Electron transport chain and oxidative phosphorylation

  • NADH electrons from glycolysis enter mitochondria via the malate-aspartate or glycerol-3-phosphate shuttle.
  • FADH2 electrons are transferred to complex II (at a lower energy level than NADH). The passage of electrons results in the formation of a proton gradient that, coupled to oxidative phosphorylation, drives the production of ATP.
  • ATP produced via ATP synthase
    • 1 NADH → 2.5 ATP; 1 FADH2 → 1.5 ATP
    • Liver, kidney and heart utilizes the Malate-aspartate shuttle producing 3 ATPs=1 NADH. Skeletal muscle and brain uses glycerol-phosphate shuttle 1 NADH=2 ATP.
  • Oxidative phosphorylation poisons
    • Electron transport inhibitors
      • Directly inhibit electron transport, causing a ↓ proton gradient and block of ATP synthesis.
      • Rotenone: complex one inhibitor.
      • “An-3-mycin” (antimycin) A: complex 3 inhibitor.
      • Cyanide, carbon monoxide, azide (the -ides, 4 letters) inhibit complex IV.
    • ATP synthase inhibitors
      • Directly inhibit mitochondrial ATP synthase, causing an ↑ proton gradient. No ATP is produced because electron transport stops.
      • Oligomycin inhibits complex V
    • Uncoupling agents
      • ↑ permeability of membrane, causing a ↓ proton gradient and ↑ O2 consumption. ATP synthesis stops, but electron transport continues. Produces heat.
      • 2,4-Dinitrophenol (used illicitly for weight loss), aspirin (fevers often occur after aspirin overdose), thermogenin in brown fat (has more mitochondria than white fat).

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