Rotenone, a toxic compound isolated from plants, strongly inhibits the transfer of electrons from iron-sulfur centers in Complex I to ubiquinone in insect and fish mitochondria. Antimycin A, a toxic antibiotic, strongly inhibits the oxidation of ubiquinol.
(A) Explain why rotenone ingestion is lethal to some insect and fish species.
(B) Explain why antimycin A is a poison.
(C) Given that rotenone and antimycin A are equally effective in blocking their respective sites in the electron transfer system, which do you think would be a more potent poison

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Answer:

(A) It prevents electron flow from the iron-sulfur centers in complex 1 to the ubiquinone. Due to reduction in electron transfer rate, there is a decrease in the production of ATP which is dangerous for some insects and fish over time.

(B) It also prevents electron flow from cytochrome b to cytochrome c1 at the complex III which leads to QH2 accumulation. If oxidized Q is not present, these is alteration of electron flow and the production of ATP is altered.

(C) Rotenone only prevent electron transfer into the chain at Complex 1  but it does not affect electron transfer at Complex II. Although there is slow ETC, it does not stop completely. However, Antimycin A prevents the oxidation of QH2, the final electron acceptor crom complex I and complex II. Thereby, stopping the production of both ETC and ATP. It can be concluded that antimycin A is a more potent poison.

Explanation:

Rotenone prevents electron flow from the iron-sulfur centers in complex 1 to the ubiquinone. Due to a reduction in electron transfer rate, there is a decrease in the production of ATP which is dangerous for some insects and fish over time. Antimycin A also prevents electron flow from cytochrome b to cytochrome c1 at the complex III which leads to QH2 accumulation. If oxidized Q is not present, there is an alteration of electron flow and the production of ATP is altered. Antimycin A is more potent than rotenone.

Answer:

1.Retenone is one of the inhibitors of NADH dehydrogenase in cells. NADH dehydrogenase is an enzyme that oxidizes co-factor NADH so that electrons flow;for Electron transport chain (ECT) set up at complex I  could be available for the chemical potential energy generated  set up for  Proton Motive Force.(PMF) .

The PMF is needed for influx of protons for ATPs synthesis. Therefore ingestion of rotenone hinders electron transfer sequence of the iron-sulfur centers in complex 1 to ubiquinone (co-enzyme Q) of  membrane. Consequently, ECT will  be reduced; PMF will not occur,with   resultant reduction in ATP synthesis. This is an example of completive inhibititon, however if there is no available substrate to neutralize this effect from prolong exposure , the effects of toxicity can be high.

2. Antimycin, by stopping the oxidation of ubiquinone, prevents the  ubiquinone -cycle of enzyme( NADH dehydrogenase) turn over.

Therefore  Antimycin  A  acts as poison  by  blocking  ATP synthesis in the mitochondria; which stops the electron transport chain sequence(ETC) though  inhibition of  election transfer from cytochrome b to cytochrome c1, with consequent buildup of  QH2 concentrations in the cells.

3. Antimycin is more toxic than  Rotenone ;because it inhibits the activities of ubiqunone by preventing its oxidation to QH2; the final electron acceptor,  in  both  complex I and II.  Thus in absence of electron acceptor in both complex I and II, both ATP synthesis and electron transport Chain  are stopped.

Rotenone, is less toxic because, compare to Antimycin it only block  availability of electrons for  ECT  sequence in complex  I only, but complex II  electron flow is  not affected by its inhibition. Therefore the complex ii electron flow  still ensures ECT progress ;although ATP synthesis may be  slow.

Explanation:

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