Final answer:
Cyanide inhibits cytochrome c oxidase in the electron transport chain, leading to a decreased proton gradient and increased pH in the intermembrane space, which significantly reduces ATP synthesis.
Step-by-step explanation:
Cyanide poisoning inhibits cytochrome c oxidase, which is a crucial component of Complex IV in the electron transport chain (ETC) of cellular respiration. This inhibition has a critical impact on ATP synthesis. When cyanide binds to cytochrome c oxidase, it prevents the transfer of electrons to oxygen, which is the final electron acceptor in the ETC. As a result, the proton gradient across the mitochondrial membrane, which is generated by the movement of electrons through the ETC, cannot be maintained. This gradient is essential for the synthesis of ATP by ATP synthase.
With the ETC being compromised, the pumping of protons (H+) from the mitochondrial matrix to the intermembrane space is reduced, leading to a decreased proton gradient. This decrease in proton gradient means that the driving force for ATP synthesis is lost. As such, you would expect the pH of the intermembrane space to increase, as fewer protons are being pumped into this space, making it less acidic.
Consequently, the effect of cyanide on ATP synthesis would be a severe reduction, as ATP synthase relies on the flow of protons down the gradient to drive the synthesis of ATP from ADP and inorganic phosphate. Without a sufficient proton gradient, ATP synthase cannot function effectively, leading to decreased cellular energy production and cell death if the poisoning is not promptly treated.