Curriculum
Module 04 · 60 min
Oxidative Phosphorylation
Electron transport chain, proton-motive force, and the small drugs that uncouple them.
CoreClinicalResearch
Topics
What this module covers
- 01ETC complexes I–IV: substrates and inhibitors
- 02Chemiosmosis and ATP synthase
- 03Uncouplers: clinical and toxicologic
- 04Mitochondrial myopathies
Learning objectives
By the end of this module you will be able to
- L01Trace electron flow from NADH/FADH2 through Complex I–IV to oxygen.
- L02Explain how ATP synthase converts proton-motive force into ATP.
- L03Identify mechanisms by which cyanide, rotenone, and 2,4-DNP disrupt OXPHOS.
Expected takeaways
What you should walk away believing
- →OXPHOS produces ~26–28 of the ~30 ATP per glucose.
- →Inhibition at any complex collapses the entire chain.
- →Uncouplers dissipate proton-motive force as heat — therapeutically tempting, narrowly toxic.
Core summary
At the Core level
The mitochondrial electron transport chain shuttles electrons from NADH and FADH2 to oxygen, pumping protons to build a gradient. ATP synthase uses that gradient to phosphorylate ADP. Disrupt the chain and you disrupt nearly all cellular energy.
Evidence-graded claims
Claims, scored A–F
A
ATP synthase rotates
Direct visualization (Yoshida, Walker).
F
DNP is a safe weight-loss drug
Lethal hyperthermia.
Quiz
Check your understanding
Q1. Which complex pumps protons but accepts electrons from FADH2?
Flashcards
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Front
Final electron acceptor in OXPHOS?
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