Amphotericin B exerts its antifungal effect by a mechanism distinct from azoles. It acts by:
- A Inhibiting fungal lanosterol 14α-demethylase (CYP51), preventing ergosterol synthesis
- B Inhibiting β-1,3-glucan synthase, disrupting fungal cell wall integrity
- C Binding directly to ergosterol in the fungal cell membrane, forming transmembrane ion channels (pores) that disrupt membrane permeability and osmotic stability ✓
- D Blocking fungal dihydroorotase, inhibiting pyrimidine synthesis
Correct answer: C. Binding directly to ergosterol in the fungal cell membrane, forming transmembrane ion channels (pores) that disrupt membrane permeability and osmotic stability
Explanation
Amphotericin B is a polyene macrolide that binds with high affinity to ergosterol (the principal sterol in fungal membranes) and forms barrel-like oligomeric pores in the membrane, allowing leak of monovalent and divalent ions (K+, Mg2+, H+) down electrochemical gradients, disrupting membrane potential and killing the organism. Azoles (fluconazole, voriconazole) inhibit lanosterol 14α-demethylase. Echinocandins (caspofungin) inhibit β-1,3-glucan synthase. Flucytosine (not amphotericin B) is converted to 5-fluorouracil, disrupting pyrimidine metabolism.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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