Cyanide poisoning causes cellular hypoxia. Unlike carbon monoxide, cyanide does NOT bind haemoglobin. The mechanism of cyanide toxicity at the cellular level is:

• A Competitive inhibition of haemoglobin oxygen binding
• B Inhibition of cytochrome c oxidase (Complex IV), blocking electron transfer to oxygen ✓
• C Inhibition of NADH dehydrogenase (Complex I) of the electron transport chain
• D Uncoupling of oxidative phosphorylation by dissipating the proton gradient

Explanation

Cyanide (CN⁻) irreversibly inhibits cytochrome c oxidase (complex IV of the mitochondrial electron transport chain) by binding to the ferric (Fe³⁺) iron of the haem-a₃ site. This blocks electron transfer to molecular oxygen (the final acceptor), halting the ETC and ATP synthesis. Tissues cannot utilise oxygen despite normal delivery — producing "histotoxic hypoxia" with paradoxically high venous PO₂ and cherry-red coloration. Antidotes include sodium thiosulphate (donates sulphur to convert CN⁻ to thiocyanate via rhodanese) and dicobalt edetate (chelates CN⁻). 2,4-dinitrophenol is the classic uncoupler of oxidative phosphorylation.

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.