Question

Shortly before the four-hour mark, the researcher inhibits the activity of proton pumps in the outer mitochondrial membrane. Which of the following conclusions do the data support?

A. The protein channel in the outer mitochondrial membrane is activated by membrane potential.
B. The glucose carrier protein in the plasma membrane is activated by membrane potential.
C. The pyruvate carrier protein in the mitochondrial outer membrane is a cotransporter.
D. The cell uses cotransporters to transport pyruvate from the mitochondria to the cytosol.

Answer 1

Inhibition of proton pumps in the outer mitochondrial membrane would affect mitochondrial functions related to the proton gradient and ATP production, but the data provided do not support any of the given conclusions, as they pertain to the inner mitochondrial membrane or other unrelated processes.

Step-by-step explanation:

When looking at the inhibition of proton pumps in the mitochondrial outer membrane, we prompt a closer examination of how different transport proteins might be affected. The data you're referring to likely deal with the role of membrane potential in mitochondrial function, especially concerning ATP production and transport proteins' activity. Membrane potential is crucial for various cellular processes, including the transport of substances across cellular membranes via different types of carrier proteins, such as uniporters, symporters, and antiporters.The conformational coupling hypothesis highlights that the ATP production in the mitochondria via the FF₁ATPase is driven by conformational changes in membrane proteins due to the energy passed from the electron transport chain. Similarly, the chemi-osmotic hypothesis suggests that hydrogen ions, driven by the electrochemical gradient, return to the mitochondrial matrix through ATP synthase, facilitating ATP synthesis. Ion channels and carrier proteins are designed to control the diffusion of ions, and active transport systems, like proton pumps, use energy (often ATP) to move molecules against these gradients. Given these understandings, we can assess the scenario where the activity of proton pumps is inhibited. If proton pumps in the outer mitochondrial membrane specifically were inhibited, we'd expect some effect on the mitochondrial function related to establishing the proton gradient, potentially affecting ATP production. However, the mitochondrial membrane involved in establishing the electrochemical gradient and housing ATP synthase used in ATP production is the inner mitochondrial membrane, not the outer membrane. Therefore, none of the conclusions A, B, C, or D, which are related to membrane potential, directly pertain to the inhibition of proton pumps in the outer mitochondrial membrane.