Step 1: What rotenone does
Rotenone binds to Complex I (NADH:ubiquinone oxidoreductase) at the ubiquinone-binding site. This blocks electron transfer from FMN/Fe–S centers to ubiquinone (Q). Consequences:
Electron flow from NADH is halted at Complex I.
Complex I cannot pump protons from matrix to intermembrane space.
Mitochondrial $\Delta p$ (proton motive force) and ATP synthesis fall sharply.
Step 2: Why plants cope better than animals
Plant mitochondria possess a suite of rotenone-insensitive Type II NAD(P)H dehydrogenases embedded in the inner mitochondrial membrane:
External-facing enzymes (e.g., NDB family) oxidize cytosolic NAD(P)H and pass electrons directly to ubiquinone.
Internal-facing enzymes (e.g., NDA/NDC) oxidize matrix NAD(P)H and also reduce ubiquinone.
These enzymes bypass Complex I (they do not pump protons), maintaining electron flow to Q and onward to Complex III/IV (often assisted by alternative oxidase, AOX, to relieve over-reduction and limit ROS). Energy yield is lower (no pumping), but respiration and redox balance are sustained, conferring tolerance to rotenone.
Step 3: Eliminate incorrect options
(A) Incorrect. Plant Complex I is not intrinsically rotenone-resistant; it is inhibited similarly to animal Complex I.
(B) Unlikely/Incorrect as primary explanation. While plants can metabolize some xenobiotics, rotenone tolerance in vivo is explained chiefly by ETC bypass, not specific detoxification.
(C) Incorrect. No specific rotenone efflux channels are known to account for whole-plant tolerance.
(D) Correct. Presence of additional rotenone-insensitive NAD(P)H dehydrogenases that feed electrons to Q provides a physiological bypass of Complex I.
Therefore, the correct explanation is (D).