Fluoroquinolone mechanism of action: Ciprofloxacin and norfloxacin interfere with bacterial replication by acting on which critical function?

Introduction / Context:
Ciprofloxacin and norfloxacin are prototype fluoroquinolones. Their target explains both spectrum and the rapid bactericidal activity observed in clinical use.

Given Data / Assumptions:

• We must specify the cellular function inhibited by these drugs.
• Candidates include wall, membrane, DNA, and protein synthesis.

Concept / Approach:
Fluoroquinolones inhibit bacterial type II topoisomerases: DNA gyrase (primarily in Gram-negatives) and topoisomerase IV (often in Gram-positives). This prevents DNA supercoiling management and chromosome segregation, causing double-strand DNA breaks and cell death.

Step-by-Step Solution:
Identify drug class: fluoroquinolones (ciprofloxacin, norfloxacin). Recall target enzymes: DNA gyrase and topoisomerase IV. Connect inhibition to impaired DNA replication and transcription. Select DNA function as the correct target.

Verification / Alternative check:
Resistance mutations commonly occur in gyrA/gyrB or parC/parE genes encoding the topoisomerases, confirming the drug target.

Why Other Options Are Wrong:

• Cell wall synthesis: targeted by beta-lactams/glycopeptides.
• Cell membrane function: disrupted by polymyxins and daptomycin (in Gram-positives).
• Protein synthesis: target of macrolides, tetracyclines, aminoglycosides, etc.

Common Pitfalls:
Mixing up aminoglycosides (protein synthesis inhibitors) with fluoroquinolones; both are bactericidal but via different pathways.

Final Answer:
DNA function (DNA gyrase / topoisomerase)