Disease relevance of Tackle

• Extracts of E. coli cells transformed with the Arabidopsis PPOX cDNA had high PPOX activity, and this activity was markedly inhibited by acifluorfen, a specific inhibitor of PPOX [1].
• Effects of UVBR on three selected pesticides (Atrazine, carbaryl and Acifluorfen) and possible induction of phototoxicity are reviewed [2].
• The interaction of the herbicides acifluorfen and paraquat with the photosynthetic reaction center from Rhodobacter sphaeroides has been studied by NMR relaxation measurements [3].
• In the present study we show that long term maintenance of murine erythroleukemia (MEL) cells in acifluorfen, which is normally toxic to these cells at 5 microM concentration, results in cells that grow at a near normal rate in 100 microM acifluorfen [4].
• Toxicity tests against Daphnia magna Strauss showed that acifluorfen was not toxic at a concentration of 0.1 mM; however, photoproducts formed after 36 h of UV exposure of the herbicide induced a remarkable toxicity to the test organism [5].

High impact information on Tackle

• A homogenate of the monkey kidney COS-1 cells that had been transfected with the cDNA had much higher PPO activity than an extract of control cells, and this activity was inhibited by acifluorfen, a specific inhibitor of PPO [6].
• Two reactive oxygen generating compounds, paraquat and acifluorfen, were found to cause induction of both phytoalexin accumulation and PDF1.2 expression in wild-type plants, but this induction was almost completely abolished in esa1 [7].
• Effects of UVBR on three selected pesticides (Atrazine, carbaryl and Acifluorfen) and possible induction of phototoxicity are reviewed [8].
• Transgenic plants synthesizing hGSH in the cytosol were more tolerant to acifluorfen than wild-type plants, whereas enhanced tolerance to fomesafen was not observed [9].
• Hepatocyte COH activity was increased also by the ferrochelatase inhibitor griseofulvin and the protoporphyrinogen oxidase inhibitor acifluorfen (about 9-fold induction) [10].

Biological context of Tackle

• Tritiated acifluorfen and a diazoketone derivative of tritiated acifluorfen were specifically bound to a single class of high-affinity binding sites on yeast mitochondrial membranes with apparent dissociation constants of 7 nM and 12.5 nM, respectively [11].
• These results suggest that the photodegradation of acifluorfen proceeds via a number of reaction pathways: (1) decarboxylation, (2) dehalogenation, (3) substitution of chlorine group by hydroxyl or hydrogen groups, and (4) cleavage of ether linkage, giving phenols [12].
• Oxidative stress in cucumber (Cucumis sativus L) seedlings treated with acifluorfen [13].

Anatomical context of Tackle

• The specific binding of the herbicide acifluorfen 5-[2-chloro-4-(trifluoromethyl)phenoxy]-2-nitrobenzoic acid to corn etioplast membranes is competitively inhibited by protoporphyrinogen IX, the substrate of protoporphyrinogen oxidase [14].
• In vitro enzyme studies of hepatic mitochondria isolated from rat and chick embryos demonstrated that protoporphyrinogen oxidase, the penultimate enzyme of heme biosynthesis, was inhibited by low concentrations of acifluorfen, nitrofen, or acifluorfen methyl with the latter being the most potent inhibitor [15].

Associations of Tackle with other chemical compounds

• The photolytic degradations of asulam, triclopyr, acifluorfen, and atrazine were independently compared in air-dried soils and in moist (75% field moisture capacity at 0.33 bar) soils maintained at initial conditions through the use of a specially designed soil photolysis apparatus [16].
• Diphenyl ether (DPE) herbicides such as acifluorfen inhibit both the plant and mammalian forms of protoporphyrinogen oxidase, a heme biosynthetic enzyme [17].

Gene context of Tackle

• The diazoketone derivative of tritiated acifluorfen was used to specifically photolabel yeast protoporphyrinogen oxidase [11].
• In addition, we found that the effect of a protoporphyrinogen oxidase inhibitor such as acifluorfen on the regulation of heme synthesis in hepatocyte cultures differed from that of an iron chelator [17].
• HPLC-MS analysis (APCI and ESI in positive and negative modes) was used to identify acifluorfen photoproducts [12].
• When the ORF3 gene was overexpressed in E. coli, the extract had much higher PPO activity than a control extract, and this activity was inhibited by acifluorfen, a specific inhibitor of PPO [18].

Analytical, diagnostic and therapeutic context of Tackle

• The degradation rate of acifluorfen, determined by liquid chromatography analysis in batch cultures incubated under oxygen-limited conditions were compared [19].

References