M&n Week 2: Oxidative Phosphorylation

Front 1

NADH delivers electrons to which complex in the ETC?

Back 1

Complex I

Front 2

Succinate dehydrogenase serves as which complex in the ETC?

Back 2

Complex II
(reducuces FAD--> FADH2)

Front 3

What compound serves as the electron carrier between Complexes I --> III, and complexes II --> III ?

Back 3

Ubiquinone (coenzyme Q)

Front 4

Which compound is responsible for electron transfer from complexes III to IV?

Back 4

Cytochrome c

Front 5

At which complexes in the ETC are protons pumped from the mitochondrial matrix to the innermembrane space?

Back 5

Complex I, III, IV

*Protons are NOT pumped at complex II

Front 6

If the reaction between cyt b ----> cyt c1 was blocked, what forms will these compounds be in?

Back 6

Cyt b will be in reduced form (electron rich)
Cyt c1 will be in oxidized form (electron poor)

Front 7

Which metabolic pathways provide electrons from the cytoplasm or the matrix to ubiquinone in the ETC?

Back 7

1. Glycerol-3 phosphate dehydrogenase (glycolysis) <---CYTOSOL
2. Acyl CoA dehydrogenase (B-oxidation) <--- MATRIX

Front 8

Explain how the first enzyme in B-oxidation transfers electrons to the ETC.

Back 8

1. Acyl-CoA dehydrogenase transfers electrons to electron transport flavoprotein (ETF)
2. ETF reduces ETF:Q oxidoreductase
3. ETF:Q transfers electrons to coenzyme Q

Front 9

How are electrons transfered from glycerol 3-PO4 to the ETC?

Back 9

Electrons are transferred directly to ubiquinon (coenzyme Q) via Glycerol 3-PO4 dehydrogenase

Front 10

Describe the locations of the ATP synthase subunits.

Back 10

F0 --> submerged in lipid bilayer of innermembrane
F1 --> protrudes into the mitochondrial matrix

Front 11

Which ATP synthase subunit is the site of ATP synthesis?

Back 11

F1

Front 12

Through which ATP synthase subunit do protons pass through?

Back 12

F0

Front 13

Explain how ATP bound to the F1 subunit of the ATP synthase is released?

Back 13

During rotation, the gamma-subunit of F1 touches each B-subunit, inducing a conformational change that causes the release of bound ATP.

Front 14

Which portions of the ATP synthase rotate as protons pass through?

Back 14

F0 domain and the y-subunit of F1 domain

Front 15

What is the result of uncoupling proteins?

Back 15

They allow protons to reenter the mitochondrial matrix without capturing any energy as ATP, thus collapsing the proton gradient.

*Results in the increase in ETC and O2 consumption in attempt to reestablish the proton gradient.

*Energy is used to produce heat rather than ATP

Front 16

What kind of tissue is particularly abundant in naturally occurring uncoupling proteins?

What is the purpose of this?

Back 16

Brown adipose tissue

*Production of heat (important in newborns)

Front 17

Give an example of a synthetic uncoupling agent.

Back 17

2,4-Dinitrophenol

Front 18

Which regulatory protein prevents reverse operation of ATP synthase in ischemia?

Back 18

Protein inhibitor IF1
(induced by acidity derived from pyruvate/lactate in glycolysis)

Front 19

Which regulatory protein uncouples ATP synthesis from oxidation by providing a channel for return of protons to the matrix?

Back 19

Thermogenin.

*Energy is lost as heat; useful in brown adipose tissue

Front 20

List 4 ways oxidative phosphorylation is regulated.

Back 20

1. Thermodynamic regulation (proton gradient)
2. Acceptor control ratio (ADP:ATP ratio)
3. Protein inhibitor IF1
4. Thermogenin (uncoupling protein)

Front 21

List 2 alternative functions of the mitochondria (besides oxidative phosphorylation).

Back 21

1. Free radical production
2. Induction of programmed cell death (apoptosis)

Front 22

How can reperfusion of ischemic tissue be damaging?

Back 22

Due to increases in free radical production

Front 23

Which metabolic pathway maintains pH?

Back 23

Electron transport chain

(In absence of O2, metabolic acidosis occurs)

Front 24

Why does metabolic acidosis occur in the absence of oxygen?

Back 24

Glycolysis and Krebs cycle result in the production of acid. The ETC consumes H+, resulting in maintenance of pH. However, in the absence of O2, the ETC cannot maintain this balance.

Front 25

What are the primary sites of free radical production within mitochondria?

Back 25

Complex I and III

Front 26

List 3 ischemia-induced alterations that can occur in the ETC.

Back 26

1. Age-dependent accumulation of Ca2+
2. pH and Ca2+-dependent dissociation of cyto c
3. Complex I inactivation

Front 27

How can superoxide anion be converted to hydrogen peroxide?

Back 27

Superoxide dismutase (SOD)

Front 28

How is a hydroxyl radical produced from hydrogen peroxide?

Back 28

Metal ions (Fe2+, Cu2+) are oxidized by hydrogen peroxide, resulting in the production of hydroxyl radical (*OH).

(Superoxide anion --> H2O2 --> *OH)

Front 29

Which Kreb cycle enzymes are particularly sensitive to oxidative modification?

Back 29

1. Aconitase
2. a-ketogluterate DH

*Can undergo reversible oxidative modification that limits free radical production and oxidative damage.

Front 30

How can hydrogen peroxide be converted to H2O?

Back 30

1. Glutathione peroxidase
2. Peroxiredoxin
3. Catalase

Front 31

Which enzyme regenerates glutathionine peroxidase?

Back 31

Glutathione reductase

Front 32

Which enzyme regenerates peroxiredoxin?

Back 32

Thioredoxin reductase

Front 33

List 3 factors that can cause the transition from reversible regulation of free radicals to oxidative damage.

Back 33

1. Aging
2. Obesity
3. Diabetes