Carbon monoxide (CO) produces its cellular toxicity through all the following mechanisms EXCEPT:
- A Binds haemoglobin with 200–250 times greater affinity than oxygen, forming carboxyhaemoglobin
- B Causes a left shift of the oxyhaemoglobin dissociation curve reducing oxygen delivery
- C Activates NMDA receptors causing immediate excitotoxic neuronal death ✓
- D Directly inhibits cytochrome c oxidase (complex IV) of the mitochondrial electron transport chain
Explanation
Carbon monoxide toxicity operates via multiple mechanisms: (1) high affinity binding to haemoglobin forming carboxyhaemoglobin (HbCO) — 200–250× higher affinity than O2; (2) left-shifting the oxyhaemoglobin dissociation curve (Haldane effect) reducing tissue oxygen delivery; (3) direct binding to and inhibition of cytochrome c oxidase impairing cellular respiration. CO does NOT primarily activate NMDA receptors acutely — delayed neurological syndrome post-CO exposure may involve inflammatory and oxidative mechanisms but NMDA receptor direct activation is not a primary CO toxicity mechanism. Cyanide is the classic cytochrome oxidase inhibitor, but CO also shares this property.
Reference: The Essentials of Forensic Medicine and Toxicology (Narayan Reddy), 34th ed.
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Written and medically reviewed by the StethoPrep medical team.