The TCA Cycle and Oxidative Phosphorylation (Biochem) Flashcards Preview

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Flashcards in The TCA Cycle and Oxidative Phosphorylation (Biochem) Deck (57)
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1

Can The TCA cycle occur in anaerobic conditions?

NO. Although O2 is not directly required in the TCA cycle, the pathway won't occur anaerobically, because NADH and FADH2 will accumulate if O2 is not available for the ETC

2

How many ATP does 1 NADH yield?

- 3 ATP/1NADH
- NADH donates 3 H+
- each NADH donates 2e- to the ETC

3

Primary Function of the TCA cycle

- oxidation of Acetyl CoA to 2CO2
- Substrates: Acetyl CoA + 3NAD + FAD + GDP + Pi
- produces: 2 CO2 + 3 NADH + FADH2 + GTP
**The ONLY fate of Acetyl CoA in this pathway is its oxidation to CO2.
- therefore, the CAC does not represent a pathway by which there can be net synthesis of glucose from Acetyl CoA

4

Isocitrate dehydrogenase, the major control enzyme of the TCA cycle is:
- inhibited by ____ and
- activated by ___
- creates

Isocitrate dehydrogenase, the major control enzyme of the TCA cycle is:
- inhibited by NADH and ATP and
- activated by ADP and calcium
- converts isocitrate to alpha-ketoglutarate
- gives off CO2
- Requires NAD to be reduced to NADH (this NADH goes on to create 3 ATP in the ETC)

5

alpha ketoglutarate dehydrogenase
- what does it do?
- What does it require?

- converts alpha-ketoglutarate to succinyl Co-A
- gives off CO2
- Requires NAD to be reduced to NADH (this NADH goes on to create 3 ATP in the ETC)
- alpha ketoglutarate dehydrogenase is similar to the pyruvate dehydrogenase complex. It requires: *TLCFN*
- thiamine (Vit B1)
- lipoid acid
- CoA (from panthenate aka Vit B5)
- FAD (from riboflavin aka Vit B2)
- NAD (from niacin aka Vit B3) (may also be synthesized from tryptophan)

6

Succinyl-CoA synthetase (succinate thiokinase) catalyzes

- Succinyl Co-A to Succinate
- converts GDP + Pi to GTP!
- a substrate-level phosphorylation of GDP and GTP
*(this is our 3rd example of substrate-level phosphorylation; 2 were in glycolysis)

7

Succinate dehydrogenase is:
- catalyzes what reaction
- located on the
- it also functions as

- converts succinate to fumarate
- requires FAD that it reduces to FADH2
- this FADH2 goes on to create 2 ATP in the ETC
- Think (F)AD required to create (F)umarate
- it is located on the inner mitochondrial membrane
- where it also functions as Complex II of the ETC
* Fumarate is also a product of the urea cycle

8

How many ATP does 1 FADH2 yield?

- 2 ATP per 1 FADH2
- each FADH2 donates 2 H+
- each FADH2 donates 2 e- to the ETC

9

Citrate (intermediate of the CAC) may leave the mitochondria via the _____ to ____

Citrate (intermediate of the CAC) may leave the mitochondria via the
- citrate shuttle
- to deliver acetyl CoA into the cytoplasm for FA synthesis
- FA synthesis occurs in the cytoplasm of the liver

10

Succinyl CoA is a high-energy intermediate of the CAC that can be used for

- heme synthesis and
- to activate ketone bodies in extra hepatic tissues

11

Malate (intermediate of the CAC) can leave the mitochondria via the ____ for ____

Malate (intermediate of the CAC) can leave the mitochondria via the malate shuttle for gluconeogenesis

12

1 Acetyl CoA can yield how many ATP?

1 Acetyl CoA --> 2CO2 + 12 ATP

13

Which CAC intermediate is also a product of the urea cycle?

Fumarate

14

How many ATP are made per NADH?

- there are 3H+ per NADH, that can be converted into 3 ATP
- therefore, with NADH there is a ratio of 1 ATP/H+

15

How many ATP are made per FADH2?

- there are 2H+ per FADH2, that can be converted into 2 ATP
- therefore, with NADH there is a ratio of 1 ATP/H+

16

What is Complex I of the ETC and what does it do?

- NADH is oxidized by NADH dehydrogenase (Complex 1)
- Complex 1 accepts electrons from NADH

17

In the ETC, the electrons are passed along ga series of protein and lipid carriers. Their order is:

1. NADH dehydrogenase (Complex 1) accepts e- from NADH
2. Coenzyme Q (a lipid)
3. cytochrome b/c1 (an Fe/heme protein) aka Complex III
4. cytochrome c (an Fe/heme protein)
5. cytochrome a/a3 transfers electrons to O2 (a Cu/heme protein) aka cytochrome oxidase, aka Complex IV

- the Fe acts as an e- receptor: Fe3+ --> Fe2+
- the Cu acts as an e- receptor: Cu+ --> Cu

18

- Which components of the inner mitochondrial membrane in the ETC reoxidize their FADH2?
- and where do they pass their electrons?

- Succinate dehydrogenase and the alpha-glycerol phosphate shuttle enzymes reoxidize their FADH2
- and they pass their electrons directly to CoQ (a lipid)

19

What is another name for Complex III of the ETC?

- cytochrome b/c1
- (an Fe/heme protein)
- the Fe acts as an e- receptor: Fe3+ --> Fe2+

20

What is another name for Complex IV of the ETC?

- cytochrome a/a3 aka cytochrome oxidase
- (a Cu/heme protein)
- the Cu acts as an e- receptor: Cu+ --> Cu

21

How does ATP synthesis by oxidative phosphorylation work?

- the ATP synthase complex has the structure: F0F1, and spans the inner mitochondrial membrane
- As protons flow into the mitochondria through the F0 component, their energy is used by the F1 component (ATP synthase) to phosphorylate ADP using Pi
- 1 NADH yields 3 ATP
- 1 FADH2 yields 2 ATP

22

Where does the TCA cycle occur?

mitochondria

23

Citrate synthase condenses

the incoming acetyl group with oxaloacetate to form citrate

24

Proteins and drugs that uncouple ETC ____ rate of ETC and ____ efficiency

- Proteins and drugs that uncouple ETC increase the rate of ETC but decrease its efficiency.
- When the ETC is uncoupled it still generates heat, but doesn't make any ATP
- this increases the [ADP] which stimulates an increase in the rate of ETC, but it's not going to fix the problem

25

What is the controlled step of the CAC?

- isocitrate dehydrogenase
- it is inhibited by NADH
- causing the CAC to stop when the ETC stops in the anaerobic cell

26

Where do the ETC and Oxidative Phosphorylation occur in prokaryotes?

- on the cell membrane (bc they don't have mitochondria)

27

1. what are the consequences of inhibiting the ETC?
2. What inhibits the ETC?

1. ATP synthesis decreases, ETC decreases,
- O2 consumption decreases,
- increased intracellular NADH/NAD and FADH2/FAD ratios
2. Inhibited by:
- cyanide (complex IV, cytochrome oxidase)
- Barbiturates and rotenone (complex I, NADH dehydrogenase)
- doxorubicin (CoQ)
- antimycin (Complex III)
- Oligomycin (F0 component of F0F1 ATP synthase)
- carbon monoxide (complex IV, cytochrome oxidase)

28

1. Uncouplers of the ETC
2. consequences of uncoupling the ETC

1. Uncouplers:
- 2,4 DNP
- Aspirin in high doses (i.e. doses used to treat RA)
- uncoupling proteins (ie thermogenin aka UCP, natural uncoupling protein. Found in Brown Fat. Allows energy loss as heat to maintain a basal temperature around the kidneys, neck, breastplate and scapulae in newborns)
2. Uncouplers decrease the proton gradient causing:
- ATP synthesis decreases, ETC increases, O2 consumption increases
- uncouplers destroy the proton gradient
- produce heat rather than ATP
- increase oxidation of NADH

29

A/E of Aspirin in doses used to treat RA

- uncoupling of Oxidative Phosphorylation
- increased O2 consumption
- depletion of hepatic glycogen and
- the pyretic effect of toxic doses of salicylate
- depending on the degree of salicylate intoxication, the symptoms can vary from tinnitus to pronounced CNS and acid-base disturbances

30

Tissue hypoxia and the ETC

- hypoxia deprives the ETC of O2, decreasing the rate of ETC and ATP production
- When ATP levels fall, glycolysis increases, and in the absence of O2, all produce lactate (lactic acidosis)
- Anaerobic glycolysis is not able to meet the demand of most tissues for ATP--esp nerves and cardiac muscle