Kaplan Ch. 10 - Kreb's Cycle And ETC

Question 1

Where does the Kreb’s cycle occur?

Answer 1

Mitochondrial matrix

Question 2

What type of transport brings pyruvate into mitochondria?

Answer 2

Active transport

Question 3

Other than pyruvate from glucose, what other molecules can be made into acetyl CoA?

Answer 3

Fatty acids
Amino acids
Ketone bodies
Alcohol

Question 4

Describe beta oxidation.

Answer 4

CoA - SH forms thioester bond with carboxyl groups of FAs to form activated fatty acid. Activated FA transported into intermembrane space where transferred to carnitine, which carries fatty acyl CoA across inner membrane. There, fatty acyl CoA is transferred to another CoA - SH to form Acyl CoA. Beta oxidation is then able to occur which removes 2 carbons at a time from carboxyl end of fatty acid.

Question 5

How is alcohol converted to acetyl CoA?

Answer 5

Alcohol dehydrogenase converts it to acetyl CoA directly. But this results in buildup of NADH which inhibits Krebs cycle. Thus, acetyl co A formed from lots of alcohol is primarily used to synthesize fatty acids.

Question 6

Describe general process of how amino acids are made into acetyl co A.

Answer 6

Amino acids lose amino group via transamination and then carbon skeleton is used to form ketone bodies which are made into acetyl CoA.

Question 7

The kreb’s cycle does not require oxygen to occur. So why doesn’t it occur anaerobically?

Answer 7

Because when oxygen is not present, NADH and FADH2 build up because they can’t be used by the ETC. NADH and FADH2 inhibit the cycle so it doesn’t occur without oxygen as a result.

Question 8

When an enzyme is a dehydrogenase, what does that always mean in terms of products?

Answer 8

Reduction, either NAD+ —> NADH or FAD —> FADH2

Question 9

Mnemonic to remember Krebs cycle:

Please can I keep selling seashells for money officer?

Answer 9

P - pyruvate
C - citrate
I - isocitrate
K - AKG
S - succinyl CoA
S - succinate
F - fumarate
M - malate
O - oxaloacetate

Question 10

Step 1 of TCA cycle: formation of citrate

1) what are the reactants?
2) what is the enzyme that catalyzes the reaction?
3) what are the products?

Answer 10

1) acetyl CoA + oxaloacetate + H2O
2) citrate synthase
3) citrate + CoA - SH + H+

Question 11

Step 2 TCA: isomerization of citrate to form isocitrate

1) what are the reactants?
2) what is the enzyme that catalyzes the reaction?
3) what does this enzyme do?
4) this enzyme is a ___ that requires ___ to function.

Answer 11

1) citrate
2) aconitase
3) binds to citrate, losing H2O. Then adds H2O back in to form the isomer of citrate, isocitrate
4) metalloprotein, Fe2+

Question 12

Step 3 TCA: formation alpha ketoglutarate

1) Why is this step essential to the rest of the cycle?
2) what is the enzyme for this step?

Answer 12

1) It is the rate limiting step, first carbon is lost as CO2, first molecule NADH formed
2) isocitrate dehydrogenase

Question 13

Step 4 TCA: succinyl CoA and CO2 formation

1) what is the enzyme that catalyzes the reaction?
2) reactants —> products?

Answer 13

1) alpha ketoglutarate dehydrogenase complex, similar to PDH

2) AKG + CoA - SH + NAD+ —> succinyl CoA + CO2 + NADH

Question 14

Step 5 TCA: succinate formation

1) enzyme?
2) reactants —> products?
3) where does the energy for GTP formation come from?
4) what happens to GTP once formed?

Answer 14

1) succinyl CoA synthetase
2) succinyl CoA + GDP + Pi —> GTP + CoA - SH + succinate
3) hydrolysis of thioester bond in succinyl CoA, bond is very high energy so energy released fe breaking bond is used to phosphorylate GDP to produce GTP (rxns are coupled).
4) GTP then enzymatically transfers a phosphate to ADP to make ATP

Question 15

Step 6 TCA: fumarate formation

1) what is forms during this rxn?
2) where does this rxn occur? Why?

Answer 15

1) fumarate and FADH2

2) on the inner membrane because succinate dehydrogenase is an integral membrane protein

Question 16

What are the totals for molecules produced by TCA? How will that translate to ATP after ETC?

Answer 16

4 NADH (2.5 ATP/NADH = 10ATP)
1 FADH2 (1.5 ATP/FADH2 = 1.5 ATP)
1 GTP (1 ATP)
2 CO2
1 CoA - SH
3 H+

Total 12.5 ATP / pyruvate
2 pyruvate / glucose = 25 ATP / glucose

Question 17

What are the 4 checkpoints of TCA?

Answer 17

PDH
Citrate synthase
Isocitrate dehydrogenase
AKG dehydrogenase

Question 18

Regulation citrate synthase:

High [ ] what 4 molecules allosterically inhibits this enzyme?

Answer 18

ATP
NADH
Citrate
Succinyl CoA

Question 19

Regulation isocitrate dehydrogenase

High [ ] what 2 molecules act as allosteric inhibitors?

High [ ] what 2 molecules act as allosteric activators?

Answer 19

ATP and NADH

ADP and NAD+

Question 20

Regulation AKG dehydrogenase

1) high [ ] of what 3 molecules inhibit this enzyme?
2) high [ ] of what 2 molecules activate this enzyme?

Answer 20

1) ATP, NADH, succinyl CoA

2) ADP and Ca2+ ions

Question 21

Regulation of PDH

1) high [ ] of what 3 molecules can inhibit PDH?
2) how do these molecules inhibit PDH?
3) high [ ] of what molecule activates PDH?

Answer 21

1) acetyl CoA, ATP, NADH
2) acetyl CoA exerts negative feedback

ATP and NADH activate PDH kinase which phosphorylates PDH and inactivates it

3) ADP, activates PDH phosphatase which removes Pi from PDH this activating it

Question 22

What part of the ETC is responsible for the production of ATP?

Answer 22

The proton gradient that is created (protons are pumped from matrix to intermembrane space, creating large concentration of + charge in IMS)

Question 23

What 2 processes are couples in aerobic respiration?

Answer 23

Formation of ATP (endergonic) and electron transport (exergonic)

Question 24

What happens in complex I of the ETC?

Answer 24

2 electrons are transferred from NADH to coenzyme Q (ubiquinone) to form CoQH2. In this process, 4H+ are pumped from the mitochondrial matrix to the intermembrane space

Question 25

What happens in ETC complex II?

Answer 25

In kreb’s cycle, succinate —> fumarate via succinate dehydrogenase, which creates a molecule of FADH2 from FAD. FADH2 then transfers 2e- to iron - sulfur protein which then transfers 2e- to coenzyme Q to form CoQH2. NO H+ PUMPED INTO IMS.

Question 26

What happens in ETC complex III?

Answer 26

CoQH2 transfers 1e- to cytochrome c and then other e- to another cytochrome c, producing 2 reduced CytC per CoQH2. 4 H+ are displaced into IMS as a result.

Question 27

What happens in ETC complex IV?

Answer 27

There are 4 molecules of reduced CytC which becomes oxidized and transfers 4e- to oxygen which combines with H+ to form 2H2O.

Question 28

What are NADH shuttles? What role do they play in aerobic respiration?

Answer 28

NADH formed through glycolysis cannot directly cross into mitochondrial matrix. This results in a range of ATP produced from cellular respiration of 30-32. NADH shuttles transfer high energy e- of NADH to a carrier that can cross inner mitochondrial membrane. 2 possible shuttles are glycerol phosphate shuttle (produces 1.5 ATP per NADH) or malate aspartate shuttle (produces 2.5 ATP per NADH)

Question 29

Describe the location of ATP synthase?

Answer 29

It spans the entire inner mitochondrial membrane and protrudes into the matrix

Question 30

What part of ATP synthase does H+ interact with?

Answer 30

The F0 portion, which spans the entire membrane. F0 portion acts like ion channel so protons flow along their gradient from high [ ] in IMS to low [ ] in matrix.

Question 31

How does the flow of H+ through ATP synthase generate ATP?

Answer 31

As H+ flow through, the F1 portion of ATP synthase utilizes the energy from this electrochemical gradient to phosphorylate ADP to ATP.

Question 32

Chemiosmotic coupling

Answer 32

Describes the direct relationship between the proton gradient and the production of ATP

Question 33

How is the ETC regulated?

Answer 33

By oxygen and ADP. If [O2] is low, then the ETC will be inhibited. If there is plenty of O2 then ability of ETC to occur depends on [ADP]. If [ADP] is high, then that will allosterically activate isocitrate dehydrogenase and produce more NADH and FADH2 for ETC. If [ATP] is high then ETC will be inhibited indirectly because ATP buildup will inhibit Krebs cycle and this produce less electron carriers for ETC.