Electron Transport Chain
The cellular powerhouse finale. The electron transport chain (ETC) is where the magic happens—electrons from NADH and FADH₂ cascade through protein complexes, pumping protons to create a gradient that drives ATP synthase. This is where oxygen is consumed and 90% of cellular ATP is produced.
The Five Complexes
Complex I (NADH-DH)
Accepts electrons from NADH. Pumps 4 H⁺. Contains iron-sulfur clusters. Largest complex.
Complex II (Succinate-DH)
Accepts electrons from FADH₂. Part of Krebs cycle too. NO proton pumping. Contains FAD.
CoQ10 (Ubiquinone)
Mobile carrier. Collects from I & II. Delivers to Complex III. Lipid-soluble.
Complex III (Cytochrome bc1)
Receives from CoQ10. Pumps 4 H⁺. Q-cycle mechanism. Contains cytochromes b and c1.
Cytochrome c
Mobile carrier in intermembrane space. Connects III to IV. Also involved in apoptosis.
Complex IV (Cytochrome c Oxidase)
Final electron acceptor. O₂ reduced to H₂O. Pumps 2 H⁺. Contains copper and iron.
Complex V (ATP Synthase)
H⁺ flow back through ATP synthase. Rotation drives ATP production. ~3 H⁺ = 1 ATP. The molecular turbine that harvests proton gradient energy.
Chemiosmosis
Proton Gradient
- Electron flow: Powers proton pumping
- H⁺ buildup: Intermembrane space
- Electrochemical: Both charge and concentration
- ~10 H⁺: Pumped per NADH
ATP Synthesis
- F₀ subunit: Proton channel
- F₁ subunit: Catalytic (ATP synthesis)
- Rotation: Mechanical work → chemical
- ~2.5 ATP: Per NADH
Key Nutrients for ETC
CoQ10 (Ubiquinone)
Essential electron carrier. Declines with age, statins deplete. Supplements help.
Iron
Cytochromes contain heme iron. Iron-sulfur clusters. Critical for electron transfer.
Copper
Complex IV contains copper centers. Required for O₂ reduction.
Riboflavin (B2)
FMN in Complex I. FAD in Complex II. Essential flavin cofactors.
Oxygen
Final electron acceptor. Without O₂, chain backs up. Becomes H₂O.
PQQ
Supports mitochondrial biogenesis. May help ETC function. Newer research area.
When ETC Goes Wrong
ROS Generation
1-2% of electrons escape. Form superoxide. Source of oxidative stress. Complexes I and III leak most.
Mitochondrial Diseases
Genetic defects in ETC. Muscle weakness, neurodegeneration. Often childhood onset.
Aging
ETC efficiency declines with age. More ROS, less ATP. Mitochondrial theory of aging.
Toxin Damage
Cyanide blocks Complex IV. Rotenone blocks Complex I (Parkinson's link).
Chronic Fatigue
ETC dysfunction = less ATP. Fatigue, brain fog. ME/CFS involves mitochondria.
Neurodegeneration
Brain needs huge ATP. Complex I dysfunction in Parkinson's. Alzheimer's mitochondrial issues.