Mechanism of action — Amphotericin B (a polyene antifungal) and polymyxins (polypeptide antibiotics) primarily interfere with which critical cellular function?

Introduction / Context:
Understanding mechanisms of action helps predict spectrum, toxicity, and resistance. Amphotericin B and polymyxins both target membranes, albeit in different organisms and by distinct biochemical interactions.

Given Data / Assumptions:

• Amphotericin B binds ergosterol in fungal membranes, forming pores.
• Polymyxins (e.g., colistin) bind lipid A and phospholipids in Gram-negative outer membranes, disrupting membrane integrity.
• Other targets (cell wall, protein synthesis, DNA) are not the primary actions for these agents.

Concept / Approach:
Match each drug class to its canonical target. Both drugs compromise membrane structure and permeability, leading to leakage of essential intracellular contents and rapid cell death or fungistatic effects depending on concentration and organism.

Step-by-Step Solution:

Verification / Alternative check:
Adverse effects (e.g., nephrotoxicity for amphotericin B and polymyxins) correlate with membrane interactions in host tissues, reinforcing the membrane-targeting mechanism.

Why Other Options Are Wrong:

• Cell wall synthesis: targeted by β-lactams, glycopeptides.
• Protein synthesis: targeted by aminoglycosides, macrolides, tetracyclines.
• DNA function: targeted by fluoroquinolones, metronidazole.

Common Pitfalls:
Confusing amphotericin B with azoles; azoles inhibit ergosterol synthesis, whereas amphotericin B binds existing ergosterol.

Final Answer:
cell membrane function