Desnitroimidacloprid and Nicotine Binding Site in Rat Recombinant alpha4beta2 Neuronal Nicotinic Acetylcholine Receptor,

Common chickweed (Stellaria media Vill.) is one of the major weeds in upland and orchard in Japan and has been known to be a species poorly controlled by diphenyl ether herbicides. Laboratory experiments were conducted to determine the physiological basis of the plantʹs tolerance to the diphenyl ether herbicide oxyfluorfen (2-chloro-4-trifluoromethylphenyl 3ethoxy-4-nitrophenyl ether). Uptake, translocation, and metabolism of the herbicide, sensitivity of the action site, porphyrin accumulation, and tolerance to singlet oxygen in common chickweed were compared with slender amaranth (Amaranthus viridis) and large crabgrass (Digitaria adscendens), oxyfluorfen-sensitive species. Common chickweed showed a little visible herbicide injury to 10 muM of sprayed oxyfluorfen, while the herbicide significantly reduced the fresh weight of large crabgrass and slender amaranth at 1 muM. Uptake of 14C following [14C]oxyfluorfen application to the adaxial surface of the second leaf for 2 h was similar for common chickweed and large crabgrass, although the initial rate was greater in large crabgrass. No translocation of the herbicide out of the treated leaf was observed in either species. The major part of absorbed 14C was identified as unmetabolized oxyfluorfen in common chickweed and large crabgrass 24 h after application. The herbicide caused protoporphyrin IX accumulation in slender amaranth and large crabgrass. In contrast, no accumulation of the photosensitizing tetrapyrrole was observed in common chickweed. When excised leaf disks of slender amaranth and large crabgrass were treated with the herbicide, the porphyrin accumulation occurred faster than in intact plants. However, no accumulation was detected in leaf disks of common chickweed. Furthermore, vacuum infiltration of oxyfluorfen solution into the leaf disks of common chickweed did not promote the porphyrin accumulation. Protoporphyrinogen oxidase, the target enzyme of the herbicide, in common chickweed was inhibited by oxyfluorfen in vitro. The plant was also more tolerant to the singlet oxygen generating agent, rose bengal, than the susceptible species. However, tolerance of common chickweed to oxyfluorfen is considered to be due mainly to the mechanism which prevents protoporphyrin IX accumulation.