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ELECTRON TRANSPORT CHAIN

ECDA September 2009. ELECTRON TRANSPORT CHAIN. ELECTRON TRANSPORT CHAIN. The cells of almost all eukaryotes (animals, plants, fungi, algae, protozoa – in other words, the living things except bacteria) contain intracellular organelles called mitochondria, which produce ATP.

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ELECTRON TRANSPORT CHAIN

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  1. ECDA September 2009 ELECTRON TRANSPORT CHAIN

  2. ELECTRON TRANSPORT CHAIN • The cells of almost all eukaryotes (animals, plants, fungi, algae, protozoa – in other words, the living things except bacteria) contain intracellular organelles called mitochondria, which produce ATP. • Energy sources such as glucose are initially metabolized in the cytoplasm. • The products are imported into mitochondria.

  3. ELECTRON TRANSPORT CHAIN • Mitochondria continue the process of catabolism using metabolic pathways including the Krebs cycle, fatty acid oxidation, and amino acid oxidation. • The end result of these pathways is the production of two kinds of energy-rich electron donors, NADH and FADH2. When metabolized: • One NADH molecule = 3 ATP molecules • One FADH2 molecule = 2 ATP molecules

  4. ELECTRON TRANSPORT CHAIN • Electrons from NADH and FADH2 are passed through an electron transport chain to oxygen, which is reduced to water. • This is a multi-step redox process that occurs on the mitochondrial inner membrane.

  5. ELECTRON TRANSPORT CHAIN

  6. ELECTRON TRANSPORT CHAIN • Four membrane-bound complexes have been identified in mitochondria. • Each is an extremely complex transmembrane structure that is embedded in the inner membrane. • Three of them are proton pumps (Complexes I, III, and IV). • The structures are electrically connected by lipid-soluble electron carriers and water-soluble electron carriers.

  7. ELECTRON TRANSPORT CHAIN

  8. ETC–Complex I • Complex I removes two electrons from NADH and transfers them to a lipid-soluble carrier, ubiquinone (Q) • When NADH binds to complex I, it binds to a prosthetic group called flavin mononucleotide (FMN), and is immediately re-oxidized to NAD. • FMN then receives the hydrogen from the NADH and two electrons. • The reduced FMN form passes the electrons to iron-sulfur clusters that are part of the complex, and forces two protons into the intermembrane space.

  9. ETC–Complex I

  10. ETC–Complex I • Electrons pass from complex I to a carrier (Coenzyme Q) embedded by itself in the membrane. • From Coenzyme Q electrons are passed to a complex III which is associated with another proton translocation event. • Note that the path of electrons is from Complex I to Coenzyme Q to Complex III. • Complex II, the succinatedehydrogenase complex, is a separate starting point, and is not a part of the NADH pathway.

  11. ETC–Complex II • Complex II (succinatedehydrogenase) is not a proton pump. It serves to funnel additional electrons into the quinone pool (Q) by removing electrons from succinate and transferring them (via FAD) to Q. • Complex II consists of four protein subunits: SDHA, SDHB, SDHC, and SDHD. Other electron donors (e.g., fatty acids and glycerol 3-phosphate) also funnel electrons into Q (via FAD), again without producing a proton gradient.

  12. ETC-Complex II

  13. ETC-Complex III • Complex III (cytochromebc1 complex) removes in a stepwise fashion two electrons from QH2 at the QO site and sequentially transfers them to two molecules of cytochromec, a water-soluble electron carrier located within the intermembrane space. • From Complex III the pathway is to cytochrome c then to a Complex IV (cytochromeoxidase complex).

  14. ETC-Complex III

  15. ETC-Complex IV • Complex IV (cytochrome c oxidase) removes four electrons from four molecules of cytochrome c and transfers them to molecular oxygen (O2), producing two molecules of water (H2O). • Molecular oxygen serves as the final electron sink or acceptor, clearing the way for carriers in the sequence to be reoxidized so that electron transport process can continue

  16. ETC • KEY POINTS: • Protons are translocated across the membrane, from the matrix to the intermembrane space • Electrons are transported along the membrane, through a series of protein carriers • Oxygen is the terminal electron acceptor, combining with electrons and H+ ions to produce water • As NADH delivers more H+ and electrons into the ETS, the proton gradient increases, with H+ building up outside the inner mitochondrial membrane, and OH- inside the membrane.

  17. ETC INHIBITORS • Electron transport chain may be blocked by some compounds known as ETC Inhibitors. • ETS inhibitors act by binding somewhere on the electron transport chain, literally preventing electrons from being passed from one carrier to the next. • They all act specifically, that is, each inhibitor binds a particular carrier or complex in the ETS. • No matter what substrate is used to fuel electron transport, only two entry points into the electron transport system are known to be used by mitochondria: Complexes I and II.

  18. Two entry points into the ETC system

  19. ETC INHIBITORS

  20. ETC INHIBITORS • A consequence of having separate pathways for entry of electrons is that an ETS inhibitor can affect one part of a pathway without interfering with another part. In this case, respiration can still occur depending on choice of substrate. • However, some poisons may completely stop ETC and halt respiration.

  21. ETC INHIBITORS • Two Mechanism of Inhibition: • Irreversible inhibition results in a complete stoppage of respiration via the blocked pathway. • Competitive inhibition allows some oxygen consumption since a "trickle" of electrons can still pass through the blocked site. Although it allows some oxygen consumption, competitive inhibition prevents maintenance of a chemiosmotic gradient, thus the addition of ADP can have no effect on respiration.

  22. ETC INHIBITORS • An inhibitor may completely block electron transport by irreversibly binding to a binding site. • For example, cyanide binds cytochromeoxidase so as to prevent the binding of oxygen. Electron transport is reduced to zero. Breathe all you want - you can't use any of the oxygen you take in. • Rotenone, on the other hand, binds competitively, so that a trickle of electron flow is permitted. However, the rate of electron transport is too slow for maintenance of a gradient.

  23. ETC Inhibitors • Electron Transport Inhibitors • Rotenone • Antimycin • Cyanide • Oligomycin (inhibitor of oxidative phosphorylation)

  24. ETC Inhibitors • ROTENONE • Used as insecticide • Toxic to wildlife, to humans as well as to insects • Competitive inhibitor on complexes I and II, thus, blocking respiration • ANTIMYCIN • Being used in researches • binding site for antimycin can be narrowed considerably using combinations of substrates inlcuding succinate, NADH

  25. ETC Inhibitors • CYANIDE • extremely effective reversible inhibitor of cytochromeoxidase • A concentration of 1 mM KCN is sufficient to inhibit oxygen consumption by mitochondria from a vertebrate source by >98%. • Cyanide is one of the most deadly compounds in a laboratory.

  26. ATP Synthase Inhibitor • OLIGOMYCIN • An antibiotic, acts by binding ATP synthase in such a way as to block the proton channel • Inhibitor of oxydative phosphorylation • it has no direct effect on electron transport or the chemiosmotic gradient

  27. ETC Inhibitors

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