5. Mitochondria and Oxidative Phosphorylation

Question 1

How do mitochondria suggest we are descendants of prokaryotes?

Answer 1

Can only arise from pre-existing mitochondria
Possess own genome (circular, no histones)
Have own protein synthesising machinery
1st AA of transcripts is fMet as in prokaryotes
Some Antibiotics blocking protein synthesis in bacteria also blocks in mitochondria

Question 2

What type of genome do mitochondria have?

Answer 2

Circular molecule of DNA

Question 3

When there is a mutation in mitochondrial DNA…

Answer 3

Mutation transmitted to all maternal offspring

Question 4

What is the result of the deoxidation of NADH and FADH2 having a large delta G?

Answer 4

It is enough to generate several phophoanhydride bonds

Part of this energy is recovered by ETC and used to synthesise ATP

Question 5

Chemiosmotic model of oxidative phosphorylation

Answer 5

Movement of protons from within matrix into inter membrane space is controlled by ETC/ respiratory chain
Pumped protons allowed back into mitochondria through a specific channel: ATP synthase

Question 6

Where is the ETC and where does oxidative phosphorylation occur?

Answer 6

On the inner mitochondrial membrane

Question 7

Electron transport chain

Answer 7

Protein carriers accept electrons and in doing so a proton from the aq solution
As electrons pass through each complex, a H+ is pumped to inter membrane space

Question 8

How do redox potentials show that the ETC is energetically favourable?

Answer 8

Each successive unit has a more positive redox potential than the previous and thus a higher electron affinity
= energetically favourable

Question 9

What happens to the electrons in the ETC as they pass along the chain?

Answer 9

Electrons lose energy

Question 10

Reduced substrate

Answer 10

Donates electrons

Becomes oxidised

Question 11

Oxidised substrate

Answer 11

Accepts electrons

Becomes reduced

Question 12

Redox couple

Answer 12

A substrate that can exist as both

e.g. NAD+ / NADH

Question 13

Redox potential (E’0)

Answer 13

Ability to accept / donate electrons

Question 14

Negative redox potential indicates

Answer 14

Redox couple tends to donate electrons

Has more reducing power than hydrogen

Question 15

Positive redox potential indicates

Answer 15

Redox couple tends to accept electrons

Has more oxidising power than hydrogen

Question 16

ATP synthase

Answer 16

Multimeric enzyme consisting of a membrane bound part (F0) and a part which projects into the matrix space (F1)

Question 17

What does rotation of ATP synthase due to proton movement drive?

Answer 17

Transition states with altering affinities for ATP and ADP

Question 18

What does direction of proton flow through ATP synthase dictate?

Answer 18

ATP synthesis vs ATP hydrolysis

Question 19

Which Krebs’ Cycle enzyme is located on the inner surface of the inner mitochondrial membrane?

Answer 19

Succinate Dehydrgenase

Question 20

Why is Succinate Dehydrogenase located on the inner mitochondrial membrane?

Answer 20

Responsible for catalysing reaction which produces FADH2

Location allows communication with Ubiquinone (coenzyme Q)

Question 21

What is ubiquinone the entry point for?

Answer 21

Electrons donated by FADH2

Question 22

What is the function of an oxygen electrode?

Answer 22

Measures concentration of oxygen in a solution in a chamber

Question 23

How does cyanide act as a metabolic poison?

Answer 23

Binds to Fe3+ in the cytochrome oxidase complex and blocks the flow of electrons through the ETC and consequently, the production of ATP

Question 24

How does malonate act as a metabolic poison?

Answer 24

Competitive Inhibitor of Succinate Dehydrogenase
Slows down the flow of electrons from succinate to ubiquinone by inhibiting the oxidation of succinate to fumarate by succinate dehydrogenase

Question 25

How does oligomycin act as a metabolic poison?

Answer 25

Binds to stalk of ATP synthase and inhibits oxidative phosphorylation
Blocks flow of protons through ATP synthase and so causes a backlog of protons in the intermembrane space.
Intermembrane space becomes saturated with protons meaning that protons can no longer be pumped into the space by the ETC components.
This means that the flow of electrons through the ETC, and hence respiration, stops.

Question 26

How does carbon monoxide act as a metabolic poison?

Answer 26

Binds to Fe2+ in cytochrome oxidase and blocks electron flow

Question 27

How does dinitrophenol (DNP) act as a metabolic poison?

Answer 27

Uncouples oxidative phosphorylation from ATP production by transporting protons across the mitochondrial membrane

Question 28

What is non-shivering thermogenesis?

Answer 28

Drop in body temperature
In response: Thermogenin (UCP-1) channel can be activated
Like DNP, it allows protons to bypass ATP synthase thereby releasing heat from the dissipation of the proton gradient

Question 29

How does DNP induce weight loss?

Answer 29

Transports protons across the mitochondrial membrane, thereby uncoupling oxidative phosphorylation from ATP production
Markedly increases metabolic rate and body temperature.

Question 30

How does Rotenone act as a metabolic poison?

Answer 30

Inhibits transfer of electrons from complex I

to ubiquinone.