Question:
The fluoroquinolones act by:
The fluoroquinolones act by:
Updated On: Jul 14, 2026
- Inhibiting folic acid synthesis, reducing nucleotide production and DNA synthesis
- Inhibiting DNA gyrase and topoisomerase IV, causing supercoiling and fragmentation of bacterial DNA
- Disrupting peptidoglycan cross-linking, weakening the bacterial cell wall
- Inhibiting ribosomal subunits, leading to the cessation of protein synthesis
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The Correct Option is B
Approach Solution - 1
The correct option is (B): Inhibiting DNA gyrase and topoisomerase IV, causing supercoiling and fragmentation of bacterial DNA.
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Approach Solution -2
The question asks about the mechanism of action of the fluoroquinolone class of antibiotics. Let's check each proposed mechanism against how fluoroquinolones actually work.
- Inhibiting folic acid synthesis, reducing nucleotide production and DNA synthesis: This describes the mechanism of sulfonamides and trimethoprim, which block enzymes in the folate pathway. Fluoroquinolones have a completely different target.
- Inhibiting DNA gyrase and topoisomerase IV, causing supercoiling and fragmentation of bacterial DNA: Fluoroquinolones bind to and inhibit bacterial DNA gyrase (topoisomerase II) and topoisomerase IV, enzymes needed to relax and unwind supercoiled DNA during replication. Blocking them traps the DNA in a state that leads to double-strand breaks and cell death. This is exactly how this drug class acts.
- Disrupting peptidoglycan cross-linking, weakening the bacterial cell wall: This is the mechanism of beta-lactam antibiotics such as penicillins and cephalosporins, which act on the cell wall, not the DNA replication machinery targeted by fluoroquinolones.
- Inhibiting ribosomal subunits, leading to the cessation of protein synthesis: This describes antibiotics like aminoglycosides, macrolides and tetracyclines, which act on the bacterial ribosome. Fluoroquinolones do not target the ribosome at all.
Fluoroquinolones are unique among these options in acting on the bacterial enzymes that control DNA supercoiling, rather than the cell wall, ribosome, or folate pathway.
Therefore, the correct answer is inhibiting DNA gyrase and topoisomerase IV, causing supercoiling and fragmentation of bacterial DNA.
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