Electron Transport Chain And Oxidative Phosphorylation Flashcards

1
Q

Briefly describe oxidative phosphorylation

A
  • Oxidize NADH and FADH2
  • Generate electrical energy by passing electrons to Oxygen
  • create a proton gradient across inner mitochondrial membrane
  • proton gradient drives phosphorylation of ADP to ATP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where is the electron transport chain?

A

Inner mitochondrial membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The ETC uses NADH and FADH2, where are these generated?

A

In the make ATP and ADP using energy stored in NADH and FADH2

Generated through catabolic processes such as glycolysis , Pyruvate dehydrogenase (PDH ) and TCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What structures and enzymes are located within the mitochondria?

A

-ATP synthesizing structures (ATP synthase) and San electron transport assembly in the inner mitochondrial membrane.

The following in the mitochondrial matrix:

  • TCA cycle enzymes
  • Fatty acid oxidation enzymes
  • mtDNA, mtRNA
  • Mitochondrial ribosomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe briefly the mitochondrial inner membrane

A

Impermeable to most small ions, small and 9arge molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 2 stages we can break this process down to?

A
  1. Electron transport

2. Oxidative phosphorylation and the Chemiosmotic hypothesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the role of NADH and FADH2 in electron transport?

A
  • NADH and FADH2 donate electrons to complexes in the inner mitochondrial membrane
  • the electrons flow Through the complexes and are eventually donated to oxygen forming water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens to protons in the Electron transport chain?

A
  • Process pumps protons (H+) into the inter-membrane space
  • this establishes a H+ gradient across the inner mitochondrial membrane
  • There is a high concentration of protons in the in the inter-membrane space and low concentration in the matrix
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain the chemiosmotic hypothesis and oxidative phosphorylation

A
  • this proton gradient causes protons to flow through ATP synthase in the inner membrane resulting in production of ATP
  • the H+ gradient couples electron transport to ATP synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 4 protein complexes of the Electron transport chain?

A

Complex 1 - NADH dehydrogenase

Complex 2- Succinate dehydrogenase

Complex 3- cytochrome reductase

Complex 4 - cytochrome oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the functions of 4 protein complexes in ETC?

A

These four complexes accept or donate electrons to relatively mobile electron carriers such as :

Coenzyme Q

Cytochrome C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do protein ETC complexes interact with prosthetic groups?

A

Prosthetic groups in each complex reversibly accept and release electrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the prosthetic groups for ETC Complexes I and II?

A

-FMN and FAD (riboflavin derivative), respectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the prosthetic group of Compex III in the ETC?

A

Heme group (Fe2+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the prosthetic groups of protein complex IV in the ETC?

A

Cu2+ and heme group(Fe2+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Complexes I, II and III also contain….

A

Iron-sulfur proteins

17
Q

Where do Complex 1 electrons come from?

A

-NADH electrons come from malate dehydrogenase(MDH, a-keto glutamate dehydrogenase(a-KGDH), isocitrate dehydrogenase(IDH), Pyruvate dehydrogenase (PDH) as well as fatty acid B-oxidation and from cytosolic sources such as glycolysis

18
Q

Where do the electrons for Complex 2 come from?

A

-FADH2 electrons from Succinate dehydrogenase (SDH) or the associated Coenzyme Q(CoQ) gets them from glycerol phosphate shuttle or from fatty acid B-oxidation

19
Q

Outline the flow of electrons during electron transport

A
  1. NADH oxidized by CoQ at complex I and/or FADH2 oxidized by CoQ at complex II
  2. CoQ oxidized by Cytochrome c and Complex II
  3. Cytochrome c oxidized by oxygen at complex IV
  4. O2 is the final electron acceptor at complex IV
20
Q

Explain the ending of Oxidative Phosphorylation and chemiosmotic hypothesis

A
  • As electrons flow down electrochemical potential, protons are pumped into the inter membrane space
  • Protons are pumped into the intra membrane space at complexes I, III and IV
  • This creates a pH gradient that is relieved by pumping protons back through F0F1-ATP synthase(COMPLEX V).

The energy released in this process is coupled to ATP synthesis from ADP and Pi

21
Q

Explain the inhibition of electron transport

A
  • Rotenone, piericidin A(bacterial antibiotic) and the barbiturate Amytal inhibit NADH dehydrogenase in complex 1
  • Antimycin (an antibiotic) inhibits cytochrome b of cytochrome reductase(complex III)
  • CO, azide, hydrogen sulphide(H2S) and cyanide (CN-) inhibit cytochrome oxidase(complex IV)
  • Oligomycin(a streptomyces antibiotic) inhibits ATP synthase
22
Q

What are the effects of ETC inhibitors?

A

Inhibitors decrease ATP synthesis, decrease ETC and Oxygen consumption

23
Q

How are ATP and ADP transported?

A
  • Adenine nucleotide translocase: unidirectional exchange of ATP for ADP(antiport)
  • Symporters of Pi and H+ is electro-neutral
24
Q

What chemicals inhibit ADP/ATP transport?

A

Atractyloside

Bongkrekic acid

Effects of both of these are similar to oligomycin

25
Q

How does Atractyloside inhibit ADP/ATP transport?

A

Atractyloside: a toxic glycoside(molecule with a sugar and a non carbohydrate element) from thistle plant Atractylis gummifera)

-Binds the outward facing (inter-membrane space) portion of the adenine nucleotide transporter

26
Q

How does Bongkrekic acid inhibit ADP/ATP transport?

A

Respiratory toxin produced in coconuts contaminated with Burkholderia gladioll

-Binds the inward facing (matrix) portion of the adenine nucleotide transporter

27
Q

What is the purpose of uncoupled of oxidative phosphorylation?

A

Uncouplers decrease ATP synthesis, increase ETC and OXYGEN consumption

28
Q

How do certain uncouplers act?

A

Certain uncouplers (e.g. DNP(dinitrophenol) ASA(aspirin), thermogin, ionophores) act by destroying the proton gradient

29
Q

What is the mechanism of uncouplers of oxidative phosphorylation?

A

Uncoupling proteins create a “proton leak”, allowing protons to renter the mitochondrial matrix without capturing any energy as ATP

30
Q

Why are shuttle mechanisms needed?

A
  • inner mitochondrial membrane is impermeable to most proteins and coenzymes
  • Need shuttle to deliver electrons from NADH (from glycolysis in the cytosol) across the inner mitochondrial membrane
31
Q

What are the 2 shuttle mechanisms?

A
  • Glycerol phosphate shuttle

- malate-Aspartate shuttle

32
Q

What is the P/O ratio?

A

The P/O ratio= ratio of ATP formed per Onatom reduced divided by Phosphorylated nucleotide/oxygen needed
Varies between NADH and FADH2

33
Q

What is the P/O ratio of NADH?

A

P/O ratio for NADH is 3 ATP: 1 NADH oxidized by the ETC

34
Q

What is the P/O ratio for FADH2?

A

P/O ratio FADH2 is 2 ATP :1 FADH2 oxidized by the ETC

35
Q

Describe the energy yield of the ETC

A

The oxidation of 1 NADH yields enough energy for:

  • 3 moles of ATP(malate-Aspartate shuttle)
  • 2 moles of ATP (glycerol phosphate shuttle)

The oxidation of 1 FADH2 yields enough energy for about 2 moles of ATP

36
Q

What are the principle controls of ATP production ?

A

[NADH][NAD+]

And

[ATP][ADP]

I.e. ETC will be active when

[ADP][ATP] and [NADH][NAD+]

37
Q

What is hypoxia? What are the effects?

A
  • Hypoxia decreases the rate of ETC and ATP production
  • A drop in cellular ATP increases anaerobic glycolysis and lactic acidosis production, anaerobic glycolysis cannot meet most tissue demands (neural tissue, cardiac muscle)
  • Myocardial infarction (heart attack) can result from hypoxia