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AI Questions (232) > Electron Transport and Oxidative Phosphorylation – I > Flashcards

Electron Transport and Oxidative Phosphorylation – I Flashcards

1
Q

What are the three requirements for the electron transport chain (ETC)?

A

An ion-impermeable membrane.

A mechanism for moving protons (H⁺) across the membrane to produce a proton gradient.

A mechanism to capture the energy as protons move down the gradient.

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2
Q

How many ATP molecules are produced from the complete oxidation of NADH and FADH₂ in the ETC?

A

NADH = 2.5 ATP

FADH₂ = 1.5 ATP

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2
Q

What is the role of oxygen in the ETC?

A

Oxygen acts as the final electron acceptor, combining with electrons and protons to form water (H₂O).

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3
Q

Name the four complexes of the ETC and their prosthetic groups.

A

Complex I (NADH-CoQ Reductase): FMN, Fe-S

Complex II (Succinate-CoQ Reductase): FAD, Fe-S

Complex III (CoQ-Cyt c Reductase): iron-porphyrin, Fe-S

Complex IV (Cytochrome Oxidase): iron-porphyrin, Cu

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4
Q

Which complex in the ETC does not pump protons across the membrane?

A

Complex II (Succinate-CoQ Reductase) because the energy released is insufficient for proton pumping.

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5
Q

What is the Q cycle, and where does it occur?

A

The Q cycle describes electron transfer in Complex III (Ubiquinol-Cytochrome c Reductase).

It involves two ubiquinone binding sites and translocates 4 protons per 2 electrons transferred to cytochrome c.

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6
Q

What is the central component of cytochromes involved in redox reactions?

A

An iron atom (in the heme group).

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7
Q

What is chemiosmosis?

A

The process by which the proton gradient (protonmotive force) drives ATP synthesis via ATP synthase.

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8
Q

What are uncouplers, and how do they work?

A

Uncouplers (e.g., 2,4-DNP) dissipate the proton gradient by making the membrane permeable to H⁺.

This stops ATP synthesis but allows continued electron transport, releasing energy as heat.

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9
Q

What is the P/O ratio for NADH and FADH₂?

A

NADH: 2.5 ATP per ½ O₂

FADH₂: 1.5 ATP per ½ O₂

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9
Q

What is the function of brown adipose tissue?

A

It generates heat (thermogenesis) via UCP-1, which uncouples proton flow from ATP synthesis.

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10
Q

What is the role of ATP synthase (Complex V)?

A

It uses the proton gradient to synthesize ATP from ADP and inorganic phosphate (Pᵢ).

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11
Q

Which mitochondrial transporter exchanges ADP for ATP?

A

The adenine nucleotide translocator (ANT).

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12
Q

What happens if the proton gradient is disrupted?

A

Electron transport continues, but ATP synthesis stops, and energy is released as heat (e.g., in uncoupling).

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13
Q

Name two inhibitors of Complex IV.

A

Cyanide (binds to cytochrome a₃)

Carbon monoxide (binds to heme iron).

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14
Q

What are the two main mitochondrial shuttles for transferring reducing equivalents (NADH) from the cytosol to the matrix?

A

Malate-Aspartate Shuttle (produces NADH in the matrix, yielding ~2.5 ATP).

Glycerol-3-Phosphate Shuttle (produces FADH₂ in the matrix, yielding ~1.5 ATP).

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15
Q

Why does Complex II (Succinate Dehydrogenase) not pump protons?

A

The energy released from succinate oxidation (FADH₂ → Q) is insufficient to drive proton translocation.

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16
Q

What is the terminal electron acceptor in Complex IV, and what is produced?

A

Oxygen (O₂) accepts 4 electrons and 4 protons to form 2 H₂O, preventing toxic reactive oxygen species (ROS).

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17
Q

Name two inhibitors of Complex I and their effects.

A

Rotenone (blocks electron transfer from Fe-S to Q).

Piericidin A (mimics Q, halting electron flow).
→ Both stop NADH oxidation and proton pumping.

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18
Q

What is the role of cytochrome c in the ETC?

A

A mobile electron carrier that shuttles electrons from Complex III to Complex IV.

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19
Q

How does thermogenin (UCP-1) work in brown fat?

A

It uncouples proton flow from ATP synthesis, dissipating the gradient as heat (non-shivering thermogenesis).

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20
Q

What is the difference between the inner and outer mitochondrial membranes in terms of permeability?

A

Outer membrane: Porous (allows small molecules/nucleotides).

Inner membrane: Impermeable (requires transporters like ANT for ATP/ADP).

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21
Q

Which enzyme in the TCA cycle is also part of Complex II?

A

Succinate Dehydrogenase (links TCA to ETC via FADH₂).

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22
Q

What happens if ATP synthase is removed from the inner membrane?

A

Electron transport continues, but no proton gradient is maintained (no ATP synthesis).

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22
Name two mitochondrial transporters and their substrates.
Adenine Nucleotide Translocator (ANT): Exchanges ADP (in) for ATP (out). Phosphate Transporter (Pᵢ): Co-imports H₂PO₄⁻ with H⁺.
23
What is the significance of the Nernst equation in the ETC?
It relates redox potential (ΔE) to free energy (ΔG), predicting electron flow direction between carriers.
24
How does aspirin act as an uncoupler?
At high doses, it increases membrane permeability to H⁺, dissipating the gradient and causing fever.
25
What are the subunits of ATP synthase, and which part catalyzes ATP synthesis?
F₀: Membrane-embedded proton channel (a, b, c subunits). F₁: Catalytic head (α, β, γ, δ, ε subunits; β subunits synthesize ATP).
26
What prevents ROS formation in Complex IV?
Tight binding of O₂ to the heme a₃-Cuᴮ binuclear center, ensuring full reduction to H₂O.
27
Why is the malate-aspartate shuttle more efficient than the glycerol-3-P shuttle?
It transfers electrons to NADH (yields 2.5 ATP) vs. FADH₂ (1.5 ATP) in the glycerol-3-P shuttle.
28
What is the role of Fe-S clusters in the ETC?
They are one-electron carriers that shuttle electrons between flavins (FMN/FAD) and cytochromes/Q.
28
What is the effect of oligomycin on ATP synthase?
It blocks the F₀ proton channel, halting ATP synthesis and electron transport (no H⁺ backflow).
29
Which complex is inhibited by cyanide, and what is the mechanism?
Complex IV (Cytochrome Oxidase); binds to heme a₃, blocking O₂ reduction.
30
How does antimycin A inhibit the ETC?
Binds to Complex III’s Qᵢ site, blocking electron transfer to cytochrome b and halting the Q cycle.
31
What happens to the P/O ratio if electrons enter at Complex II (via FADH₂)?
It drops to 1.5 ATP/½ O₂ (vs. 2.5 for NADH) because fewer protons are pumped.
32
Name two enzymes located in the mitochondrial matrix.
Citrate Synthase (TCA cycle). Pyruvate Dehydrogenase (links glycolysis to TCA).
33
What is the protonmotive force (Δp)?
The combined electrochemical gradient (ΔΨ + ΔpH) driving protons through ATP synthase.
34
Why is CoQ (ubiquinone) unique among ETC carriers?
It is lipid-soluble, shuttling electrons between complexes while transporting protons across the membrane.
35
What is the role of cristae in mitochondria?
They increase surface area for ETC complexes and ATP synthase, boosting oxidative phosphorylation.
36
How does the binding-change model explain ATP synthesis?
Proton flow rotates the γ subunit of F₁, inducing conformational changes in β subunits to synthesize/release ATP.
37
What happens to oxygen consumption when an uncoupler (e.g., DNP) is added to mitochondria inhibited by oligomycin?
O₂ consumption increases because the uncoupler dissipates the proton gradient, allowing electron transport to continue without ATP synthesis.
37
Name two inhibitors of Complex I and their mechanism.
Rotenone and piericidin A block electron transfer from Fe-S clusters to ubiquinone (Q). → Halts NADH oxidation and proton pumping.
37
What is the clinical presentation of carbon monoxide (CO) poisoning?
Cherry-red skin/lips (pulse oximeter falsely normal). Headache, nausea, tachypnea, tachycardia. Treatment: 100% O₂ or hyperbaric O₂.
38
How does cyanide (CN⁻) inhibit the ETC, and how is it treated?
Binds to Complex IV (cytochrome oxidase), blocking O₂ reduction. Treatment: Sodium thiosulfate (converts CN⁻ to thiocyanate) + nitrites (form methemoglobin to bind CN⁻).
39
What is the effect of oligomycin on ATP synthase and the proton gradient?
Blocks the F₀ proton channel, stopping ATP synthesis. Proton gradient builds up, halting electron transport (no H⁺ backflow).
39
Why does antimycin A inhibit the Q cycle?
Binds to Complex III’s Qᵢ site, preventing electron transfer to cytochrome *b* and ubiquinone recycling.
40
What mitochondrial transporter exchanges ADP for ATP?
Adenine nucleotide translocator (ANT). Inhibited by atractyloside and bongkrekic acid.
41
Which part of ATP synthase forms the proton channel?
The F₀ subunit (embedded in the membrane). F₁ subunit catalyzes ATP synthesis.
42
What are the clinical symptoms of CN⁻ poisoning?
Seizures, tachycardia, tachypnea, headache, flushing. Sources: Nitroprusside, burning plastics, mining.
43
How does 2,4-DNP affect O₂ consumption and ATP production?
↑ O₂ consumption (uncouples ETC from ATP synthesis). ↓ ATP production (proton gradient dissipated as heat).
44
What is the role of the F₁ subunit in ATP synthase?
Contains catalytic β subunits that synthesize ATP via conformational changes induced by proton flow through F₀.
45
Which ETC complex is inhibited by myxothiazol?
Complex III (blocks electron transfer at the Q₀ site).
46
What happens to NADH/NAD⁺ ratio if Complex I is inhibited?
NADH accumulates (cannot donate electrons to ETC).
47
Why is TMPD used in ETC experiments?
It donates electrons directly to cytochrome c, bypassing Complexes I–III to test Complex IV activity.
48
What is the chemiosmotic hypothesis?
Proton gradient (Δp) drives ATP synthesis via ATP synthase Requires: Impermeable membrane to H⁺. Proton pumping by ETC. Coupled ATP synthase activity.
49
Which inhibitor blocks both ATP synthesis and electron transport?
Oligomycin (blocks ATP synthase, causing proton gradient to stall ETC).
50
What is the source of CO poisoning in enclosed spaces?
Incomplete combustion (e.g., car engines, grills, fireplaces).
51
How does FCCP uncouple oxidative phosphorylation?
As a protonophore, it dissipates the proton gradient by carrying H⁺ across the membrane.
52
What is the correct sequence of electron acceptors in Complex IV?
Cytochrome *c* → Cuₐ → heme *a* → heme a₃-Cuᴮ → O₂.
53
What happens to ATP production if the malate-aspartate shuttle is blocked?
ATP yield (cytosolic NADH cannot enter mitochondria; backup glycerol-3-P shuttle produces FADH₂ → 1.5 ATP).
54
y does cyanide (CN⁻) poisoning cause a bright red appearance in victims despite hypoxia?
CN⁻ inhibits Complex IV, blocking O₂ utilization → venous blood remains oxygenated (unable to offload O₂ to tissues).
55
What is the mechanism of DCCD (dicyclohexylcarbodiimide) as an ATP synthase inhibitor?
Binds to Asp61 in the *c* subunit of F₀, blocking proton flow through the channel.
56
How does atractyloside inhibit oxidative phosphorylation?
Blocks the ANT (ADP/ATP translocator), preventing ADP entry into mitochondria → halts ATP synthesis.
57
What is the significance of TMPD (tetramethyl-p-phenylenediamine) in ETC experiments?
Artificial electron donor to cytochrome *c*, bypassing Complexes I–III to test Complex IV activity (e.g., in the presence of cyanide).
58
Why do uncouplers (e.g., DNP) cause hyperthermia?
Dissipated proton gradient releases energy as heat instead of ATP production (used in brown fat for thermogenesis).
59
What happens to intracellular [Ca²⁺] during ETC inhibition?
↑ Ca²⁺ (due to reduced ATP for Ca²⁺ pumps) → activates apoptotic pathways.
60
What is the primary defect in Leigh syndrome (mitochondrial disease)?
Mutations in Complex IV (cytochrome oxidase) or other ETC components → severe ATP deficiency in CNS/muscle.
61
Why does methemoglobin treat cyanide poisoning?
CN⁻ binds preferentially to Fe³⁺ in methemoglobin over cytochrome a₃, sparing Complex IV.
62
What is the P/O ratio when electrons enter via glycerol-3-phosphate shuttle?
1.5 ATP/O₂ (electrons enter as FADH₂ at Q, bypassing Complex I proton pumps).
63
What is the role of Cuₐ and Cuᴮ in Complex IV?
Cuₐ: Accepts electrons from cytochrome *c*. Cuᴮ: Part of the binuclear center with heme a₃ to reduce O₂ → H₂O.
64
Why does CO poisoning initially cause tachycardia/tachypnea?
Tissue hypoxia triggers compensatory sympathetic response despite normal SpO₂ (CO binds Hb 200× tighter than O₂).
65
What happens to ROS production if Complex III is inhibited?
↑ Superoxide (O₂⁻) due to electron leakage from stalled ubiquinone (Q cycle intermediates).
66
What is the clinical triad of severe cyanide poisoning?
Coma/seizures (CNS hypoxia). Cardiovascular collapse (myocardial hypoxia). Lactic acidosis (anaerobic metabolism).
67
Why does malonate inhibit the ETC?
Competitive inhibitor of succinate dehydrogenase (Complex II) → blocks FADH₂ production.
68
Why is nitroprusside a risk for CN⁻ toxicity?
Metabolized to release CN⁻ → requires co-administration of thiosulfate for detoxification.
69

AI Questions (232) (22 decks)

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