Herbicidal action of nitrophenyl pyrazole ether MON 12800: immunolocalization, ultrastructural, and physiological studies

The effects of MON 12800 [4-chloro-3-(3-methoxy-4-nitrophenoxy)-1-methyl-5-trifluoro methylpyrazole] photosynthetic electron transport in chloroplasts from velvetleaf (Abutilon theophrasti) plants, on the ultrastructural morphology of morning glory (Ipomea hederecia) leaves, and on immunolocalization of incorporated herbicide are described, as are correlations of herbicidal injury with light quality. Application of herbicide caused leaf desiccation in light-grown plants, whereas plants incubated in the dark did not develop desiccation symptoms. Phytotoxicity was attenuated in plants exposed to red light, an observation consistent with data implicating accumulated protoporphyrin IX as the mediator of photodamage. At the ultrastructural level, leaves of morning glory plants exposed to light for 4-24 hr developed abnormalities in the plasma membrane, tonoplast, chloroplasts, and mitochondria of palisade and mesophyll cells. Immunolocalization studies on morning glory plants incubated 24 hr in the dark after herbicide application indicated that herbicide MON 12800 was present in mitochondria, chloroplasts, peroxisomes, and nuclei; the herbicide was associated with grana and stroma in chloroplasts and with mitochondrial cristae. Unlike acifluorfen, MON 12800 is an effective inhibitor of electron transport in vitro, though not as potent an inhibitor as oxyfluorfen. This difference probably accounts for the relatively greater and more rapid effects on chloroplast ultrastructure than have been reported for acifluorfen. Overall, our results are consistent with the hypothesis that this pyrazole phenyl ether herbicide acts primarily by inhibiting protoporphyrinogen oxidase, and illustrates the interplay among organellar systems in mediating damage by accumulated protoporphyrin IX.