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The electron transport chain (which I will now conveniently refer to as ETC) couples a chemical reaction between an electron donor (such as NADH) and an electron acceptor (such as O2) to the transfer of H+ ions across a membrane, through a set of mediating biochemical reactions. These H+ ions are used to produce relatively large amounts of adenosine triphosphate (ATP), the main energy intermediate in living organisms, as they move back across the membrane.

Without a working ETC, the cell will be reduced to other forms of ATP producing pathways, most of which are highly inefficient as well as slow to produce ATP. In humans, the result of inhibiting or blocking the ETC is most pronounced. There are several well-known drugs and toxins that inhibit the ETC. Although any one of these toxins inhibits only one enzyme in the ETC, inhibition of any step in this process will halt the rest of the process.

One well known example is cyanide. Cyanide is an inhibitor of the enzyme cytochrome c oxidase in the fourth complex of the ETC (found in the membrane of the mitochondria of eukaryotic cells). It attaches to the iron within this protein. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the ETC is disrupted, meaning that the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. At a micro-level, Cells are unable to keep up with the essential production of ATP and begin to die off. At a macro-level, the cell death manifests as a coma with seizures, apnea and cardiac arrest, with death following in a matter of minutes.

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16y ago

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