Final answer:
Dinitrophenol (DNP) acts as an uncoupler by making the inner mitochondrial membrane leaky to protons, thus disrupting the proton gradient required for ATP synthesis during glucose oxidation. This can potentially increase metabolic rate, which was why DNP was used as a weight-loss drug. Other compounds mentioned, such as cyanide, inhibit components of the electron transport chain but do not act as uncouplers.
Step-by-step explanation:
The compound that can act as an "uncoupler" of glucose oxidation and ADP phosphorylation is dinitrophenol (DNP). Uncouplers like DNP make the inner mitochondrial membrane permeable to protons (H+), allowing them to leak back into the mitochondrial matrix without passing through ATP synthase. This disrupts the proton gradient necessary for ATP synthesis, effectively decoupling electron transport from ATP production.
In relation to the provided scenarios, DNP would be expected to decrease the pH gradient across the inner mitochondrial membrane, which might be an effective weight-loss mechanism because it forces the cell to use more glucose to generate the same amount of ATP, resulting in increased metabolic rate and hence fat burn. On the other hand, cyanide poisoning which inhibits cytochrome c oxidase would cause a buildup of protons in the intermembrane space, likely increasing the pH in that space, and halting ATP synthesis due to the cessation of electron transport.
Hydrogen ion diffusion through the mitochondrial membrane without the need for integral membrane proteins would result in the dissipation of the proton gradient and a direct halt in ATP synthesis as the gradient is crucial for the function of ATP synthase.