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19.8: The Electron Transport Chain
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The Electron Transport Chain
 
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19.8: The Electron Transport Chain

The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.

Inhibitors of the electron transport chain

Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in complex I by blocking the Q-binding site. Inhibition of complex I function results in the increased production of reactive oxygen species or ROS. This rotenone-induced ROS production can be detrimental to mitochondrial components, including mitochondrial DNA, and can eventually lead to cell death.

Another competitive inhibitor of ubiquinone is carboxin, a potent fungicide that interferes with the Q-binding site on complex II. The binding of carboxin inhibits the transfer of electrons from FADH2 to ubiquinone, thus blocking the respiratory chain.

Certain antibiotics are also known to inhibit the respiratory chain complexes. For instance, antimycin A, an antibiotic produced by Streptomyces species, interferes with the ubiquinone binding site of complex III, thereby blocking the Q-cycle. The absence of Q-cycle prevents electron transfer between complex III subunits, cytochrome b and cytochrome c, thus inhibiting the electron transport chain.

Sometimes, toxins generated during metabolic activities of the cell can act as an inhibitor of mitochondrial function. For example, carbon monoxide, a by-product of heme catabolism, inhibits complex IV by competing with oxygen for the oxygen-binding sites. This leads to electron accumulation at complex III and results in the generation of superoxide radicals.

The mitochondrial ATP synthase, or complex V, is inhibited by oligomycin, an antibiotic that binds and inhibits its proton channel. This inhibition prevents proton flow through the ATP synthase, thus preventing the rotary motion of the complex needed for catalytic conversion of ADP to ATP.

While these toxins are potent inhibitors of respiratory functions, they can also act as valuable agents in studying individual complexes and enzyme kinetic research.


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