Paraquat (methyl viologen) produces its primary pulmonary toxicity through which mechanism?
- A Direct alkylation of alveolar type II cell DNA causing irreversible apoptosis
- B Redox cycling generating superoxide anion radicals that destroy alveolar membranes ✓
- C Competitive inhibition of surfactant phospholipid synthesis by type II pneumocytes
- D Depletion of glutathione in Clara cells leading to oxidative lipid peroxidation
Explanation
Paraquat is selectively concentrated in lung tissue via the polyamine uptake system in type II alveolar cells. It undergoes redox cycling — accepting an electron from NADPH via NADPH-cytochrome P450 reductase to form a paraquat radical cation, which then donates the electron to oxygen generating superoxide radical (O2•−). This superoxide is converted to hydrogen peroxide and hydroxyl radical (via Fenton reaction), causing lipid peroxidation of alveolar membranes, progressive fibrosis, and 'wet lung' destruction. This cyclic process continues as long as paraquat is present, depleting NADPH.
Reference: The Essentials of Forensic Medicine and Toxicology (Narayan Reddy), 34th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.