Answer:
Several studies have shown that persons admitted to hospital due to fire accidents may have been carbon monoxide as well as cyanide. In fact the most common source of CN poisoning in humans arise from fire exposures.In fires CN is developed when the temperature reaches 315 degree and is released from the toxic fumes in the gaseous form.HCN is developed from an incomplete combustion of nitrogen containing materials such as silk, plastic etc. HCN is still produced when the fire is producing embers. HCN is easily absorbed from all the routes of exposure. Since CN is a small lipid molecule which is mainly undissociated but penetration in cells could be rapid. CN distribution in the body within seconds and death can occur within minutes.Symptoms include a brief period of hyperpnoea, sensation of dryness & burning in nose & throat.In mild cases the symptoms are headache, nausea, vertigo,anxiety, altered mental status, hypertension.In more severe cases the symptoms are bradycardia, unconsciousness, hypotension, arrhythmia,convulsions,pulmonary oedema,CV collapse & death.
Step-by-step explanation:
Cyanide is dangerous because CN binding of erythrocytes does not hampers the oxygen transfer.Both CO & CN leads to the influencing of the mitochondria by binding of enzyme cytochrome-c oxidase a,a3(CCO) which is the terminal enzyme complex of the respiratory chain in complex IV.The active (O2) binding site of the CCO is binuclear consists of heme a3 and CuB.CO binds to the reduced form of CCO &CN binds to either the reduced CCO heme (Fe2) or oxidized heme.The primary effect of CN is a blockage of the mitochondrial respiration chain & intracellular adenosine triphosphate(ATP). The consequence is the formation of cytotoxic hypoxia which is caused by the inhibition of CCO by the high affinity of CN to heme a3 of the enzyme. The result is a structural change and a decreased activity of the enzyme & rise in the lactate production which cause metabolic acidosis.