scholarly journals Protoporphyrin IX Accumulation in Lemna paucicostata Hegelm. Caused by Diphenyl Ether Herbicides and Their Herbicidal Activity.

1991 ◽  
Vol 36 (4) ◽  
pp. 318-323
Author(s):  
Shuuichi Kojima ◽  
Hiroshi Matsumoto ◽  
Kozo Ishizuka
Weed Science ◽  
1989 ◽  
Vol 37 (2) ◽  
pp. 152-160 ◽  
Author(s):  
Stephen O. Duke ◽  
John Lydon ◽  
Rex N. Paul

Oxadiazon (10 μM) caused rapid, light-dependent membrane damage to cucumber cotyledon discs. Electrolyte leakage was detected within 1 h of exposure to light, as were cytoplasmic vesiculation and breakage of the tonoplast and plasmalemma. The ultrastructure of chloroplasts was not affected until the cytoplasm was dispersed. Photosynthetic inhibitors had no effect on activity and, after a period of dark incubation with oxadiazon, there was little effect of temperature on the light-caused membrane destruction. Porphyrin synthesis inhibitors (gabaculine and 4,6-dioxoheptanoic acid) almost completely prevented the herbicidal activity of oxadiazon. Oxadiazon treatment caused accumulation of protoporphyrin IX, a photodynamic pigment. Oxadiazon caused physiological effects on cucumber cotyledons that were virtually identical to those ofp-nitro-diphenyl ether herbicides like acifluorfen and its methyl ester, which have recently been shown to also cause protoporphyrin IX accumulation.


1993 ◽  
Vol 48 (3-4) ◽  
pp. 326-333 ◽  
Author(s):  
Beate Nicolaus ◽  
Gerhard Sandmann ◽  
Peter Böger

Abstract Protoporphyrinogen oxidase, the last enzyme of the common tetrapyrrole biosynthetic pathway, is inhibited by several peroxidizing compounds resulting in accumulation of photodynamic tetrapyrroles, mainly protoporphyrin IX. The inhibition characteristics of two chemi­cally unrelated compounds were studied using membrane bound protoporphyrinogen oxidase from corn etioplasts. As shown by Lineweaver-Burk-analysis, the inhibition of enzyme activity by the diphenyl ether oxyfluorfen and the cyclic imide MCI 15 are competitive with respect to the substrate. The competitive interaction of protoporphyrinogen and the two chemically un­related inhibitors indicate a relative specificity of the binding site. The reversibility of oxyfluorfen inhibition was evaluated by dilution experiments and was shown to be independent of the presence of DTT. The analysis of structure-activity-relationship on protoporphyrinogen oxidase inhibition was investigated with para-substituted derivatives of phenyl-3,4,5,6-tetrahydro-phthalimides. The results obtained by QSAR -calculation yielded a good correlation of the inhibitory activity determined by the lipophilicity of the para-substituent. These data point to one binding region of the inhibitors within a lipophilic environment associated with the active center of the enzyme.


1989 ◽  
Vol 260 (1) ◽  
pp. 231-235 ◽  
Author(s):  
M Matringe ◽  
J M Camadro ◽  
P Labbe ◽  
R Scalla

Diphenyl ether herbicides induce an accumulation of protoporphyrin IX in plant tissues. By analogy to human porphyria, the accumulation could be attributed to decreased (Mg or Fe)-chelatase or protoporphyrinogen oxidase activities. Possible effects of acifluorfen-methyl on these enzymes were investigated in isolated corn (maize, Zea mays) etioplasts, potato (Solanum tuberosum) and mouse mitochondria, and yeast mitochondrial membranes. Acifluorfen-methyl was strongly inhibitory to protoporphyrinogen oxidase activities whatever their origins [concn. causing 50% inhibition (IC50) = 4 nM for the corn etioplast enzyme]. By contrast, it was roughly 100,000 times less active on (Mg or Fe)-chelatase activities (IC50 = 80-100 microM). Our results lead us to propose protoporphyrinogen oxidase as a cellular target for diphenyl ether herbicides.


Weed Science ◽  
1995 ◽  
Vol 43 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Terry R. Wright ◽  
E. Patrick Fuerst ◽  
Alex G. Ogg ◽  
Ujjana B. Nandihalli ◽  
Hee Jae Lee

Laboratory and greenhouse studies were conducted to determine the mode of action of soil- and foliar-applied UCC-C4243. Experiments demonstrated that UCC-C4243 required light for phytotoxicity, phytotoxic symptoms were similar to inhibitors of porphyrin synthesis such as acifluorfen, and UCC-C4243 potently inhibited protoporphyrinogen oxidase. Germination and emergence of field pennycress and lentil in the dark were not affected by soil-incorporated UCC-C4243 at rates more than 10 times greater than like treatments that killed all plants in the light. Soil-incorporated UCC-C4243 required light for activity and killed seedlings within 1 d after emergence; sublethal doses caused desiccation, veinal necrosis, and leaf deformation. Field pennycress and lentil were susceptible to soil-incorporated UCC-C4243 and acifluorfen in the light, but were 5 to 93 times less sensitive to the herbicides in the dark. Wheat was not affected by either herbicide in the light or dark. Injury symptoms from UCC-C4243 applied POST to redroot pigweed were similar to symptoms from diphenyl ether and bipyridinium herbicides: rapid, light-dependent chlorophyll bleaching, desiccation, and necrosis. UCC-C4243, acifluorfen-methyl, and acifluorfen acid caused light- and concentration-dependent chlorophyll bleaching and electrolyte leakage from cucumber leaf disks (I50= 1.0, 1.8, and 4.3 μM, respectively). An inhibitor of the porphyrin synthesis pathway, 4,6-dioxoheptanoic acid, almost completely inhibited herbicide-induced electrolyte leakage. δ-Aminolevulinic acid, a tetrapyrrole precursor and stimulator of the porphyrin synthesis pathway, caused synergistic effects with each herbicide. Protoporphyrinogen oxidase from barley etioplast preparations was inhibited 50% by 40 nM UCC-C4243. Barley leaf sections treated with 100 μM UCC-C4243 accumulated protoporphyrin IXin vivoto levels > 75 times non-treated controls. These data indicate the light-requiring herbicide activity of UCC-C4243, like acifluorfen, is due to inhibition of protoporphyrinogen oxidase.


1993 ◽  
Vol 48 (3-4) ◽  
pp. 339-344 ◽  
Author(s):  
Hiromichi Oshio ◽  
Hideyuki Shibata ◽  
Nobuaki Mito ◽  
Masako Yamamoto ◽  
Elizabeth H. Harris ◽  
...  

A group of highly active N -phenylimide photobleaching herbicides have been synthesized. These N -phenylimide herbicides as well as diphenyl ether herbicides induce protoporphyrin IX accumulation and inhibit protoporphyrinogen oxidase activity at extremely low concentrations in higher plants. The binding of a 14C -labeled N -phenylimide herbicide S-23121 [N-[4-chloro- 2-fluoro-5-[(1-m ethyl-2-propynyl)oxy]phenyl]-3,4,5,6-tetrahydrophthalimide] to the solubilized plastid fractions of greening corn seedlings is competed by the diphenyl ether herbicide acifluorfen-ethyl, but not by diuron, an inhibitor of photosynthetic electron transport. These results indicate a similar mode of action for both N -phenylimide and diphenyl ether herbicides.In order to investigate the mechanism of photobleaching herbicides at the molecular level, a strain of Chlamydomonas reinhardtii RS-3 resistant to N -phenylimide S-23142 [N -(4-chloro- 2-fluoro-5-propargyloxyphenyl)-3,4,5,6-tetrahydrophthalimide] was isolated by mutagenesis with N -m ethyl-N′-nitro-N -nitrosoguanidine. The 90% inhibition concentration of N -phenylimide S-23142 for growth of RS-3 was 100 times higher than that for wild type. Maximum accumulation of protoporphyrin IX was reached at 0.03 μᴍ of S-23142 for the wild type and 3 μᴍ for RS-3. RS-3 was resistant to oxadiazon, oxyfluorfen and acifluorfen-ethyl which had been shown to have the same mechanism of action as N -phenylimide herbicides, but not to paraquat, diuron or fluridone. Genetic analysis of RS-3 strain showed that the resistance results from a dominant mutation ( rs-3) in the nuclear genome. The magnesium protoporphyrin IX synthesizing activity from 5-am inolevulinic acid in chloroplast fragments isolated from RS-3 was less sensitive to S-23142 than that from wild type (CC-407). Protoporphyrinogen oxidase activity in Percoll™ -purified chloroplasts from RS-3 was also less sensitive to S-23142 than that from wild type. These results indicate that the resistance of RS-3 is specific for photobleaching herbicides, and that the mutation is related to protoporphyrinogen oxidase, the primary site of the photobleaching herbicide action.


1990 ◽  
Vol 30 (4) ◽  
pp. 367-378 ◽  
Author(s):  
Stephen O. Duke ◽  
José M. Becerril ◽  
T. D. Sherman ◽  
John Lydon ◽  
Hiroshi Matsumoto

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Mohd Ali ◽  
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Liang Lv ◽  
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1991 ◽  
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pp. 432-437 ◽  
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