemia, weakened immune response, and developmental abnormalities. Rapidly dividing tissues, such as bone marrow and epithelial cells, are particularly sensitive to folate deficiency. Biochemically, insufficient tetrahydrofolate disrupts purine and thymidylate synthesis, leading to defective DNA replication and cell cycle arrest [1,2]. Sulfonamide drugs exert a bacteriostatic effect by interfering with bacterial folic acid synthesis. These agents are structural analogs of para-aminobenzoic acid (PABA) and competitively inhibit the enzyme dihydropteroate synthase, thereby blocking the formation of dihydrofolic acid in microorganisms. Since bacteria synthesize folate de novo, inhibition of this pathway prevents DNA synthesis and bacterial proliferation. In contrast, human cells obtain folic acid from dietary sources, which explains the selective toxicity of sulfonamides [3,4]. Understanding the biochemical basis of folic acid metabolism and the mechanism of action of sulfonamides is essential for rational antimicrobial therapy and prevention of drug resistance.

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