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metabolism > TCA cycle and ETC > Flashcards

TCA cycle and ETC Flashcards

1
Q

what is the pyruvate dehydrogenase complex made up of?

A

it’s made up of 3 different enzymes

E1, E2. E3

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2
Q

what is enzyme E1?

A

pyruvate dehydrogenase

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3
Q

what reaction is catalysed by E1?

A

TPP being added to pyruvate to make acyl-TPP

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4
Q

what is enzyme E2?

A

dihyrolipoamide acyltransferase

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5
Q

what reaction is catalysed by E2?

A

lipoamide arm replaces the TPP to form acyl-lipoate

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6
Q

what is enzyme E3?

A

Dihydrolipoyl dehydrogenase

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7
Q

what reaction is catalysed by E3?

A

Regenerate lipoamide arm through the reduction of FAD to FADH

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8
Q

what vitamin is TPP derived from?

A

vitamin B1

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9
Q

what is PDC controlled by?

A

feedback inhibition - when acetyl coA and NADH levels are high, the enzyme is inhibited
covalent modification - phosphorylation

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10
Q

what effect does phosphorylation have on PDC?

A

activates it

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11
Q

what effect does insulin have on PDC?

A

dephosphorylation - activates glucose metabolism

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12
Q

where does the TCA cycle occur?

A

mitochondrial matrix

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13
Q

what process forms GTP in the TCA cycle?

A

substrate level phosphorylation

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14
Q

what are reduced coenzymes used for?

A

oxidised and feed electrons into the ETC
ETC uses these electrons to pump protons across the mitochondrial membrane
produces ATP

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15
Q

explain what each of the 4 complexes does in the ETC?

A

1 - 2 electrons removed from NADH to UQ
2 - FADH2 - electrons transferred to UQ
3 - UQ to cytochrome C
4 - electrons removed from cytochrome C to combine with O2 –> H2O

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16
Q

what substances inhibit the ETC

A

carbon monoxide

cyanide

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17
Q

what complex do CO and cyanide inhibit and what effect does this have?

A

complex 4 - causes a backlog of electrons

18
Q

what is coupling?

A

using the proton gradient to make ATP

how the ETC and oxidative phosphorylation are coupled by a proton gradient across the inner mitochondrial membrane

19
Q

what is uncoupling?

A

using the energy from the ETC in other processes

20
Q

how can uncoupling occur?

A

removing the proton gradient

equalising the charges on either side –> removing the charge gradient

21
Q

what is non-shivering thermogenesis?

A

process by which babies keep warm and how we keep warm without shivering

22
Q

what is thermogenin?

A

uncoupling protein 1 - membrane channel

23
Q

how does non-shivering thermogenesis work?

A

thermogenin allows protons to flow through it and produce heat rather than ATP

24
Q

explain how Gramicidin works?

A

forms 2 half channels – neutralises the charge gradient and kills the bacteria

25
Q

explain how Nigericin works?

A

neutralises charge gradient and kills bacteria

protons can permeate the membrane

26
Q

explain how valinomycin works?

A

allows for dissipation of charge through movement of K+ across the membrane

27
Q

what is valinomycin used clinically?

28
Q

what makes dinitro-phenol membrane soluble?

A

its negative charge is spread throughout the molecule

29
Q

what does dinitro-phenol do?

A

acts as a proton carrier across the mitochondrial membrane and neutralises the charge
releases the energy as heat - makes you feel hot

30
Q

what are the problems with dinitro-phenol?

A

has a very close therapeutic between weight loss and death
lethal dose
not allowed

31
Q

what are the intermediates of the TCA used to make?

A

amino acids
fatty acids
steroids
nucleotides

32
Q

how can the citrate of the TCA cycle be used?

A

turned into oxaloacetate and acetyl coA –> fatty acids and cholesterol

33
Q

what does the TCA rate depend on?

A

NAD+ availability –> depends on ETC rate –> linked to ATP:ADP ratio

34
Q

in muscle, what are dehydrogenases stimulated by?

35
Q

wat causes hypoxia?

A

altitude
trauma
exercise too much

36
Q

what complex of the ETC does hypoxia block?

37
Q

how are ROS formed?

A

electrons flow near the surface of complex 1
when they build up, alternative electron routes start occurring
ROS formed

38
Q

why are ROS bad for the cell?

A

react with things in the cell and damage them

39
Q

how can body limit the damage by ROS?

A

limit ATP by switching off non-essential cell functions
improve anaerobic ATP production efficiency
limit oxidative stress - providing protection against ischaemia

40
Q

explain what happens to HIF1a in normal and hypoxic conditions?

A

normal - HIF1a subunit is degraded

hypoxia - stabilised and binds to upstream elements of promoters

41
Q

what does HIF do and how does this reduce damage by ROS?

A

downregulates mitochondria respiration during hypoxia – promotes loss of mitochondria (autophagy) and suppresses biogenesis

reduce no of mitochondria –> reduce no of ETC –> lower oxygen demand –> fewer ROS

metabolism (23 decks)

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