Sesh 2- TCA cycle and oxidative phosphorylation Flashcards

1
Q

Where does the TCA cycle occur?

A

Mitochondrial matrix

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2
Q

Why are there no known genetic defects in the TCA cycle?

A

They would be lethal, as it is a central pathway of catabolism.

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3
Q

Apart from its role in the TCA cycle, what else can citrate be used for?

A

Fatty acid synthesis

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4
Q

What is the role of pyruvate carboxylase?

A

Converts pyruvate to oxaloacetate

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5
Q

Which 2 ratios are used to control the TCA cycle?

A
  • ATP:ADP

- NADH: NAD+

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6
Q

What reaction does isocitrate dehydrogenase catalyse?

A

The irreversible conversion of isocitrate to alpha-ketoglutarate

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7
Q

What are the 2 major functions of the TCA cycle?

A
  • Break all C-C bonds in acetyl CoA

- Oxidise C atoms to CO2

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8
Q

Which carrier molecule contains the highest energy electrons?

A

NADH

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9
Q

What is the net yield of ATP from one mole of glucose?

A

32 ATP

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10
Q

Where does oxidative phosphorylation occur?

A

Inner mitochondrial membrane

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11
Q

Why can the electron transport chain only occur in the presence of oxygen?

A

Oxygen is the terminal acceptor of electrons.

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12
Q

What is normally the only way that protons can re-enter the mitochondrial matrix?

A

Via the ATP synthase complex.

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13
Q

How is the proton motive force generated?

A

Electrons are transferred from NADH/FADH2 sequentially to proton translocating complexes, which use this free energy to drive H+ into the intermembrane space.

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14
Q

Why does FADH2 yield less ATP compared to NADH?

A

The electrons in FADH2 contain less energy, so it feeds in to the electron transport chain at proton translocating complex 2 rather than 1.

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15
Q

What does the efficiency of ATP synthesis in oxidative phosphorylation depend on?

A

How impermeable the inner mitochondrial membrane is to H+, as this affects generation of the proton motive force.

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16
Q

How does the proton motive force affect the relative production of ATP?

A

Greater the proton motive force, more ATP produced.

17
Q

What happens to oxidative phosphorylation, and therefore the rest of glucose metabolism when [ATP] is high?

A
  • Means [ADP] is low, so ATP synthase stops working
  • Leads to buildup of H+ in inter membrane space, so proton translocating complexes stop
  • This prevents re-oxidation of carriers, so negative feedback on prior pathways
18
Q

How does dinitrophenol lower ATP production?

A

Uncouples electron transport chain from ATP synthesis by increasing inner mitochondrial membrane permeability to H+. Less of a proton motive force is set up and more energy is lost as heat.

19
Q

What is the role of Uncoupling Protein 1 (UCP1)?

A

Expressed in brown adipose tissue, to uncouple electron transport from ATP synthesis by increasing inner mitochondrial membrane permeability to H+.
More energy lost as heat for non-shivering thermogenesis.

20
Q

How does cyanide inhibits the electron transport chain?

A

Binds the haem group of the terminal proton translocating complex (cytochrome C oxidase), meaning O2 cannot bind and act as the terminal electron acceptor.

21
Q

Which molecule combines with acetyl CoA to form citrate in the first step of the TCA cycle?

A

Oxaloacetate

22
Q

Which stage in the metabolism of glucose produces the most ATP?

A

Electron transport chain