Q.48 Rotenone is a chemical often used to kill insect pests on crop plants and fishes in
lakes. Rotenone acts by inhibiting electron transport from the NADH
dehydrogenase enzyme in Complex I to ubiquinone in the mitochondrial electron
transport chain. Which one of the following explains why plants can tolerate
rotenone application?
(A) The Complex I in plants is resistant to rotenone.
(B) Plants inactivate rotenone by enzymatic degradation.
(C) Plants have specific channels that efflux rotenone out of the cell.
(D) Plants have additional NAD(P)H dehydrogenases that are resistant to rotenone.
Plants tolerate rotenone due to alternative respiratory pathways bypassing Complex I inhibition. This mechanism allows continued electron transport despite rotenone blocking NADH dehydrogenase in the standard chain. The correct answer is option (D).
Rotenone Mechanism
Rotenone inhibits Complex I (NADH:ubiquinone oxidoreductase) by blocking electron transfer from iron-sulfur centers to ubiquinone, halting NADH oxidation and ATP production in animals and insects. This generates reactive oxygen species (ROS) and causes cell death in sensitive organisms. Plants face this on crops yet survive through unique adaptations.
Option Analysis
(A) Incorrect. Plant Complex I remains sensitive to rotenone, as shown by initial respiration drops in treated Arabidopsis cells before recovery. No evidence supports inherent resistance in plant Complex I.
(B) Incorrect. Plants do not primarily inactivate rotenone enzymatically; rapid biodegradation occurs in soil via microbes and light, but tolerance stems from respiratory bypasses, not degradation inside cells.
(C) Incorrect. No specific channels efflux rotenone; persistence in cell supernatants confirms uptake and retention, with acclimation via metabolic shifts rather than export.
(D) Correct. Plants possess rotenone-insensitive type II NAD(P)H dehydrogenases (internal NDA, external NDB) on the inner mitochondrial membrane, bypassing Complex I to oxidize NADH/NADPH and sustain respiration. These non-proton-pumping enzymes, plus alternative oxidase (AOX), enable recovery, as seen in induced NDA2, NDB2, and AOX1a transcripts post-treatment.
Plants tolerate rotenone, a potent insecticide targeting mitochondrial Complex I, through unique respiratory bypasses absent in animals and insects. This adaptation supports safe crop applications while killing pests.
Rotenone Action on Mitochondria
Rotenone blocks electron flow from NADH dehydrogenase (Complex I) to ubiquinone, disrupting ATP synthesis and elevating ROS in sensitive cells. Insects and fish succumb rapidly, but plants recover respiration within hours via alternative pathways .
Key Resistance: Alternative Dehydrogenases
Plants feature rotenone-insensitive NAD(P)H dehydrogenases (type II: NDA internal, NDB external) that oxidize matrix and cytosolic NAD(P)H directly to ubiquinone. Studies on Arabidopsis show upregulated NDA2, NDB2 post-rotenone, restoring NADH oxidation without proton pumping .
Additional Bypass Pathways
Alternative oxidase (AOX) doubles capacity, handling electrons from ubiquinone to oxygen and reducing ROS. No Complex I structural changes or efflux channels contribute; tolerance relies on these flexible ETC components.
Implications for CSIR NET
This explains crop tolerance in exams: plants sustain metabolism via bypasses, unlike lethal effects in pests. Mutants lacking Complex I (e.g., tobacco CMSII) survive similarly, confirming the mechanism .
