Final answer:
Cyanide acts as a competitive inhibitor of cytochrome c oxidase, halting the electron transport chain and leading to an increased pH in the intermembrane space due to a lack of proton accumulation. This disruption prevents ATP synthesis, critically affecting cellular energy production.
Step-by-step explanation:
The biochemical mechanism by which cyanide blocks O2 consumption involves its role as a competitive inhibitor of the enzyme cytochrome c oxidase (COX, also known as Complex IV), which is a crucial component of the electron transport chain (ETC) in mitochondria. This inhibition impairs the final step of aerobic respiration, preventing the transfer of electrons to oxygen and stopping the production of water. As a consequence, the ETC cannot function, which halts oxidative phosphorylation and the creation of the proton gradient necessary for ATP synthesis.
Since the proton gradient is not maintained, protons do not flow back into the mitochondrial matrix through ATP synthase. This implies that if cyanide poisoning occurs, the pH of the intermembrane space would increase as the accumulation of protons is diminished. The increase in pH signals that the intermembrane space is becoming less acidic. Without the proton gradient, ATP synthase cannot function properly to synthesize ATP, severely affecting the cell's energy supply and potentially leading to cell death.