How is Kreb's cycle regulated by ADP?

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In summary, the concentration of ADP plays a critical role in regulating the rate of reactions that produce ATP. When ADP is limited, ATP production decreases due to a lack of phosphate acceptors. This also causes the accumulation of NADH and FADH2, which inhibits the oxidation of acetyl CoA by the TCA cycle. The conversion of succinyl coA is the only step in the cycle that requires ADP or GDP. This lack of ADP can lead to an increase in NADH levels, which can inhibit enzymes involved in the Krebs cycle. The cycle is activated by high ADP/ATP or NAD+/NADH ratios, with isocitric dehydrogenase
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sameeralord
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My textbook says,
Increase in the concentration of ADP accelerates the rate of reactions that use ADP to generate ATP. If ADP is present in limiting concentration, the formation of ATP by oxidative phosphorylation decreases owing to lack of phosphate acceptor or inorganic phosphate. As NADH and FADH2 accumulate, their oxidized forms become depleted, causing the oxidation of acetyl CoA by TCA cycle to be inhibited, owing to lack of oxidized coenzymes.

I checked the whole citric acid cycle, and only the conversion of succinyl coA requires ADP or GDP. I don't understand how a lack of this would make NADH accumulate. Could anyone explain this. Thanks a lot :smile:
 
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sameeralord said:
My textbook says,I checked the whole citric acid cycle, and only the conversion of succinyl coA requires ADP or GDP. I don't understand how a lack of this would make NADH accumulate. Could anyone explain this. Thanks a lot :smile:

All dehydrogenases involved in Krebs are sensitive to the redox potential (mainly NADH / NAD+ ratio). NADH is an inhibitor of those enzymes. Since Electron transport chain & oxidative phosphorylation produce ATP relaying on NADH to provide the energy for ADP phosphorylation to ATP, you can then say ATP is an inhibitor. So the cycle is "turned on" by high ADP/ATP or NAD+ / NADH ratios.

IIRC, the rate limiting enzime in Krebs is isocitric dehydrogenase.
 
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1. How does ADP regulate the Kreb's cycle?

The Kreb's cycle, also known as the citric acid cycle, is regulated by ADP through its role in ATP synthesis. When the level of ADP in the cell is high, it signals the need for more energy and the Kreb's cycle is stimulated to produce more ATP. Conversely, when the level of ATP is high, it acts as a negative regulator and slows down the Kreb's cycle to conserve energy.

2. What is the relationship between ADP and ATP in the regulation of the Kreb's cycle?

ADP and ATP are closely related in the regulation of the Kreb's cycle. ADP is the precursor molecule for ATP synthesis, and its conversion to ATP is an essential step in the cycle. The ratio of ADP to ATP levels in the cell determines the rate of the Kreb's cycle, as it indicates the energy needs of the cell.

3. Can other molecules besides ADP regulate the Kreb's cycle?

Yes, there are other molecules that can regulate the Kreb's cycle, such as NADH and ATP. NADH acts as an inhibitor of the cycle, while ATP serves as a negative feedback regulator. These molecules work together with ADP to maintain the balance of energy production and consumption in the cell.

4. How does the regulation of the Kreb's cycle by ADP affect cellular respiration?

The regulation of the Kreb's cycle by ADP is crucial for efficient cellular respiration. By responding to the energy needs of the cell, ADP ensures that the Kreb's cycle is producing enough ATP to fuel cellular processes. This helps to maintain the overall balance of energy production and consumption in the cell.

5. Can the regulation of the Kreb's cycle by ADP be disrupted?

Yes, the regulation of the Kreb's cycle by ADP can be disrupted by various factors, such as changes in cellular pH or the presence of metabolic inhibitors. These disruptions can lead to an imbalance in energy production and consumption, which can have negative effects on cellular function.

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