Final: citric acid cycle/TCA cycle/Krebs cycle Flashcards

1
Q

What kind of process do cells need to generate ATP?

A

a process that generates electricity in the mitochondria

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2
Q

How do we create electricity?

A

electron-rich molecules must transfer electrons to chain of complexes (electron transport chain)

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3
Q

what is the final electron acceptor in ETC?

A

oxygen!

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4
Q

electron donor molecules (2)

A

NADH

FADH2

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5
Q

how do we produce NADH and FADH2?

A

dehydrogenase enzymes!

in the citric acid cycle (Krebs cycle)

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6
Q

CAC overview

A

8 rxns
acetyl-coa –> CO2
oxidation of pyruvate to CO2

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7
Q

starving state (what is our source of acetyl-coa and what are hormone levels like)

A

increase in glucagon, epinephrine, and cortisol

fatty acids are source of acetyl-coa

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8
Q

fed state (what is our source of acetyl-coa and what are hormone levels like)

A

increase in insulin

have plenty of acetyl-coa from breaking down glucose (mainly), fructose, and galactose

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9
Q

in the liver (source of acetyl-coa?)

A

alcohol!

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10
Q

external sources of acetyl-coA?

A

proteins

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11
Q

CAC starting with glucose

A

1) glycolysis converts 1 glucose to 2 pyruvate
2) 2 pyruvate enter mitochondria
3) pyruvate dehydrogenase makes acetyl-CoA, CO2, and NADH (from NAD+)

*this links glycolysis and CAC

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12
Q

what inhibits isocitrate dehydrogenase

A

high ATP and high NADH inhibit isocitrate dehydrogenase

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13
Q

what stimulates isocitrate dehydrogenase

A

high ADP stimulates isocitrate dehydrogenase because it tells the cell more energy is needed

high Ca2+ levels (calcium rises during work, work requires energy)

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14
Q

rate-limiting step of CAC

A

isocitrate dehydrogenase step!

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15
Q

what can disrupt CAC?

A

vitamin deficiency

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16
Q

what else is succinate dehydrogenase a part of?

A

the ETC

it is complex II!

17
Q

what do we do with oxaloacetate product?

A

oxaloacetate can join a new acetyl-CoA and start new cycle

18
Q

control of CAC

A

speeds up when there is need for energy

slows down when there is a lot of energy

19
Q

do hormones control CAC?

A

NO!

20
Q

how does fatty acid synthesis fit into this?

A

Fatty acid oxidation produces acetyl-CoA which can enter CAC

21
Q

pyruvate dehydrogenase complex

A

combines pyruvate with CoASH

1 CO2 released, 1 NADH produced

22
Q

regulation of PDC

A

product inhibition or covalent modification

23
Q

regulation of PDC by product inhibition

A

high acetyl-CoA or NADH allosterically inhibit PDC

24
Q

regulation of PDC by covalent modification

A

pyruvate dehydrogenase kinase is part of mammalian PDC

pyruvate dehydrogenase kinase is activated by NADH and acetyl-CoA (leads to phosphorylation and inactivation of E1)

25
Q

citrate synthase regulation

A

oxaloacetate binds, induces conformational change and facilitates binding of acetyl-CoA
NADH and succinyl-CoA allosterically inhibit citrate synthase

26
Q

succinate dehydrogenase…why is it unique?

A

it’s the only membrane-bound enzyme in the CAC

FAD is covalently bound to it and electrons stored in FADH2 are sent directly to ETC

27
Q

ATP from 1 glucose

A

38 ATP
glycolysis: 2ATP + 2NADH (2 ATP + 6 ATP = 8 ATP)
PDC: 1 NADH per pyruvate (3 ATP x 2 = 6 ATP)
TCA: 3 NADH + FADH2 + GTP per acetyl-CoA (9+2+1)x2 = 24

28
Q

succinyl-CoA

A

feedback inhibitor of CAC

29
Q

is CAC catabolic or anabolic?

A

catabolic bc endpoint is oxidative degradation of fuel

BUT, intermediates of CAC can be removed for biosynthetic processes (this makes it amphibolic - BOTH!)

30
Q

cataplerotic reactions

A

reactions that use CAC intermediates

31
Q

anaplerotic

A

reactions that replenish CAC intermediates