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Explain the biological purpose of the electron transport chain
Transfers electrons from NADH/FADH₂ to O₂ while pumping protons to build proton-motive force
Explain the biological purpose of oxidative phosphorylation
Uses proton-motive force to synthesize ATP from ADP and Pi
Explain why ETC and oxidative phosphorylation are separate but coupled processes
ETC generates proton gradient; ATP synthase uses it to make ATP
Explain why electrons flow spontaneously through the ETC
Move from lower to higher reduction potential carriers toward O₂
Explain why oxygen is the terminal electron acceptor
Highest reduction potential; forms stable H₂O
Explain why ETC stops when oxygen is absent
Electrons cannot be passed off; carriers remain reduced
Explain the reaction catalyzed by Complex I
NADH transfers electrons to ubiquinone while protons are pumped
Explain the role of FMN in Complex I
Accepts two electrons from NADH
Explain the role of iron–sulfur clusters in Complex I
Transfer single electrons stepwise
Explain how proton pumping occurs in Complex I
Electron transfer induces conformational changes that move protons
Explain why Complex I is a major regulatory entry point
Handles most cellular NADH
Explain the reaction catalyzed by Complex II
Succinate → fumarate; electrons transferred to ubiquinone
Explain why Complex II does not pump protons
Insufficient free energy from succinate oxidation
Explain why FAD is used instead of NAD⁺ in Complex II
Succinate oxidation potential too low for NAD⁺ reduction
Explain why Complex II is part of both TCA and ETC
Catalyzes TCA reaction and feeds electrons into ETC
Explain the role of ubiquinone in the ETC
Mobile lipid-soluble electron carrier
Explain why ubiquinone can carry both electrons and protons
Can exist in oxidized, semiquinone, and reduced forms
Explain why ubiquinone is essential for ETC flexibility
Accepts electrons from multiple complexes
Explain the reaction catalyzed by Complex III
Transfers electrons from ubiquinol to cytochrome c
Explain the Q cycle
Mechanism that couples electron transfer to proton translocation
Explain why the Q cycle amplifies proton pumping
Two electrons result in four protons released
Explain the role of cytochrome b and c₁
Sequential electron transfer via heme groups
Explain the role of cytochrome c
Mobile protein that transfers electrons to Complex IV
Explain why cytochrome c carries only one electron
Heme iron cycles between Fe²⁺ and Fe³⁺
Explain the reaction catalyzed by Complex IV
Electrons reduce O₂ to H₂O
Explain why Complex IV is the most tightly regulated complex
Controls oxygen consumption
Explain the role of copper and heme centers in Complex IV
Facilitate electron transfer and oxygen reduction
Explain how proton pumping occurs in Complex IV
Electron transfer drives conformational proton movement
Explain what the proton-motive force consists of
Membrane potential (Δψ) + proton gradient (ΔpH)
Explain why proton pumping stores energy
Creates electrochemical gradient across membrane
Explain why inner mitochondrial membrane must be impermeable to protons
Prevents energy dissipation
Explain the structure of ATP synthase
F₀ proton channel + F₁ catalytic head
Explain the binding-change mechanism
Rotation forces β subunits through loose, tight, open states
Explain how proton flow drives ATP synthesis
Proton movement rotates c-ring and γ shaft
Explain why ATP synthesis does not require a phosphorylated intermediate
Mechanical energy drives ATP formation
Explain why ATP synthase is reversible
Can hydrolyze ATP to pump protons if gradient collapses
Explain what coupling means in oxidative phosphorylation
Electron transport linked to ATP synthesis via proton gradient
Explain respiratory control by ADP
High ADP increases ETC rate; low ADP slows ETC
Explain why ETC slows when ATP demand is low
Proton gradient builds and resists pumping
Explain why oxidative phosphorylation controls ETC rate
ETC activity depends on proton gradient usage
Explain what uncoupling is
Proton gradient dissipated without ATP synthesis
Explain how chemical uncouplers work
Carry protons across membrane, bypassing ATP synthase
Explain the effect of uncoupling on oxygen consumption
Oxygen consumption increases
Explain the effect of uncoupling on ATP production
ATP synthesis decreases
Explain why uncoupling produces heat
Energy released as thermal motion
Explain how cyanide inhibits oxidative phosphorylation
Binds Complex IV; blocks oxygen reduction
Explain how rotenone inhibits the ETC
Blocks electron transfer in Complex I
Explain how antimycin A inhibits the ETC
Blocks electron transfer in Complex III
Explain how oligomycin inhibits ATP synthesis
Blocks F₀ proton channel
Explain what happens to proton gradient when ATP synthase is inhibited
Gradient increases; ETC slows
Explain how superoxide is formed in the ETC
Electron leakage to oxygen at Complex I or III
Explain why excessive ROS is dangerous
Damages proteins, lipids, and DNA
Explain the ATP yield per NADH
Approximately 2.5 ATP
Explain the ATP yield per FADH₂
Approximately 1.5 ATP
Explain why FADH₂ yields less ATP than NADH
Bypasses proton-pumping Complex I
Explain how the ETC links to glycolysis and TCA
Uses NADH/FADH₂ produced upstream
Explain why ETC activity influences TCA cycle rate
Controls NAD⁺ availability
Explain why ETC inhibition affects gluconeogenesis
High NADH inhibits gluconeogenic enzymes
Explain everything you know about ETC and oxidative phosphorylation
ETC transfers electrons to oxygen, builds proton gradient, ATP synthase uses gradient to make ATP; tightly regulated by ADP and oxygen
Explain ETC and oxidative phosphorylation in the context of whole-body metabolism
Primary ATP source in aerobic tissues; integrates with all fuel pathways
Summarize ETC and oxidative phosphorylation in one sentence
A coupled system where electron transfer to oxygen drives proton pumping, which powers ATP synthesis via ATP synthas