The role of protoporphyrin IX in the mechanism of action of diphenyl ether herbicides

Abstract

AbstractPhotobleaching diphenyl ether, cyclic imide and oxadiazole herbicides inhibit protoporphyrinogen oxidase (Protox), resulting in uncontrolled, non‐enzymic oxidation of accumulated protoporphyrinogen to protoporphyrin IX (Proto). Proto accumulation is stimulated by deregulation of the porphoyrin pathway due to blockage of heme synthesis. Heme is a Proto product and a feedback inhibitor of δ‐aminolevulinic acid synthesis. Strong correlations were found in several species under various conditions (e.g. sprayed on intact plants or taken up by leaf dises) between the accumulation of Proto and the degree of herbicidal damage caused by these herbicides. Levels of protochlorophyllide, Mg‐Proto, or Mg‐Proto monomethyl ester did not correlate significantly with herbicidal damage. Kinetic data indicated that elevated levels of protochlorophyllide in tissues treated with these herbicides only occurred after Proto had accumulated to high levels. Thus, Proto apparently re‐enters the porphyrin pathway to a significant extent after other cellular sites are saturated. Fluorescence microscopy indicated that considerable amounts of Proto accumulated outside the plastid in herbicide‐treated cells. All of the data were consistent with the hypothesis that Proto plays a critical role as a photosensitizing pigment in the mode of action of Protox‐inhibiting herbicides and that chlorophyll precursors that are derivatives of Proto are not significantly involved in the mode of action of these herbicides.