Oxidative Phosphorylation & Electron Transport System

Vocabulary flashcards covering major components, mechanisms, and inhibitors of the mitochondrial electron transport chain and oxidative phosphorylation.

Oxidative phosphorylation

Process that converts the energy of electrons from NADH/FADH2 into ATP, coupling electron transfer to oxygen with ATP synthesis.

Electron transport chain (ETC) / Electron transport system (ETS)

Series of protein complexes in the inner mitochondrial membrane that pass electrons to O2 and create a proton gradient.

Mitochondrion

Organelle where the citric-acid cycle, electron transport, and oxidative phosphorylation occur; number correlates with tissue energy demand.

Inner mitochondrial membrane (IMM)

Location of ETC complexes, proton pumping, and ATP synthase.

NADH

High-energy electron carrier that donates electrons to Complex I and drives pumping of 4 H⁺ per molecule.

FADH2

Electron carrier that donates to Complex II and yields fewer pumped protons (no pumping at Complex II).

Complex I (NADH oxidase/NADH dehydrogenase)

Large L-shaped protein (≈43–47 subunits) that accepts electrons from NADH, passes them to ubiquinone, and pumps 4 H⁺.

FMN (flavin mononucleotide)

Initial electron acceptor within Complex I before electrons reach Fe-S centers.

Iron-sulfur (Fe-S) complexes

Clusters within Complex I & II that relay electrons toward ubiquinone.

Ubiquinone (Coenzyme Q10, Q)

Lipid-soluble carrier that moves within IMM, accepting electrons from Complex I/II and delivering them to Complex III.

Semiquinone

Half-reduced intermediate form of ubiquinone (one electron added).

Ubiquinol (QH2)

Fully reduced form of ubiquinone containing two alcohol groups; donates electrons in the Q-cycle.

Complex II (Succinate dehydrogenase)

Citric-acid-cycle enzyme that feeds electrons from FADH2 to ubiquinone; does not pump protons.

Succinate

Citric-acid-cycle substrate oxidized to fumarate at Complex II, generating FADH2.

Fumarate

Product of succinate oxidation in the citric-acid cycle and Complex II reaction.

Q-cycle

Mechanism in Complex III that transfers 4 H⁺ to the intermembrane space while moving electrons one at a time to cytochrome c.

Complex III (Cytochrome bc1 complex)

Receives ubiquinol, conducts the Q-cycle, moves 4 H⁺ (via chemistry, not pumping).

Cytochrome c

Soluble protein on IMM surface that carries one electron at a time from Complex III to Complex IV.

Complex IV (Cytochrome c oxidase, CCO)

Final ETC complex; pumps 2 H⁺ and reduces O2 to 2 H2O.

Chemiosmosis

ATP synthesis powered by H⁺ flow back into the matrix through ATP synthase.

ATP synthase

Enzyme that uses the proton gradient to convert ADP + Pi into ATP.

Proton motive force (PMF)

Electrochemical gradient of H⁺ across IMM generated by ETC activity.

Substrate-level phosphorylation

ATP production by direct transfer of a phosphate group in glycolysis and the citric-acid cycle, distinct from oxidative phosphorylation.

Redox potential (E°)

Measure of a molecule’s tendency to gain electrons; ETC proceeds from low (–0.315 V for NADH) to high (+0.815 V for O2).

Respirasome (super-complex)

Structural assembly of Complexes I, III, and IV that streamlines electron flow and proton pumping (10 H⁺ per NADH).

Proton pumping stoichiometry (NADH)

Complexes I, III, IV together move 10 H⁺ per NADH oxidized.

Proton pumping stoichiometry (FADH2)

Complexes II, III, IV together move 6 H⁺ per FADH2 oxidized.

Rotenone

Plant-derived poison that blocks electron transfer at Complex I.

Amytal / Barbiturates

Anesthetic drugs that inhibit Complex I activity.

Myxothiazol (or antimycin A)

Antibiotic that blocks electron transfer within Complex III.

Cyanide (CN⁻)

Potent poison that binds Complex IV, preventing O2 reduction.

Carbon monoxide (CO)

Gas that competitively inhibits O2 binding at Complex IV.

Nitric oxide (NO)

Endogenous signaling molecule that can reversibly inhibit Complex IV.

Hydrogen sulfide (H2S)

Toxic gas that interferes with Complex IV activity.

Chemiosmotic theory ("~" concept)

Idea proposed to explain how the proton gradient, rather than direct phosphorylation steps, drives ATP formation.

Citric acid cycle

Mitochondrial pathway that supplies NADH and FADH2 for the ETC by oxidizing acetyl-CoA.