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Cyanide poisoning primarily affects cellular respiration by inhibiting cytochrome oxidase, which is a vital component of the electron transport chain in oxidative phosphorylation. This enzyme, specifically complex IV of the mitochondrial respiratory chain, is responsible for transferring electrons from cytochrome c to molecular oxygen, which is a crucial step for the production of adenosine triphosphate (ATP).

When cyanide binds to cytochrome oxidase, it prevents oxygen from binding and being reduced to water, effectively halting ATP production despite the presence of oxygen in the system. This disruption causes a cellular energy crisis, as cells are unable to carry out aerobic respiration and produce ATP. As a result, even though oxygen may be present in the bloodstream, cells cannot utilize it efficiently, leading to tissue hypoxia despite adequate oxygen delivery.

In contrast, options related to increased oxygen absorption at tissues, decreased perfusion of oxygen, and increased arterial PO2 do not occur as a direct consequence of cyanide poisoning. Oxygen may still be delivered to tissues, but the interference with its utilization at the cellular level is what leads to critical metabolic dysfunction. Therefore, the key consequence of cyanide poisoning is the inhibition of cytochrome oxidase, fundamentally impacting cellular respiration.