19.9
電子伝達鎖
電子伝達連鎖→電子伝達鎖または酸化的リン酸化は、電子伝達反応中に放出される自由エネルギーが ATP 合成に結合する発熱過程です。 この過程は好気性細胞の重要なエネルギー源であるため、電子伝達鎖の阻害剤は細胞の代謝プロセスに悪影響を与える可能性があります。
電子伝達鎖の阻害剤
広く使用されている殺虫剤…
The electron transport chain or ETC is the final stage of cellular respiration, where NADH and FADH2 begin a series of redox reactions.
At complex I, NADH donates two electrons across different electron acceptors, reducing Q to QH2.
At complex II, FADH2 transfers electrons via Fe-S to a Q-molecule, forming another QH2.
The QH2 generated in these reactions then diffuse to complex III and transfer electrons to cytochrome c via a series of reactions called the Q cycle.
The reduced cytochrome c moves to complex IV, where after a series of electron transfers, oxygen accepts electrons and combines with protons to produce water.
As electrons pass through complexes I, III, and IV, the energy released is used to pump protons into the intermembrane space.
The pumped protons can then flow down their concentration gradient and activate complex V or ATP synthase to produce ATP from ADP and inorganic phosphate.
Overall, the ETC produces 32 ATP molecules from one molecule of glucose, making it the major energy contributing stage of cellular respiration.
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Q1: What happens to electrons as they move through the electron transport chain?
Electrons from NADH and FADH2 pass through a series of protein complexes, losing energy at each step. At complex I, NADH donates electrons that reduce ubiquinone to QH2. These electrons continue through electron transport chain complex III and IV, where oxygen finally accepts them and combines with protons to produce water.
Q2: How does the electron transport chain generate ATP?
As electrons move through complexes I, III, and IV, energy released pumps protons into the intermembrane space, creating a concentration gradient. Protons flow back through ATP synthase down this gradient, activating the enzyme to convert ADP and inorganic phosphate into ATP, producing approximately 32 ATP molecules per glucose molecule.
Q3: What role does ubiquinone play in the electron transport chain?
Ubiquinone, or Q, acts as a mobile electron carrier between complexes. At complex I, NADH reduces Q to QH2. At complex II, FADH2 also transfers electrons to Q. The QH2 then diffuses to complex III, where it participates in the Q cycle to transfer electrons to cytochrome c.
Q4: Why are electron transport chain inhibitors dangerous to cells?
Inhibitors like rotenone block electron transfer and cause reactive oxygen species accumulation, damaging mitochondrial DNA and cellular components. Carbon monoxide inhibits complex IV by competing for oxygen-binding sites, causing electron accumulation and superoxide radical generation. These effects disrupt ATP production and can lead to cell death.
Q5: How does rotenone interfere with complex I function?
Rotenone, a pesticide, blocks the Q-binding site at complex I, preventing electron transfer from the Fe-S cluster to ubiquinone. This inhibition halts the electron transport chain and increases reactive oxygen species production, which damages mitochondrial components and can ultimately cause cell death.
Q6: What is the Q cycle and where does it occur?
The Q cycle is a series of reactions at complex III where reduced cytochrome c receives electrons from QH2. This process involves electron transfer between cytochrome b and cytochrome c subunits. Antimycin A, an antibiotic, blocks this cycle by interfering with the ubiquinone binding site, halting electron transport.
Q7: How does oligomycin inhibit ATP production?
Oligomycin, an antibiotic, binds to and blocks the proton channel of ATP synthase, preventing protons from flowing through the enzyme. Without proton flow, the rotary motion needed for ATP synthesis cannot occur, stopping the conversion of ADP to ATP despite an active electron transport chain.