Photosensitizing Porphyrins as Herbicides

Several porphyrin intermediates of heme and/or chlorophyll biosynthesis are potent photosensitizers which generate high levels of singlet oxygen in the presence of molecular oxygen and light. Many compounds that affect the heme and/or chlorophyll pathways are strongly herbicidal due to accumulation of phytotoxic levels of these porphyrins in response to the chemical. For instance, several commercial and experimental herbicides inhibit protoporphyrinogen oxidase, the enzyme that converts protoporphyrinogen to protoporphyrin IX (PPIX). This leads to uncontrolled autooxidation of the substrate and results in massive accumulation of PPIX. In plants treated with these herbicides, damage is light dependent and closely correlated with the level of PPIX that accumulates. PPIX accumulation is apparently largely extraplastidic. Treatment with the porphyrin precursor δ-aminolevulinic acid (ALA), in combination with the heme and chlorophyll pathway inhibitor 2,2'-dypyridyl (DP), results in the accumulation of toxic levels of primarily Mg-PPIX monomethylester. DP deregulates porphyrin synthesis and ALA provides additional substrate. DP and other chlorophyll synthesis modulators in combination with ALA can increase the selectivity as well as enhance the efficacy of ALA as a herbicide. Exogenously applied porphyrins are far less effective as herbicides than treatment with compounds that cause plants to accumulate their own porphyrins.