Clofazimine, used in multidrug regimens for leprosy and MDR-TB, exerts its antimycobacterial effect through which primary mechanism?
- A Binding to single-stranded mycobacterial DNA, inhibiting transcription
- B Generating reactive oxygen species (superoxide) via redox cycling and also inhibiting mycobacterial potassium channels ✓
- C Competitive inhibition of dihydropteroate synthase preventing folate synthesis
- D Blocking arabinosyl transferase (EmbB) enzyme in arabinogalactan synthesis
Explanation
Clofazimine's antimycobacterial activity involves two complementary mechanisms: it intercalates into mycobacterial DNA (causing inhibition), and more importantly, the iron-clofazimine complex participates in redox cycling that generates reactive oxygen species (particularly superoxide and hydrogen peroxide), oxidatively damaging the organism. Additionally, clofazimine disrupts mycobacterial potassium ion transport, acidifying the cell. The combination of ROS generation and membrane disruption accounts for its bactericidal activity against Mycobacterium leprae and its usefulness in MDR-TB.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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