In organophosphate poisoning, pralidoxime (PAM) reactivates acetylcholinesterase by:
- A Nucleophilic attack on the phosphorylated serine of AChE, regenerating the active site ✓
- B Binding the carbamate ester linkage and restoring enzyme conformation
- C Displacing organophosphate from the anionic site before aging occurs
- D Competitive inhibition of cholinesterase at the nicotinic receptor
Explanation
PAM (2-pyridine aldoxime methiodide) is an oxime whose nucleophilic oxygen attacks the phosphorus atom on the phosphorylated serine of AChE, displacing the organophosphate moiety and regenerating free active enzyme. This mechanism requires the bond to be 'un-aged' (non-oxidised); aging renders PAM ineffective. It acts primarily at nicotinic (NMJ) sites and has less effect on muscarinic symptoms.
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.