Amphotericin B is fungicidal due to its mechanism of forming membrane pores. The specific interaction enabling this is:

• A Covalent binding to ergosterol in the fungal cell membrane, forming barrel-shaped ion channels
• B Competitive displacement of cholesterol from lipid rafts, disrupting signal transduction
• C Inhibition of squalene epoxidase, depleting ergosterol and causing membrane instability
• D Aggregation with ergosterol to form amphotericin-ergosterol complexes that insert as aqueous pores, allowing ion leakage ✓

Explanation

Amphotericin B has a hydrophilic polyol side and a hydrophobic polyene region. Multiple molecules insert into fungal membranes rich in ergosterol, aggregating to form transmembrane pores (channels) that allow leakage of monovalent cations (K+, Na+) and protons, leading to loss of membrane potential and cell death. Its selective toxicity for fungi over mammalian cells relates to its higher affinity for ergosterol than cholesterol, though residual interaction with cholesterol causes nephrotoxicity.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.