Oxidative Phosphorylation Flashcards

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1
Q

Describe permeability of outer mitochondrial membrane.

A

Permeable to small molecules and small proteins.

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2
Q

Describe permeability of inner membrane.

A

Impermeable to small and large molecules

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3
Q

Where does oxidative phosphorylation occur?

A

Inner mitochondrial membrane

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4
Q

Explain how you can have an electrochemical gradient with no membrane potential.

A

Negative membrane potential inside, positive membrane potential outside.

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5
Q

What is the fastest way and preferred way for NADH to shuttle H+?

A

Take it straight to complex I of ETC from cytosol to mitochondrial matrix

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6
Q

What is a slower, irreversible way for NADH to shuttle H+ to ETC?

A

NADH transfers H+ to glycerol 3-phosphate which then moves into the inner mitochondrial matrix where FAD takes the H+ and moves it to CoQ of the ETC.

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7
Q

Describe the function of the first complex in ETC and its name.

A

NADH Dehydrogenase complex

Transfer electron from NADH to chain of iron-sulfur clusters. Reduces ubiquinone to ubiquinol. Then Ubiquinone or CoQ transfers protons to next complex.

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8
Q

Describe function of third complex in ETC.

A

Cytochrome b-c1 complex - CoQ recycling and transfer of electrons to cytochrome C

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9
Q

Describe function of fourth complex in ETC.

A

Cytochrome oxidase

  • 4 electrons enter one at a time from cytochrome c
  • Cu, protein side chains, Fe atom on cytochrome oxidase collect all the electrons
  • O2 binds to the active site and is reduced
  • 4 protons are pumped out of matrix back into intermembrane space
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10
Q

How many H+ ions does it take to make 1 ATP?

A

About 3

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11
Q

Describe protein transport conformations of cytochrome oxidase.

A

Conformation A - high affinity for H+, proton uptake
Conformation B - H+ binds to cytochrome oxidase
Conformation C - low affinity for H+, proton released to outside of cell

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12
Q

What is the total aerobic energy yield from one molecule of glucose? Break down where the ATPs come from.

A

32 ATP total

Glycolysis (2 NADH, 2 ATP)
PDH complex (2 NADH)
TCA (6 NADH, 2 FADH2, 2 GTP)

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13
Q

What is the total anaerobic energy yield from one molecule of glucose?

A

2 ATP total

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14
Q

What binding-specificity does electron transport rely on for stability and energy efficiency?

A

Binding-specificity of mobile carriers with complexes I-IV

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15
Q

Where is ubiquinone a free carrier?

A

Lipids

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16
Q

Where is cytochrome C a free carrier?

A

intermembrane space

17
Q

How will a low NAD:NADH ratio affect respiration?

A

It will slow it b/c there is no reducing agent available

18
Q

How will a steep proton gradient affect respiration?

A

It will slow it b/c it will slow electron transfer

19
Q

How will a high ADP level affect respiration?

A

It will increase it

20
Q

What is an NADH dehydrogenase inhibitor of ETC?

A

Amytal rotenone

21
Q

What is a cytochrome b-c1 complex inhibitor of ETC?

A

Antimycin A

22
Q

What are some cytochrome c oxidase inhibitors of ETC?

A

CN, CO, azide

23
Q

What is an F1FoATPase inhibitor?

A

Oligomycin

24
Q

What is an ATP/ADP exchange inhibitor?

A

Atractyloside bongkrektate

25
Q

What are some uncouplers of respiration? How do they work?

A

FCCP, DNP (they collapse the H+ gradient)

They collapse the proton gradient and thus allow protons to re-enter the mitochondrial matrix without energy being captured as ATP—the energy is released as heat and the
process is called non-shivering thermogenesis. This prevents the synthesis of ATP but will normally increase respiration and electron transport.

26
Q

What is a reactive oxygen species and how does it form?

A

Electron transfer in the mitochondria occasionally allows oxygen to escape before it is fully reduced to water. Escape as a superoxide anion radical (-O2) can lead to the formation of H2O2 or the hydroxyl radical (ROS) which can induce DNA and protein damage.

27
Q

What do superoxide dismutase and glutathione peroxidase do?

A

Converts superoxide anion radical into intermediary H2O2 before glutathione peroxidase adds an H, making a water molecule.

28
Q

How are mitochondrial myopathies obtained?

A

They are maternally inherited defects in genes encoding mitochondrial tRNAs. Mitochondrial DNA mutates at a much faster rate than nuclear DNA, increasing chance of mitochondrial myopathies.

29
Q

How do mitochondrial myopathies present?

A

Muscle weakness and/or neurological symptoms

30
Q

What are the two categories for mitochondrial myopathies?

A

MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, stroke-like episodes)
MERRF (myoclonic epilepsy and ragged red fibers)