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You recently identified a new compound, TX32, present in e-cigarette vapor that

ID: 274206 • Letter: Y

Question

You recently identified a new compound, TX32, present in e-cigarette vapor that you suspect causes mitochondrial dysfunction. Your preliminary data from Part 1 indicated that TX32 reduces mitochondrial membrane potential in a dose-dependent manner. However, you do not know whether membrane potential is reduced due to:
1. decreased proton pumping, or 2. increased proton leakage.
If option 1 (decreased proton pumping) is correct, you expect TX32 will a. Increase or b. Decrease. unsubmitted mitochondrial oxygen consumption independent of whether ATP is synthesized.

If option 2 (increased proton leakage) is correct, you expect TX32 will a. Increase or b. Decrease. unsubmitted mitochondrial oxygen consumption independent of whether ATP is synthesized.
Note that now we can distinguish which option TX32 exploits to reduce the mitochondrial membrane potential without having to measure ATP synthesis levels. Instead, we can simply focus on how much oxygen is consumed by the ETC under different conditions.
You recently identified a new compound, TX32, present in e-cigarette vapor that you suspect causes mitochondrial dysfunction. Your preliminary data from Part 1 indicated that TX32 reduces mitochondrial membrane potential in a dose-dependent manner. However, you do not know whether membrane potential is reduced due to:
1. decreased proton pumping, or 2. increased proton leakage.
If option 1 (decreased proton pumping) is correct, you expect TX32 will a. Increase or b. Decrease. unsubmitted mitochondrial oxygen consumption independent of whether ATP is synthesized.

If option 2 (increased proton leakage) is correct, you expect TX32 will a. Increase or b. Decrease. unsubmitted mitochondrial oxygen consumption independent of whether ATP is synthesized.
Note that now we can distinguish which option TX32 exploits to reduce the mitochondrial membrane potential without having to measure ATP synthesis levels. Instead, we can simply focus on how much oxygen is consumed by the ETC under different conditions.
You recently identified a new compound, TX32, present in e-cigarette vapor that you suspect causes mitochondrial dysfunction. Your preliminary data from Part 1 indicated that TX32 reduces mitochondrial membrane potential in a dose-dependent manner. However, you do not know whether membrane potential is reduced due to:
1. decreased proton pumping, or 2. increased proton leakage. You recently identified a new compound, TX32, present in e-cigarette vapor that you suspect causes mitochondrial dysfunction. Your preliminary data from Part 1 indicated that TX32 reduces mitochondrial membrane potential in a dose-dependent manner. However, you do not know whether membrane potential is reduced due to:
1. decreased proton pumping, or 2. increased proton leakage.
If option 1 (decreased proton pumping) is correct, you expect TX32 will a. Increase or b. Decrease. unsubmitted mitochondrial oxygen consumption independent of whether ATP is synthesized.

If option 2 (increased proton leakage) is correct, you expect TX32 will a. Increase or b. Decrease. unsubmitted mitochondrial oxygen consumption independent of whether ATP is synthesized.
Note that now we can distinguish which option TX32 exploits to reduce the mitochondrial membrane potential without having to measure ATP synthesis levels. Instead, we can simply focus on how much oxygen is consumed by the ETC under different conditions.

Explanation / Answer

If TX32 causes decreased proton pumping,

i. It would lead to less mitochondrial respiration i.e. reduced oxygen consumption and reduced NADH oxidation rates.

If TX32 causes increased proton leakage,

i. It would lead to increased mitochondrial respiration i.e. increased oxygen consumption and increased NADH oxidation rates.

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