Final answer:
Cyanide binds to cytochrome c oxidase, stopping the electron transport chain and increasing the pH of the intermembrane space due to disrupted proton pumping, which leads to a cessation of ATP synthesis.
Step-by-step explanation:
Cyanide is known to be a potent inhibitor of cytochrome c oxidase, which is a crucial component of the electron transport chain (ETC) involved in aerobic respiration. When cyanide binds to this enzyme, it prevents the transfer of electrons to oxygen, the final electron acceptor, effectively halting the ETC. This inhibition leads to a disruption in the proton gradient across the mitochondrial membrane since protons are no longer being pumped into the intermembrane space. As a result, the pH of the intermembrane space would increase, becoming less acidic because the protons are not being pumped out of the mitochondrial matrix.
Moreover, because the ATP synthesis is driven by the flow of protons back into the mitochondrial matrix through ATP synthase, cyanide poisoning prevents this flow, leading to a halt in ATP production. Without the production of ATP, which is the energy currency of the cell, cellular functions can't be carried out, leading to cell death. Cyanide, therefore, has a lethal effect on cellular metabolism due to its direct inhibition of a critical step in ATP production.