From the Research
The correct answer is "A slight, short-term increase in oxygen consumption, followed by no oxygen consumption." Atractyloside inhibits the adenine nucleotide translocase (ANT), which is responsible for exchanging ADP from the cytosol with ATP from the mitochondrial matrix. When atractyloside is present, ADP cannot enter the mitochondrial matrix, preventing it from being phosphorylated to ATP.
Key Points to Consider
- Initially, there might be a slight increase in oxygen consumption as the electron transport chain begins to function with the available substrates (pyruvate) and any ADP already present in the matrix.
- However, this oxygen consumption would quickly cease because without the ability to import more ADP, oxidative phosphorylation cannot continue.
- The proton gradient would initially form but would not be utilized for ATP synthesis due to the lack of ADP substrate, eventually leading to respiratory control where electron transport slows down because the proton gradient cannot be dissipated through ATP synthase, as supported by the principles of oxidative phosphorylation 1.
Mechanism of Action
The mechanism of atractyloside inhibition of ANT is crucial in understanding the impact on oxygen consumption and ATP production.
- The inhibition of ANT by atractyloside prevents the exchange of ADP for ATP across the mitochondrial membrane.
- This prevention of ADP entry into the mitochondria halts the oxidative phosphorylation process, as there is no substrate (ADP) for the electron transport chain to phosphorylate into ATP.
Implications for Cellular Metabolism
The effects of atractyloside on mitochondrial function have significant implications for cellular metabolism, particularly in the context of energy production and consumption, as discussed in the context of mitochondrial function and disease 2, 3.
- The cessation of oxygen consumption after initial increase indicates the dependence of oxidative phosphorylation on the continuous supply of ADP.
- The role of oxidative phosphorylation in setting and maintaining metabolic homeostasis is critical, and its regulation by the energy state ([ATP]/[ADP][Pi]) is essential for cellular function 1.