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74 Cards in this Set

  • Front
  • Back
Reduction is a _____ of electrons.
Gain (OIL RIG)
Oxidation is a _____ of electrons.
Loss (OIL RIG)
What is the standard half reaction for SRP?
2H+ + 2e- <--> H2
What does a negative E mean? Good oxidizing or good reducing agent?
Good reducing agent!
How does the SRP differ between standard and physiological conditions?
pH 7, not pH 0
What is the E value of the standard half-reaction at physiological conditions?
E = - 0.421 V
(know that it is lower)
How do you calculate the change in SRP?
∆E = E (e- acceptor) - E (e- donor)
If the ∆E is negative, will the reaction be spontaneous? Why?
Non-spontaneous
∆G = - nF∆E
Which equation would you use to calculate the SRP of reaction NOT under standard conditions? i.e. not 1:1 ratios of reductant and oxidant
Nernst equation
∆E = ∆E˚ - (RT/nF)(ln ([Ared][Box+])/[Ared+][Box]))
Which compound donates its electrons to Complex I of the ETC?
NADH
What donates its electrons to Complex II of the ETC? Which enzyme creates this compound?
FADH2
Succinyl dehydrogenase (CAC)
What is the total energy released by the full ETC reaction from NADH?
218 kJ/mol
Is the energy released from Complex II sufficient to produce ATP?
No, only 16.4 kJ/mol are released
How much energy is need to drive the following reaction reaction:
ADP + Pi --> ATP
30.5 kJ/mol
Why is the physiological efficiency of ATP synthesis coupled to the ETC only 70%?
[H+] diffuse back to matrix without going through ATP synthase.
e.g. Pyruvate translocase
What are the inhibitors of the ETC complexes?
Complex I --> Rotenone
Complex II -->Antimycin A
Complex III --> Cyanide
Is ATP directly produced from the ETC?
NO!!!!!!! ATP synthase is a COMPLETELY separate complex.
How many ATP can be produced from the energy released by FADH2 oxidation? Why?
2 ATP, since the electrons are released at complex II.
How many ATP are produced from NADH oxidation?
3 ATP
What is the final electron recipient of the ETC? What is formed?
Oxygen.
1/2 O2 + 2H+ ---> H2O
Why does the P/O ratio diminish with electron entry further down the ETC?
Less oxidation steps occur and less free energy is released to drive the proton gradient.
Is Cytochrome C mobile or immobile? Coenzyme Q?
They are both mobile
What is the active centre of cytochrome?
Heme
How many electrons can a heme handle at once?
1 electron
Does the SRP increase or decrease along the ETC?
Increases
NADH --> NAD+ (-0.315 V)
1/2 O2 + 2H+ --> H2O (+0.815 V)
What are the three states of Coenzyme Q?
Oxidized: Quinone
Partially reduced: Semiquinone
Reduced: Hydroquinone
Name a role of Cytochrome C outside of the ETC.
Apoptosis
In which complexes are FeS clusters found?
Complex I and III
Where is cytochrome C located? In or on the membrane?
On the membrane
Can ATP synthase work in reverse? If yes, when?
It can work in reverse when proton gradient is present.
How does the ETC store energy? (This is a really easy question)
Proton gradient in the IMS.
Name the 5 points supporting chemiosomotic theory?
- Oxphos needs intact membrane
- IMM impermeable to ions
- ETC associated with proton transport out of matrix
- reconstitution experiments
- uncoupling agents increase permeability of IMM and stop ATP synthesis
What is the chemiosmotic theory?
ATP synthesis requires a proton gradient created by pumping of protons from matrix to IMS.
Which lipids make the IMM impermeable?
Cardiolipins (comes from 2X PG)
Name an uncoupling agent? Compound that increases permeability of IMM
DNP or FCCP
In what tissue does natural coupling occur? What is its utility?
- Brown Fat Tissue
- Used in thermogenesis
Which hormone regulates natural uncoupling? What is its mechanism of action?
Norepinephrine --> Adenylate cyclase --> cAMP --> PKA --> UCP1 --> thermogenin
Which proton channel is opened in natural uncoupling? What are its inhibitors?
- Thermogenin
- Inhibited by ATP, ADP, GTP, GDP
What are the two mechanisms for proton transport? Which one is more plausible?
- Redox loop (redox centre accepts H+ and e- at same time)

- Proton pump (binds H+, reduction causes conformation change, release of H+, reoxidation) --> more plausible
Which subunits compose Fo ATP synthase?
a1 b2 c12
What is the function of the c subunits of Fo ATP synthase? What are they attached to?
Act as a rotor attached to the gamma subunit.
Is Fo ATP synthase located outside of the membrane or inside?
Integral membrane protein
Where is the proton channel of ATP synthase located?
Where the a and c subunits meet
What are the five subunits that compose F1 ATP synthase?
alpha3, beta3, gamma, delta, epsilon
Where is F1 ATP synthase located?
In the matrix of the mitochondria, attached to the IMM
What is the rotor of ATP synthase composed of?/
gamma, epsilon, c12 subunits
What composes the stator of ATP synthase?
ab2 - alpha3, beta3, delta
What is the purpose of the b2delta structure of the stator?
Prevents the alpha3, beta3 subunits from moving
What are the 3 states of the alpha3,beta3 subunit? aka mechanism of ATP synthesis
O: low affinity, catalytically inactive
L: loose affinity, catalytically inactive
T: high affinity, catalytically active
What does the L state subunit of ATP synthase bind?
ADP + Pi
Where does the energy for the change of state of the ATP synthase subunits come from?
H+ gradient turns rotor, provides energy for the change of state.
What does the T state become with energy?
O state
How was the rotation of ATP synthase demonstrated?
Bound fluorescent actin filament to ATP synthase and watched it turn in presence of ATP.
BADASS!
How is phosphate transported inside the mitochondria?
H+/Pi symport
How is ADP moved into the mitochondria? ATP? How is this driven?
They simultaneously moved by adenine nucleotide translocase.
Negative charge is transported out, so proton gradient drives the reaction.
Does gluconeogenesis use carbohydrate precursors?
NO, only non-carbohydrate precursors.
What is the starting material for gluconeogenesis?
Oxaloacetate
Is there a NET pathway to convert Acetyl-CoA to oxaloacetate? An indirect pathway?
No net pathway.
Can go indirectly through CAC
True or False?
Gluconeogenesis is a reversal of glycolysis.
False
What are the four main enzymes involved in gluconeogenesis?
Pyruvate carboxylase
PEPCK
FBPase
G6Pase
What are the substrate of pyruvate carboxylase? Does it use ATP?
- Pyruvate and CO2
- Uses 1 ATP
What is released by PEPCK? Does it use ATP?
- CO2 is released
- Uses GTP, not ATP
How is oxaloacetate transported out of the mitochondria?
Malate/Aspartate Shuttle
Which path is favoured for the export of oxaloacetate from the mitochondria under normal conditions? When doing exercise?
- Malate --> produces 1 NADH
- Aspartate, since the gluconeogenic precursor is lactate, which can be oxidized back to pyruvate to form NADH
True or False?
G6Pase is found in almost every tissue.
False, only in the liver
What is the energetic cost of gluconeogenesis?
2 ATP, 2 GTP
Is the cost of doing gluconeogenesis worth it?
Yes, it is the price to pay to maintain independent regulation.
What are the inhibitors of FBPase?
AMP, F26P
What activates Pyruvate carboxylase?
Acetyl-CoA
What stimulates PEPCK? Inhibits?
- Stimulated by glucagon, thyroid hormone, glucocorticoids
- Inhibited by insulin
What is the Cori cycle?
Regulation between two tissues through bloodstream.
Lactate from muscle goes to liver, where it undergoes gluconeogenesis. Glucose is then sent back in blood.
Under long fasting conditions, what is Acetyl-CoA converted to?
Ketone bodies
What does the metabolism of alcohol produce in large quantities?
NADH
What effect does Alcohol have on the CAC? Gluconeogenesis?
- Inhibition of CAC, due to high NADH level
- pyruvate shifts to lactate, oxaloacetate shifts to malate