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John B Barnett - One of the best experts on this subject based on the ideXlab platform.
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in vitro nephrotoxicity induced by Propanil
Environmental Toxicology, 2008Co-Authors: Gary O Rankin, Christopher Racine, Adam Sweeney, Alyssa Kraynie, Dianne K Anestis, John B BarnettAbstract:Propanil is a postemergence herbicide used primarily in rice and wheat production in the United States. The reported toxicities for Propanil exposure include methemoglobinemia, immunotoxicity, and nephrotoxicity. A major metabolite of Propanil, 3,4-dichloroaniline (3,4-DCA), has been shown to be a nephrotoxicant in vivo and in vitro, but the nephrotoxic potential of Propanil has not been examined in detail. The purpose of this study was to determine the nephrotoxic potential of Propanil using an in vitro kidney model, determine whether in vitro Propanil nephrotoxicity is due to metabolites arising from Propanil hydrolysis, and examine mechanistic aspects of Propanil nephrotoxicity in vitro. Propanil, 3,4-DCA, propionic acid (0.1–5.0 mM), or vehicle was incubated for 15–120 min with isolated renal cortical cells (IRCC; ∼4 million cells/mL) obtained from untreated male Fischer 344 rats. Cytotoxicity was determined by measuring lactate dehydrogenase release from IRCC. In 120-min incubations, Propanil induced cytotoxicity at concentrations >0.5 mM. At 1.0 mM, Propanil induced cytotoxicity following 60- or 120-min exposure. Cytotoxicity was observed with 3,4-DCA (2.0 mM) at 60 and 120 min, while propionic acid (5.0 mM) induced cytotoxicity at 60 min. In IRCC pretreated with an antioxidant, cytochrome P450(CYP) inhibitor, flavin adenine dinucleotide monooxygenase activity modulator, or cyclooxygenase inhibitor before Propanil exposure (1.0 mM; 120 min), only piperonyl butoxide (0.1 mM), a CYP inhibitor, pretreatment decreased Propanil cytotoxicity. These results demonstrate that Propanil is an in vitro nephrotoxicant in IRCC. Propanil nephrotoxicity is not primarily due to metabolites resulting from hydrolysis of Propanil, but a metabolite resulting from Propanil oxidation may contribute to Propanil cytotoxicity. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2008.
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evidence for a novel endocrine disruptor the pesticide Propanil requires the ovaries and steroid synthesis to enhance humoral immunity
Toxicological Sciences, 2006Co-Authors: Keith D Salazar, John B Barnett, Michael R Miller, Rosana SchaferAbstract:Steroid hormones are known to affect the humoral immune response to a variety of antigens. However, the mechanisms regulating these effects are poorly understood. The immunotoxic chemical Propanil and estrogen have similar effects on the immune system including augmentation of humoral immune responses. Propanil enhances the number of phosphorylcholine (PC)-specific IgG2b, IgG3, and IgM antibody-secreting cells (ASCs) in the spleen four- to sixfold 7 days after vaccination of female C57BL/6 mice with heat-killed Streptococcus pneumoniae. Several experiments were performed to test the hypothesis that Propanil increases the response via an estrogenic pathway. Ovariectomy abrogated the effect of Propanil on the PC-specific ASC response. Both in vitro and in vivo assays indicate that Propanil does not bind either estrogen receptor (ER) a or b. Exogenous estradiol administration in ovariectomized mice failed to restore the effect of Propanil on the PC response. Treatment of female mice with a pure ER antagonist, ICI 182,780, or the progesterone antagonist RU486 did not inhibit the increase in ASCs. These data suggest that estrogen and progesterone do not regulate the effect of Propanil. However, complete inhibition of steroid synthesis with the gonadotropinreleasing hormone (GnRH) antagonist antide abrogated the increased response in Propanil-treated mice, indicating a necessary role for steroid synthesis. Experiments in male mice demonstrated that Propanil increased the number of ASCs comparable to female mice. However, orchiectomy did not inhibit this effect, suggesting that androgens do not regulate the amplification of the humoral response. These data suggest a novel role for the ovarian hormones in the regulation of the PC-specific antibody response.
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Propanil inhibits tumor necrosis factor α production by reducing nuclear levels of the transcription factor nuclear factor κb in the macrophage cell line ic 21
Toxicology and Applied Pharmacology, 2001Co-Authors: Laura L Frost, Rosana Schafer, Yilin Xie Neeley, Laura F Gibson, John B BarnettAbstract:Abstract Tumor necrosis factor-α (TNF-α) is an essential proinflammatory cytokine whose production is normally stimulated by bacterial cell wall components, such as lipopolysaccharide (LPS), during an infection. Macrophages stimulated with LPS in vitro produce several cytokines, including TNF-α. LPS-stimulated primary mouse macrophages produced less TNF-α protein and message after treatment with the herbicide Propanil (Xie et al., Toxicol. Appl. Pharmacol. 145, 184–191, 1997). Nuclear factor-κB (NF-κB) tightly regulates TNF-α transcription. Therefore, as a step toward understanding the mechanism of the effect of Propanil on TNF-α transcription, IC-21 cells were transfected with a TNF-α promoter–luciferase construct, and the effect of Propanil on luciferase activity was measured. Cells transfected with promoter constructs containing a κB site showed decreased luciferase activity relative to controls after Propanil treatment. These observations implicated NF-κB binding as an intracellular target of Propanil. Further studies demonstrated a marked reduction in the nuclear levels of the stimulatory p65 subunit of NF-κB after Propanil treatment, as measured by fluorescence confocal microscopy and Western blot analysis. The p50 subunit of NF-κB was not found to be reduced after Propanil exposure by Western blot. Electrophoretic mobility gel shift assays showed decreased DNA binding of both p65/p50 heterodimers and p50/p50 homodimers to the κB3 site of the TNF-α promoter of Propanil-treated cells. The marked reduction in nuclear p65/p50 NF-κB levels and diminished binding to the TNF-α promoter in Propanil-treated cells are consistent with reduced TNF-α levels induced by LPS.
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Propanil affects transcriptional and posttranscriptional regulation of il 2 expression in activated el 4 cells
Toxicology and Applied Pharmacology, 1999Co-Authors: Wei Zhao, Rosana Schafer, John B BarnettAbstract:Abstract The amide-class herbicide, Propanil, causes numerous immunomodulary effects in animal models. In the present study, we investigated the effect of Propanil on IL-2 expression and production in the murine lymphoma T cell line, EL-4. When supernatants of cells stimulated with phorbol 12-myristate 13-acetate in the presence of Propanil were assessed by enzyme-linked immunosorbent assay, IL-2 levels were dose-dependently decreased by 20 and 50 μM of Propanil but not at 10 μM. Quantitative Northern blot analysis of peak IL-2 message levels also showed a dose-dependent decrease. The kinetic pattern of message production, however, was unaffected. To determine if the reduced message production was due to reduced signaling or message stability, nuclear run-on and mRNA stability assays were performed. Nuclear run-on assays determined that the transcription rate of the IL-2 gene was decreased approximately 50% in the presence of 20 μM Propanil, indicating that it was able to interfere with signal transduction. IL-2 message stability assays also demonstrated a reduction in message stability. Thus, Propanil appears to reduce IL-2 production by affecting the signal transduction pathway and IL-2 message stability.
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Cytokine production by C57BL/6 mouse spleen cells is selectively reduced by exposure to Propanil
Journal of Toxicology and Environmental Health, 1998Co-Authors: Wei Zhao, Rosana Schafer, John B BarnettAbstract:Numerous immunomodulatory effects are caused by Propanil, an extensively used postemergent herbicide. The T-dependent antibody response is suppressed after exposure to Propanil, raising the question of Propanil's effect on T-helper-cell populations. In the present study, we show that the production of several T-cell cytokines is affected by Propanil after in vivo or in vitro exposure. In vivo exposure to Propanil caused the reduction of interleukin (IL)-2, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interferon (IFN)- production in concanavalin A-stimulated spleen cell cultures established 2 d after exposure. IFN- and GM-CSF production had recovered by d 4 postexposure; however, IL-2 and IL-6 levels continued to be depressed through d7 postexposure. Continuous in vitro treatment of normal spleen cells with Propanil decreased IL-2, IL-6, GM-CSF, and IFN- production after concanavalin A activation. Pulsing normal spleen cell cultures with Propanil for up to 8 h before T-cell activati...
Rosana Schafer - One of the best experts on this subject based on the ideXlab platform.
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evidence for a novel endocrine disruptor the pesticide Propanil requires the ovaries and steroid synthesis to enhance humoral immunity
Toxicological Sciences, 2006Co-Authors: Keith D Salazar, John B Barnett, Michael R Miller, Rosana SchaferAbstract:Steroid hormones are known to affect the humoral immune response to a variety of antigens. However, the mechanisms regulating these effects are poorly understood. The immunotoxic chemical Propanil and estrogen have similar effects on the immune system including augmentation of humoral immune responses. Propanil enhances the number of phosphorylcholine (PC)-specific IgG2b, IgG3, and IgM antibody-secreting cells (ASCs) in the spleen four- to sixfold 7 days after vaccination of female C57BL/6 mice with heat-killed Streptococcus pneumoniae. Several experiments were performed to test the hypothesis that Propanil increases the response via an estrogenic pathway. Ovariectomy abrogated the effect of Propanil on the PC-specific ASC response. Both in vitro and in vivo assays indicate that Propanil does not bind either estrogen receptor (ER) a or b. Exogenous estradiol administration in ovariectomized mice failed to restore the effect of Propanil on the PC response. Treatment of female mice with a pure ER antagonist, ICI 182,780, or the progesterone antagonist RU486 did not inhibit the increase in ASCs. These data suggest that estrogen and progesterone do not regulate the effect of Propanil. However, complete inhibition of steroid synthesis with the gonadotropinreleasing hormone (GnRH) antagonist antide abrogated the increased response in Propanil-treated mice, indicating a necessary role for steroid synthesis. Experiments in male mice demonstrated that Propanil increased the number of ASCs comparable to female mice. However, orchiectomy did not inhibit this effect, suggesting that androgens do not regulate the amplification of the humoral response. These data suggest a novel role for the ovarian hormones in the regulation of the PC-specific antibody response.
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Propanil inhibits tumor necrosis factor α production by reducing nuclear levels of the transcription factor nuclear factor κb in the macrophage cell line ic 21
Toxicology and Applied Pharmacology, 2001Co-Authors: Laura L Frost, Rosana Schafer, Yilin Xie Neeley, Laura F Gibson, John B BarnettAbstract:Abstract Tumor necrosis factor-α (TNF-α) is an essential proinflammatory cytokine whose production is normally stimulated by bacterial cell wall components, such as lipopolysaccharide (LPS), during an infection. Macrophages stimulated with LPS in vitro produce several cytokines, including TNF-α. LPS-stimulated primary mouse macrophages produced less TNF-α protein and message after treatment with the herbicide Propanil (Xie et al., Toxicol. Appl. Pharmacol. 145, 184–191, 1997). Nuclear factor-κB (NF-κB) tightly regulates TNF-α transcription. Therefore, as a step toward understanding the mechanism of the effect of Propanil on TNF-α transcription, IC-21 cells were transfected with a TNF-α promoter–luciferase construct, and the effect of Propanil on luciferase activity was measured. Cells transfected with promoter constructs containing a κB site showed decreased luciferase activity relative to controls after Propanil treatment. These observations implicated NF-κB binding as an intracellular target of Propanil. Further studies demonstrated a marked reduction in the nuclear levels of the stimulatory p65 subunit of NF-κB after Propanil treatment, as measured by fluorescence confocal microscopy and Western blot analysis. The p50 subunit of NF-κB was not found to be reduced after Propanil exposure by Western blot. Electrophoretic mobility gel shift assays showed decreased DNA binding of both p65/p50 heterodimers and p50/p50 homodimers to the κB3 site of the TNF-α promoter of Propanil-treated cells. The marked reduction in nuclear p65/p50 NF-κB levels and diminished binding to the TNF-α promoter in Propanil-treated cells are consistent with reduced TNF-α levels induced by LPS.
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Propanil affects transcriptional and posttranscriptional regulation of il 2 expression in activated el 4 cells
Toxicology and Applied Pharmacology, 1999Co-Authors: Wei Zhao, Rosana Schafer, John B BarnettAbstract:Abstract The amide-class herbicide, Propanil, causes numerous immunomodulary effects in animal models. In the present study, we investigated the effect of Propanil on IL-2 expression and production in the murine lymphoma T cell line, EL-4. When supernatants of cells stimulated with phorbol 12-myristate 13-acetate in the presence of Propanil were assessed by enzyme-linked immunosorbent assay, IL-2 levels were dose-dependently decreased by 20 and 50 μM of Propanil but not at 10 μM. Quantitative Northern blot analysis of peak IL-2 message levels also showed a dose-dependent decrease. The kinetic pattern of message production, however, was unaffected. To determine if the reduced message production was due to reduced signaling or message stability, nuclear run-on and mRNA stability assays were performed. Nuclear run-on assays determined that the transcription rate of the IL-2 gene was decreased approximately 50% in the presence of 20 μM Propanil, indicating that it was able to interfere with signal transduction. IL-2 message stability assays also demonstrated a reduction in message stability. Thus, Propanil appears to reduce IL-2 production by affecting the signal transduction pathway and IL-2 message stability.
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Cytokine production by C57BL/6 mouse spleen cells is selectively reduced by exposure to Propanil
Journal of Toxicology and Environmental Health, 1998Co-Authors: Wei Zhao, Rosana Schafer, John B BarnettAbstract:Numerous immunomodulatory effects are caused by Propanil, an extensively used postemergent herbicide. The T-dependent antibody response is suppressed after exposure to Propanil, raising the question of Propanil's effect on T-helper-cell populations. In the present study, we show that the production of several T-cell cytokines is affected by Propanil after in vivo or in vitro exposure. In vivo exposure to Propanil caused the reduction of interleukin (IL)-2, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interferon (IFN)- production in concanavalin A-stimulated spleen cell cultures established 2 d after exposure. IFN- and GM-CSF production had recovered by d 4 postexposure; however, IL-2 and IL-6 levels continued to be depressed through d7 postexposure. Continuous in vitro treatment of normal spleen cells with Propanil decreased IL-2, IL-6, GM-CSF, and IFN- production after concanavalin A activation. Pulsing normal spleen cell cultures with Propanil for up to 8 h before T-cell activati...
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the immunomodulatory effects of the herbicide Propanil on murine macrophage interleukin 6 and tumor necrosis factor α production
Toxicology and Applied Pharmacology, 1997Co-Authors: Rosana Schafer, John B BarnettAbstract:Abstract Intraperitoneal (ip) exposure to Propanil (3,4-dichloropropionanilide) has previously been shown to affect macrophage cytotoxicity. In this study, we compared the immunotoxic effects of Propanil, after different routes of in vivo administration, on cytokine production by thioglycollate-elicited peritoneal macrophages. C57B1/6 mice were treated with either vehicle or 200 mg/kg Propanil ip, or with vehicle, 40, or 400 mg/kg Propanil orally. Three or 7 days later, ex vivo production of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) by macrophages after lipopolysaccharide (LPS) stimulation was determined. Both oral and ip Propanil exposure resulted in up to a 60–70% reduction in IL-6 and TNF-α production by the LPS-stimulated macrophages, depending on the route, postexposure time, and dose of Propanil administered. Oral exposure to Propanil also caused splenomegaly and thymic atrophy in animals in much the same manner as animals exposed via the ip route. In vitro exposure to Propanil also significantly reduced macrophage cytokine production. Thioglycollate-elicited macrophages from normal mice were cultured in the continuous presence of 0, 10, or 20 μ m Propanil plus LPS. This exposure caused a significant reduction in IL-6 and TNF protein production by these macrophages in a concentration-dependent manner. Northern blot analysis demonstrated that the message levels of these cytokines were reduced by approximately the same percentage as the protein levels in Propanil-treated macrophages, indicating a possible transcriptional or pretranscriptional target(s) for Propanil.
Ronald E. Talbert - One of the best experts on this subject based on the ideXlab platform.
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metabolically based resistance to the herbicide Propanil in echinochloa species
Weed Science, 2004Co-Authors: Robert E Hoagland, Jason K Norsworthy, F Carey, Ronald E. TalbertAbstract:Abstract Propanil is an acylanilide herbicide introduced in the early 1960s to control dicotyledonous weeds and grasses, including Echinochloa species in cultivated rice. Since then, Propanil has been used extensively in rice production in the United States and in several other countries. Propanil is an inhibitor of photosystem II, but rice is tolerant to Propanil because of the presence of a high level of aryl acylamidase that catalytically degrades the compound to nonphytotoxic products, i.e., 3,4-dichloroaniline and propionic acid. About 10 yr ago, biotypes of barnyardgrass and junglerice were discovered to be resistant to Propanil. The resistance mechanism of these two biotypes has been shown to be elevated levels of aryl acylamidase activity. Various strategies to combat Propanil resistance and to more fully understand the biochemistry involved in this resistance have been investigated. These include studies on the interactions of herbicides and other chemicals with Propanil, rotation of rice with ot...
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Chemical interactions with the herbicide Propanil on Propanil-resistant barnyardgrass†
Pesticide Science, 1999Co-Authors: Robert E Hoagland, Jason K Norsworthy, Ronald E. TalbertAbstract:We are examining the interaction of compounds with the herbicide Propanil to find synergistic or additive actions that can increase efficacy against Propanil-resistant barnyardgrass [Echinochloa crus-galli] (R-BYG) without substantial injury to rice. Field tests (herbicidal injury) and laboratory tests (chlorophyll quantification in excised leaves; measurement of chlorophyll fluorescence to determine PSII inhibition) have been conducted on R-BYG and rice tissue exposed to various rates of Propanil and additive. Important synergistic interactions on R-BYG in laboratory and field tests were found with Propanil plus either the herbicides anilophos or piperophos, or the insecticide carbaryl. In laboratory tests, the insecticide methiocarb and PPG-124 (p-chlorophenyl N-methylcarbamate) were highly effective synergists with Propanil on R-BYG. Other important interactions occurred with certain concentrations/application rates when Propanil was combined with the herbicides quinclorac, thiobencarb, molinate, or pendimethalin (field tests). Combinations of these or other chemicals with Propanil may provide additive or synergistic action useful to control R-BYG without increasing rice injury. Such mixtures might also prevent or delay the development of Propanil resistance in this weed species.
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Agrichemical Interactions with Propanil on Propanil-Resistant Barnyardgrass (Echinochloa crus-galli)
Weed Technology, 1999Co-Authors: Jason K Norsworthy, Jeffery S. Rutledge, Ronald E. Talbert, Robert E HoaglandAbstract:Agrichemical interactions between Propanil; the herbicides HOE 30374, pendimethalin, piperophos, quinclorac, and thiobencarb; and the insecticide carbaryl were evaluated under field conditions to find synergistic or additive interactions useful to control a barnyardgrass biotype resistant to Propanil (R-BYG) without injuring rice. Propanil and each compound were evaluated at four rates for a total of 16 rate combinations for each additive. Averaged over all experiments, 2- to 3-leaf R-BYG control with Propanil alone at 0.83, 1.65, 3.3, and 6.6 kg ai/ha was 33, 53, 62, and 81% at 7 d after treatment (DAT). Propanil-susceptible barnyardgrass (S-BYG) response to Propanil alone at similar rates was 52, 73, 88, and 94% control. HOE 30374, carbaryl, piperophos, or pendimethalin in combination with Propanil produced synergistic effects on R-BYG. For each compound tested, at least one rate combination with Propanil controlled R-BYG > 80% with minimal rice injury (< 20%) at 7 DAT. Use of these combinations of compounds could provide more effective control of this resistant biotype and help prevent its spread.
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control of Propanil resistant barnyardgrass echinochloa crus galli in rice oryza sativa with carbaryl Propanil mixtures
Weed Technology, 1999Co-Authors: Hassane Daou, Ronald E. TalbertAbstract:Propanil and carbaryl mixtures, Propanil formulated with carbaryl, the package mixture of Propanil plus molinate (alone and plus pendimethalin), Propanil plus quinclorac, and Propanil plus pendimethalin were evaluated in field experiments for control of Propanil-resistant and -susceptible barnyardgrass in 1995 and 1996 in Arkansas. Propanil alone at 3.3 kg ai/ha did not control Propanil-resistant barnyardgrass when applied to two-leaf and repeated at four-leaf barnyardgrass. Propanil at 3.3 kg/ha with carbaryl at 0. 1 to 0.3 kg ai/ha controlled Propanil-resistant barnyardgrass at least 90% when applied at the two-leaf stage with no rice yield reduction. Applications repeated at the four-leaf stage also controlled Propanil-resistant barnyardgrass, but rice injury was 66% with 0.3 kg/ha carbaryl in 1 of 2 yr, and rice yield was reduced. Control of resistant barnyardgrass with the commercial formulation of Propanil plus carbaryl and Propanil plus molinate was lower with a single application than with repeat applications. Propanil plus quinclorac, Propanil plus pendimethalin, and Propanil plus molinate plus pendimethalin controlled resistant barnyardgrass with one application at the two-leaf stage. Nomenclature: Carbaryl, 1-naphthyl N-methylcarbamate; molinate, S-ethyl hexahydro-1H-azepine-1-carbothioate; pendimethalin, N-(1-ethylpropyl)-3,4-dimethyl-2,6-dinitrobenzenamine; Propanil, N-(3,4-dichlorophenyl)propanamide: quinclorac, 3,7-dichloro-8-quinolinecarboxylic acid; barnyardgrass, Echinochloa crus-galli (L.) Beauv. # 3 ECHCG; rice, Oryza sativa L. Lemont,' Kaybonnet'.
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Control of Propanil-resistant barnyardgrass (Echinochloa crus-galli) in rice (Oryza sativa) with carbaryl/Propanil mixtures
Weed Technology, 1999Co-Authors: Hassane Daou, Ronald E. TalbertAbstract:Propanil and carbaryl mixtures, Propanil formulated with carbaryl, the package mixture of Propanil plus molinate (alone and plus pendimethalin), Propanil plus quinclorac, and Propanil plus pendimethalin were evaluated in field experiments for control of Propanil-resistant and -susceptible barnyardgrass in 1995 and 1996 in Arkansas. Propanil alone at 3.3 kg ai/ha did not control Propanil-resistant barnyardgrass when applied to two-leaf and repeated at four-leaf barnyardgrass. Propanil at 3.3 kg/ha with carbaryl at 0. 1 to 0.3 kg ai/ha controlled Propanil-resistant barnyardgrass at least 90% when applied at the two-leaf stage with no rice yield reduction. Applications repeated at the four-leaf stage also controlled Propanil-resistant barnyardgrass, but rice injury was 66% with 0.3 kg/ha carbaryl in 1 of 2 yr, and rice yield was reduced. Control of resistant barnyardgrass with the commercial formulation of Propanil plus carbaryl and Propanil plus molinate was lower with a single application than with repeat applications. Propanil plus quinclorac, Propanil plus pendimethalin, and Propanil plus molinate plus pendimethalin controlled resistant barnyardgrass with one application at the two-leaf stage. Nomenclature: Carbaryl, 1-naphthyl N-methylcarbamate; molinate, S-ethyl hexahydro-1H-azepine-1-carbothioate; pendimethalin, N-(1-ethylpropyl)-3,4-dimethyl-2,6-dinitrobenzenamine; Propanil, N-(3,4-dichlorophenyl)propanamide: quinclorac, 3,7-dichloro-8-quinolinecarboxylic acid; barnyardgrass, Echinochloa crus-galli (L.) Beauv. # 3 ECHCG; rice, Oryza sativa L. Lemont,' Kaybonnet'.
Andreas Schaffer - One of the best experts on this subject based on the ideXlab platform.
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uptake and decomposition of the herbicide Propanil in the plant bidens pilosa l dominating in the yangtze three gorges reservoir tgr china
Environmental Science and Pollution Research, 2017Co-Authors: Zhongli Chen, Burkhard Schmidt, Andreas SchafferAbstract:Propanil (3′,4′-dichloropropionanilide) is a selective post emergence herbicide for controlling broad leaf and grass weeds in rice (Oryza sativa L.). After being taken up by plants, the fate of Propanil in decomposing plant material is of particular importance to the phytoremediation of the environment. Therefore, we investigated the biotransformation of Propanil in the plant Bidens pilosa under conditions close to those present in the Three Gorges Reservoir (TGR), China. Plants pre-treated with 14C-ring-labeled Propanil were either (treatment a) directly submerged in TGR water for 90 days or (treatment b) pre-extracted with organic solvents, and subsequently only insoluble materials and non-extractable residues (NER) of the pesticide fractions were similarly incubated. After incubation in TGR water (treatment a), 30 % of applied radioactivity was released into water and simultaneously, amounts of NER in the plant debris appeared to increase with time finally amounting to 40 % of applied 14C. The radioactivity contained in the extractable fractions were identified as Propanil, 3,4-dichloroaniline (DCA), and N-β-D-glucopyranosyl-3,4-dichloroaniline (DCA-Glu). In treatment b, significant 14C amounts were released to the water (6 % of applied 14C) and the solubilized radioactivity fractions were demonstrated to agree with those found in the extractable fractions. Therefore, if residues of the pesticide Propanil are taken up by plants, it may enter again the aquatic environment after plant death and submergence. This phenomenon may have a potential impact on aquatic organisms, which to our knowledge has not been reported before. As plant uptake and degradation of xenobiotics are recognized as detoxification, we consider B. pilosa with its high uptake potential, at least for Propanil, as suitable species for phytoremediation.
Aldo Ferrero - One of the best experts on this subject based on the ideXlab platform.
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dissipation of Propanil and 3 4 dichloroaniline in three different rice management systems
Journal of Environmental Quality, 2012Co-Authors: Marco Milan, Francesco Vidotto, Serenella Piano, Michele Negre, Aldo FerreroAbstract:: This study focused on the dissipation of Propanil and 3,4 dichloroaniline (3,4 DCA) over time in the soil, field water, inlet water, and outlet water of paddy fields under three management systems: conventional water seeding (CON), conventional water seeding with supplied liquid manure (LMA), and dry seeding (DRY). Propanil dissipation in water was also investigated under laboratory conditions. The field study was conducted from 2004 to 2006 at Vercelli, northern Italy. Propanil and 3,4 DCA showed rapid dissipation in water and soil environments both in the field and in the laboratory. Under controlled conditions, chemical hydrolysis was not detected for either compounds for up to 100 d at pHs of 5, 7, and 9. In the laboratory, the half-life of Propanil in irrigation water was 1.1 d; its half-life in soil was routinely measured at <1.0 d (between 0.17 and 1.77 d). 3,4 DCA was found to persist much longer. Measured in all three study years at 50 d after treatment, its concentration ranged between 44 μg kg (CON) and 140 μg kg (DRY). Propanil and 3,4 DCA concentrations in paddy water were particularly high in samples collected at 4 d (2004) and 2 d (2005) after treatment. Maximum concentrations were 54.4 μg L (CON) for Propanil (2005) and 113.7 μg L (LMA) for 3,4 DCA (2004). The concentrations of Propanil and 3,4 DCA in inlet water were never above 1.1 and 0.3 μg L, respectively, whereas the highest concentration of each compound in outlet water was in samples collected first after treatment in 2005 and 2006. Both chemicals dissipated rapidly in all the soil-water environments but displayed no important differences among the three management systems. In conclusion, Propanil and 3,4 DCA did not persist longer in paddy fields. A risk of water network contamination by these compounds may occur only early after herbicide spraying. A water-holding period after herbicide spraying may reduce this risk.
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Dissipation of Propanil and 3,4 dichloroaniline in three different rice management systems.
Journal of Environmental Quality, 2012Co-Authors: Marco Milan, Francesco Vidotto, Serenella Piano, Michele Negre, Aldo FerreroAbstract:: This study focused on the dissipation of Propanil and 3,4 dichloroaniline (3,4 DCA) over time in the soil, field water, inlet water, and outlet water of paddy fields under three management systems: conventional water seeding (CON), conventional water seeding with supplied liquid manure (LMA), and dry seeding (DRY). Propanil dissipation in water was also investigated under laboratory conditions. The field study was conducted from 2004 to 2006 at Vercelli, northern Italy. Propanil and 3,4 DCA showed rapid dissipation in water and soil environments both in the field and in the laboratory. Under controlled conditions, chemical hydrolysis was not detected for either compounds for up to 100 d at pHs of 5, 7, and 9. In the laboratory, the half-life of Propanil in irrigation water was 1.1 d; its half-life in soil was routinely measured at
