Respiratory (Electron Transport) Chain (ETC) and ATP Generation (Oxidative Phosphorylation)

Vocabulary review cards covering the Electron Transport Chain, oxidative phosphorylation, key components, mechanisms, and related concepts from the lecture notes.

Electron Transport Chain (ETC)

A series of protein-bound, membrane-embedded carriers in the inner mitochondrial membrane that transfer electrons from NADH/FADH2 to O2, while pumping protons to generate a proton-motive force for ATP synthesis.

Inner mitochondrial membrane

The membrane where the ETC resides; separates the matrix from the intermembrane space and hosts proton pumping to create a gradient.

NADH and FADH2

Reduced cofactors that donate electrons to the ETC (NADH to Complex I; FADH2 to Complex II) and become oxidized in the process.

Oxygen (O2) as final electron acceptor

The last electron acceptor in the ETC, reduced to water (H2O) at the end of electron transport.

Complex I (NADH dehydrogenase / NADH-CoQ reductase)

Transfers electrons from NADH to coenzyme Q (CoQ) and pumps protons across the inner mitochondrial membrane; contains Fe-S clusters.

Complex II (Succinate dehydrogenase / Succinate-CoQ reductase)

Transfers electrons from FADH2 to CoQ; part of the TCA cycle; contains Fe-S clusters; does not pump protons.

Coenzyme Q (CoQ; ubiquinone)

Lipophilic, membrane-bound electron carrier that shuttles electrons between Complexes I/II and III; reduced to CoQH2.

Complex III (Cytochrome b-c1 complex / ubiquinone-cytochrome c reductase)

Transfers electrons from CoQ to cytochrome c; contains Fe-S centers and hemes; contributes to proton pumping.

Cytochrome c

Small, water-soluble heme protein in the intermembrane space that transfers electrons from Complex III to Complex IV.

Complex IV (Cytochrome c oxidase)

Final ETC complex that reduces O2 to H2O; contains copper centers (CuA, CuB) and heme a/a3; pumps protons.

Fe-S clusters

Iron–sulfur prosthetic groups in ETC proteins (I, II, III) that mediate electron transfer and influence redox potentials.

Heme prosthetic groups / Cytochromes

Iron-containing heme centers in cytochromes that shuttle electrons within the ETC (e.g., in Complex III and IV).

Redox potential (E0’)

A measure of a redox couple’s tendency to acquire electrons; dictates the direction of electron flow from more negative to more positive potentials.

Redox waterfall / pathway of electron flow

Sequential transfer of electrons through ETC driven by increasingly positive redox potentials toward O2.

Proton gradient (DpH) and membrane potential (DV)

The proton-motive force Δp = Δψ + ΔpH across the inner mitochondrial membrane that drives proton re-entry and ATP synthesis.

Proton-motive force (Δp)

The combined chemical and electrical gradient that powers ATP synthesis via ATP synthase.

Chemiosmotic theory

Concept that ATP synthesis is driven by the proton gradient across the inner mitochondrial membrane, established by the ETC.

ATP synthase (F0F1-ATP synthase)

Enzyme complex that uses the proton-motive force to synthesize ATP from ADP and Pi; located in the inner mitochondrial membrane.

F0 subunit

Proton channel component of ATP synthase embedded in the inner mitochondrial membrane.

F1 subunit

Catalytic component of ATP synthase extending into the matrix; contains αβ subunits that synthesize ATP.

Gamma subunit

Stalk-like subunit that rotates within F1 to drive conformational changes in the β subunits during ATP synthesis.

Beta subunits

Catalytic αβ subunits of F1 that actually catalyze ATP formation from ADP and Pi.

ATP synthase mechanism (open/loose/tense states)

The three conformations (O, L, T) of the β-subunits drive ATP binding, synthesis, and release during catalysis.

Proton channel vs. ATPase site

F0 forms the proton channel; F1 contains the ATPase active site where ATP is produced.

Uncoupling protein 1 (UCP1) / Thermogenin

Protein in brown adipose tissue that uncouples ETC from ATP synthesis by shuttling protons back into the matrix, releasing energy as heat.

Uncouplers (e.g., DNP)

Lipophilic compounds that dissipate the proton gradient, uncoupling oxidation from phosphorylation and producing heat instead of ATP.

CoQ10 (ubiquinone)

Coenzyme Q in its ubiquinone form; fat-soluble carrier concentrated in tissues like heart; transports protons/Electrons and participates in the Q cycle.

Cyanide poisoning

CN− inhibits Complex IV (cytochrome c oxidase), blocking O2 reduction and halting the ETC.

Iron deficiency and the ETC

Reduces Fe-S cluster integrity in ETC complexes (I, II, III), impairing electron transfer and energy production.

OXPHOS diseases

Disorders caused by mutations affecting oxidative phosphorylation, including ETC complexes, ATP synthase subunits, mtDNA, or related components.

Mitochondrial DNA (mtDNA)

Maternally inherited mitochondrial genome; mutations can cause OXPHOS diseases affecting ETC components.

Water formation at Complex IV

O2 is reduced to H2O as electrons pass through Complex IV, completing the respiratory chain.