What is the mechanism of action (MOA) of cyanide poisoning?

The mechanism of action of cyanide poisoning is primarily due to its binding to cytochrome oxidase, which is a key component of the electron transport chain in cellular respiration. By binding to this enzyme, cyanide effectively inhibits the transfer of electrons, which is crucial for the production of adenosine triphosphate (ATP) through aerobic metabolism. This inhibition prevents cells from utilizing oxygen effectively, leading to cellular hypoxia even though there may be adequate oxygen available in the bloodstream. The consequence of this process is a profound disruption in cellular energy production, which results in tissue damage and can ultimately lead to death if not promptly treated.

The other options represent mechanisms of action that do not apply to cyanide. Myoglobin binding and the effects on muscle tissue hypoxia pertain to different conditions and toxins. The inhibition of carbonic anhydrase relates to a mechanism affecting acid-base balance rather than oxygen metabolism. Inhibiting hemoglobin synthesis affects the production and availability of hemoglobin itself, which is unrelated to cyanide's specific mode of action on tissue oxygen utilization. Thus, the distinctive impact of cyanide on cytochrome oxidase underlines why the correct choice accurately captures its toxicological effects.