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ESA2 - Metabolism, Endocrinology and Haematology > Energy Production - TCA and ETC > Flashcards

Energy Production - TCA and ETC Flashcards

1
Q

True or False:

Pyruvate enters directly into Stage 3 (TCA)

A

False - has to be converted into acetyl coA first

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2
Q

Which enzyme converts pyruvate into acetyl coA?

A

Pyruvate dehydrogenase

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3
Q

What is the equation for the conversion of pyruvate into acetyl coA?

A

CH3COCOOH + CoA + NAD+ –> CH3CO~CoA + CO2 + NADH + H+

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4
Q

Where does the conversion of pyruvate to acetyl coA occur?

A

Mitochondrial Matrix

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5
Q

As pyruvate dehydrogenase is a large multi-enzyme complex, how many enzymes does it consist of?

A

5

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6
Q

Why is the conversion of pyruvate to acetyl coA sensitive to Vitamin B1 deficiency?

A

The different enzyme activities require various cofactors (FAD, thiamine pyrophosphate and lipoid acid) which are provided by B-vitamins

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7
Q

Why is the link reaction a key regulatory step?

A

It is irreversible - rate limiting

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8
Q

What does pyruvate dehydrogenase deficiency cause?

A

Lactic acidosis

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9
Q

What is pyruvate dehydrogenase activated by?

A

Pyruvate, CoA, NAD+, ADP and Insulin

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10
Q

What is pyruvate dehydrogenase inhibited by?

A

Acetyl-CoA, NADH, ATP, citrate

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11
Q

Where does the Kreb’s cycle occur?

A

Mitochondria

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12
Q

What are some feature of the Kreb’s cycle?

A

Single pathway

Acetyl converted to 2CO2

Oxidative (requires NAD+, FAD)

Some energy is produced as ATP and GTP

Produces some precursors for biosynthesis

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13
Q

How many cycles of TCA are there per glucose entering glycolysis?

A

Two

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14
Q

What does acetyl coA join with to form citrate (C6)?

A

Oxaloacetate (C4)

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15
Q

How many carbons does isocitrate have?

A

6

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16
Q

What is also produced from the production of a-ketoglutarate (C5) from isocitrate (C6)?

A

NADH and CO2

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17
Q

The C5 molecule a-ketoglutarate combines with CoA to produce succinyl-CoA (C4). What is also produced?

A

CO2 and NADH

18
Q

What is produced when succinyl-CoA is converted into succinate?

A

GTP from GDP

19
Q

What is produced when succinate is converted into fumerate?

A

FADH2

20
Q

How is oxaloacetate produced?

A

Oxidation of malate (C4) - also converts NAD+ into NADH

21
Q

How many NADH, FADH2 and GTP molecules are produced per glucose from TCA?

A

6 NADH
2 FADH2
2 GTP

22
Q

How is TCA cycle regulated?

A

By energy availability i.e. ATP/ADP ratio and NADH/NAD+ ratio

23
Q

Does TCA cycle function in the absence of O2?

A

No

24
Q

What is stage 4 of catabolism and where does it occur?

A

Electron transport chain - occurs in mitochondria

25
Q

What happens to NADH and FADH2 in the ETC?

A

Reoxidised

26
Q

Which type of phosphorylation occurs in the ETC?

A

Oxidative phosphorylation

27
Q

What happens to electrons in the ETC?

A

They are transferred through a series of carrier molecules with increasing electronegativity to O2 - the final electron acceptor

28
Q

What is the role of H+ ions in the ETC?

A

Energy used to move H+ across membrane (a lot of energy released as heat) - H+ gradient established across inner mitochondrial membrane = proton motive force

29
Q

What is the only way in which protons can return across the mitochondrial membrane?

A

Via ATP synthase - driving ATP synthesis

30
Q

Why does NADH use 3 PTCs while FADH2 only uses 2?

A

Electrons in NADH have more energy than in FADH2

31
Q

How many moles of ATP are synthesised per oxidation of 2 moles of NADH?

A

5 moles of ATP

32
Q

How many moles of ATP are synthesised per oxidation of 2 moles of FADH2?

A

3 moles of ATP

33
Q

How is oxidative phosphorylation regulated?

A

Eg

When [ATP] is high, no substrate for ATP synthase as [ADP] is low

Inward flow of H+ therefore stops

Concentration of H+ in intermitochondrial space increases

This prevents further H+ pumping - stops electron transport

34
Q

What is an example of an inhibitor of electron transport?

A

Cyanide - prevents acceptance of electrons by oxygen

35
Q

What do uncouplers do?

A

Increase the permeability of the mitochondrial inner membrane to protons

Dissipate the proton gradient, thereby reducing the proton motive force - no drive for ATP synthesis

36
Q

What are some examples of uncouplers?

A

Dinitrophenol, dinitrocresol, fatty acids

37
Q

What are Ox/Phos diseases?

A

Genetic defects in proteins encoded by mtDNA - decreases in electron transport and ATP synthesis

38
Q

In brown adipose tissue, what is the degree of coupling controlled by?

A

Fatty acids (uncouplers) - allows extra heat generation

39
Q

What naturally occurring uncoupling protein does brown adipose tissue contain?

A

Thermogenesis (UCP1)

40
Q

In brown adipose tissue, in response to cold, what does noradrenaline activate?

A
  1. Lipase which releases fatty acids from triacylglycerol
  2. Fatty acid oxidation -> NADH/FADH2 -> electron transport

Fatty acids activate UCP1

UCP1 transports H+ back into mitochondria

So electron transport uncoupled from ATP synthesis meaning energy of PDF is then released as extra heat

41
Q

What is brown adipose tissue found in?

A

Newborn infants to maintain heat and hibernating animals to generate heat to maintain body temperature

42
Q

How many moles of ATP are produced per mole of glucose in respiration?

A

32 moles

ESA2 - Metabolism, Endocrinology and Haematology (19 decks)

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