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Luc Tirry - One of the best experts on this subject based on the ideXlab platform.

  • genetic and biochemical analysis of a laboratory selected spirodiclofen resistant strain of tetranychus urticae koch acari tetranychidae
    Pest Management Science, 2009
    Co-Authors: Steven Van Pottelberge, Thomas Van Leeuwen, Jahangir Khajehali, Luc Tirry
    Abstract:

    BACKGROUND: Spirodiclofen is a selective, non-systemic acaricide from the new chemical class of tetronic acid derivatives. In order to develop strategies to minimise resistance in the field, a laboratory-selected spirodiclofen-resistant strain of the two-spotted spider mite, Tetranychus urticae Koch, was used to determine genetic, toxicological, biochemical and cross-resistance data. RESULTS: Selecting for spirodiclofen resistance in the laboratory yielded a strain (SR-VP) with a resistance ratio of 274, determined on the larval stage. The egg stage remained far more susceptible. No cross-resistance was found against other established acaricides, except for spiromesifen. Based on synergist experiments and enzyme assays, it appeared that especially P450 monooxygenases, but also esterases and glutathione-S-transferases, could be involved in the Metabolic Detoxification of spirodiclofen. Genetic analysis showed that the resistance is inherited as an intermediate trait under control of more than one gene. CONCLUSIONS: Resistance to spirodiclofen exceeded by far the recommended field rate. A good acaricide resistance management programme is necessary to prevent fast resistance build-up in the field. Spirodiclofen can be used in alternation with most established acaricides, except for other tetronic acid derivatives. Without selection pressure, resistance tends to be unstable and can decrease in the presence of susceptible individuals owing to the intermediate, polygenic inheritance mode.

  • Effects of spirodiclofen on reproduction in a susceptible and resistant strain of Tetranychus urticae (Acari: Tetranychidae)
    Experimental and Applied Acarology, 2009
    Co-Authors: Steven Van Pottelberge, Thomas Van Leeuwen, Jahangir Khajehali, Luc Tirry
    Abstract:

    In this study the reproductive capacity of a laboratory-selected spirodiclofen resistant strain was investigated after treatment with spirodiclofen. Firstly, females were exposed to different concentrations of spirodiclofen (200 and 1,000 mg/l) during 6, 12 or 24 h. In contrast to the susceptible parental strain, the fecundity and fertility of resistant mites was not affected by treatment with these concentrations after any time of exposure tested. Secondly, pre-treatment of the resistant females with the synergists PBO or DEF could increase the inhibitory effect of spirodiclofen on reproduction, demonstrating the possible involvement of monooxygenases and esterases in Metabolic Detoxification of the acaricide. Because spirodiclofen interferes with lipid biosynthesis, total lipid content was measured in female adults. There were no significant differences between treated and non-treated female adults, both in the susceptible and resistant strain. However, the total lipid content in the resistant females was significantly higher than in susceptible females. Our data shows that the detection of spirodiclofen resistance should not be limited to mortality bioassays with eggs or larvae, but should be combined with inhibitory studies on female fertility and fecundity.

  • resistance mechanisms to mitochondrial electron transport inhibitors in a field collected strain of tetranychus urticae koch acari tetranychidae
    Bulletin of Entomological Research, 2009
    Co-Authors: S Van Pottelberge, T Van Leeuwen, Ralf Nauen, Luc Tirry
    Abstract:

    A Belgian field strain (MR-VP) of Tetranychus urticae (Koch) (Acari: Tetranychidae) exhibits different levels of resistance to four frequently used METI (mitochondrial electron transport inhibitor)-acaricides, i.e. tebufenpyrad, fenpyroximate, pyridaben and fenazaquin. Resistance factors for these compounds were 184, 1547, 5971 and 35, respectively. A 23.5-fold increase in 7-ethoxy-4-trifluoromethylcoumarin O-deethylation activity suggested that Metabolic resistance through elevated levels of cytochrome P450 dependent monooxygenase-activity is a possible resistance mechanism.However, synergism studies with different Metabolic inhibitors revealed some contrasting resistance mechanisms between the METI-acaricides. Tebufenpyrad resistance could only be synergized after pre-treatment with the monooxygenase inhibitor piperonyl butoxide (PBO), whereas pyridaben resistance was strongly synergized both by PBO and the esterase inhibitor S,S,S-tributylphosphorotrithioate (DEF). Resistance levels to fenpyroximate could neither be suppressed by PBO nor by DEF. Although METI-acaricides are structurally related, these findings probably reflect a different role of esterases and mono-oxygenases in Metabolic Detoxification between these compounds. The overall lack of synergism by diethylmaleate (DEM) suggests that glutathione-S-transferases are not an important factor in resistance to METIs.Reciprocal crosses between susceptible females and resistant males showed no maternal effect, and resistance to METI-acaricides was inherited generally as a dominant trait. Backcrosses with F1 females revealed striking differences in the mode of inheritance. Although resistance to fenpyroximate and pyridaben was under monogenic control, resistance to tebufenpyrad was under control of more than one gene.

Peter J Obrien - One of the best experts on this subject based on the ideXlab platform.

  • toxicity of glyoxals role of oxidative stress Metabolic Detoxification and thiamine deficiency
    Biochemical Society Transactions, 2003
    Co-Authors: Nandita Shangari, W R Bruce, R Poon, Peter J Obrien
    Abstract:

    : Glyoxals are reactive alpha-oxoaldehydes that are formed endogenously from sugars, the levels of which are increased in various pathological conditions associated with hyperglycaemia and thiamine deficiency. However, the molecular cytotoxic mechanisms of glyoxal are not known. Results presented here and in the other studies cited provide a glimpse into the cytotoxicity mechanisms involved and their pathological implications. We found that glyoxal (10 microM) markedly increased the susceptibility of hepatocyte glutathione (GSH) to oxidation by hydrogen peroxide (H(2)O(2)) and markedly increased cytotoxicity by compromising the cellular antioxidant enzyme system. At higher concentrations, glyoxal was cytotoxic towards hepatocytes, which can be attributed to GSH depletion, oxidative stress and mitochondrial toxicity. Aminoguanidine or penicillamine protected the hepatocytes. Glyoxal cytotoxicity was prevented by increasing glyoxal metabolism with thiamine or NAD(P)H generators, and was increased in GSH- or thiamine-deficient hepatocytes. It was also found that feeding rats reduced thiamine levels in a diet high in simple sugars increased the number of aberrant crypt foci/colon in the absence of clinical evidence of beriberi. This was associated with decreased plasma thiamine and low erythrocyte transketolase activity. Western diets, which are frequently poor in thiamine and high in sugars, could result in increased levels of endogenous glyoxals, which in turn may lead to a predisposition to AGE (advanced glycation end-product)-related pathologies and neoplastic conditions.

  • toxicity of glyoxals role of oxidative stress Metabolic Detoxification and thiamine deficiency
    Biochemical Society Transactions, 2003
    Co-Authors: Nandita Shangari, W R Bruce, R Poon, Peter J Obrien
    Abstract:

    : Glyoxals are reactive alpha-oxoaldehydes that are formed endogenously from sugars, the levels of which are increased in various pathological conditions associated with hyperglycaemia and thiamine deficiency. However, the molecular cytotoxic mechanisms of glyoxal are not known. Results presented here and in the other studies cited provide a glimpse into the cytotoxicity mechanisms involved and their pathological implications. We found that glyoxal (10 microM) markedly increased the susceptibility of hepatocyte glutathione (GSH) to oxidation by hydrogen peroxide (H(2)O(2)) and markedly increased cytotoxicity by compromising the cellular antioxidant enzyme system. At higher concentrations, glyoxal was cytotoxic towards hepatocytes, which can be attributed to GSH depletion, oxidative stress and mitochondrial toxicity. Aminoguanidine or penicillamine protected the hepatocytes. Glyoxal cytotoxicity was prevented by increasing glyoxal metabolism with thiamine or NAD(P)H generators, and was increased in GSH- or thiamine-deficient hepatocytes. It was also found that feeding rats reduced thiamine levels in a diet high in simple sugars increased the number of aberrant crypt foci/colon in the absence of clinical evidence of beriberi. This was associated with decreased plasma thiamine and low erythrocyte transketolase activity. Western diets, which are frequently poor in thiamine and high in sugars, could result in increased levels of endogenous glyoxals, which in turn may lead to a predisposition to AGE (advanced glycation end-product)-related pathologies and neoplastic conditions.

  • the formaldehyde Metabolic Detoxification enzyme systems and molecular cytotoxic mechanism in isolated rat hepatocytes
    Chemico-Biological Interactions, 2001
    Co-Authors: Shirley Teng, Kristin Beard, Jalal Pourahmad, Majid Y Moridani, Elaine Easson, Raymond Poon, Peter J Obrien
    Abstract:

    The toxicity and carcinogenicity of formaldehyde (HCHO) has been attributed to its ability to form adducts with DNA and proteins. A marked decrease in mitochondrial membrane potential and inhibition of mitochondrial respiration that was accompanied by reactive oxygen species formation occurred when isolated rat hepatocytes were incubated with low concentrations of HCHO in a dose-dependent manner. Hepatocyte GSH was also depleted by HCHO in a dose-dependent manner. At higher HCHO concentrations, lipid peroxidation ensued followed by cell death. Cytotoxicity studies were conducted in which isolated hepatocytes exposed to HCHO were treated with inhibitors of HCHO metabolising enzymes. There was a marked increase in HCHO cytotoxicity when either alcohol dehydrogenase or aldehyde dehydrogenase was inhibited. Inhibition of GSH-dependent HCHO dehydrogenase activity by prior depletion of GSH markedly increased hepatocyte susceptibility to HCHO. In each case, cytotoxicity was dose-dependent and corresponded with a decrease in hepatocyte HCHO metabolism and increased lipid peroxidation. Antioxidants and iron chelators protected against HCHO cytotoxicity. Cytotoxicity was also prevented, when cyclosporine or carnitine was added to prevent the opening of the mitochondrial permeability transition pore which further suggests that HCHO targets the mitochondria. Thus, HCHO-metabolising gene polymorphisms would be expected to have toxicological consequences on an individual's susceptibility to HCHO toxicity and carcinogenesis.

Troy D Anderson - One of the best experts on this subject based on the ideXlab platform.

  • effect of alachlor and metolachlor on toxicity of chlorpyrifos and major Detoxification enzymes in the aquatic midge chironomus tentans diptera chironomidae
    Archives of Environmental Contamination and Toxicology, 2008
    Co-Authors: Ying Jinclark, Troy D Anderson
    Abstract:

    The toxicities of two herbicides (alachlor and metolachlor) and an organophosphate insecticide (chlorpyrifos) were evaluated individually and with either herbicide in binary mixture with chlorpyrifos in fourth-instar larvae of the aquatic midge (Chironomus tentans). Alachlor alone up to 1,000 micrograms per liter of water (μg/L) did not exhibit significant toxicity, whereas metolachlor at 1,000 μg/L affected 58% of midges in 72-h bioassays. However, alachlor at 1,000 μg/L and metolachlor at 10, 100, and 1,000 μg/L enhanced the toxicity of chlorpyrifos to the midges. Furthermore, alachlor and metolachlor at 1,000 μg/L reduced acetylcholinesterase (AChE) activity by 34.3% and 27.6%, respectively, in the treated midges. Although alachlor at 1,000 μg/L did not significantly affect protein production in the treated midges, it reduced glutathione S-transferases (GST) total activities by 1.9- to 2.1-fold. In contrast, metolachlor at 1,000 μg/L reduced protein production by 3.2-fold, which was associated with a 2.8-fold reduction of cytochrome P450 O-deethylation total activity and 1.4- to 1.7-fold reductions of GST total activities in the treated midges. Such reduced total activities of the major Detoxification enzymes in herbicide-treated midges might impede the Metabolic Detoxification of chlorpyrifos and, therefore, increase the susceptibility of the midges to chlorpyrifos. Thus, it is likely that coexistence of chlorpyrifos and these herbicides, particularly metolachlor, in surface waters may pose increased risks to midges in aquatic environments.

  • synergistic and antagonistic effects of atrazine on the toxicity of organophosphorodithioate and organophosphorothioate insecticides to chironomus tentans diptera chironomidae
    Pesticide Biochemistry and Physiology, 2004
    Co-Authors: Troy D Anderson
    Abstract:

    Abstract The acute toxicities of two organophosphorodithioate (dimethoate and disulfoton) and two organophosphorothioate (omethoate and demeton-S-methyl) insecticides were evaluated individually and in binary combination with the herbicide atrazine using fourth-instar larvae of the aquatic midge, Chironomus tentans. Atrazine alone up to 1000 μg/L did not show significant toxicity to the midges in a 48-h bioassay. However, atrazine concentrations as low as 1 μg/L in combination with dimethoate at EC25 (concentration to affect 25% of tested midges), 100 μg/L in combination with disulfoton (EC25), and 10 μg/L in combination with demeton-S-methyl (EC25) significantly enhanced the toxicity of each organophosphate insecticide. In contrast, atrazine concentrations of 10 μg/L and above in combination with omethoate (EC25) significantly decreased the toxicity of the insecticide. Biochemical analysis indicated that increased toxicity of dimethoate, disulfoton, and demeton-S-methyl in binary combination with atrazine correlated to the increased inhibition of acetylcholinesterase. Furthermore, cytochrome P450-dependent O-deethylation activity in the midges exposed to atrazine at 1000 μg/L was 1.5-fold higher than that in the control midges. Thus, atrazine appeared to induce cytochrome P450 monooxygenases in the midges. Elevated cytochrome P450 monooxygenase activity may increase the toxicities of dimethoate, disulfoton, and demeton-S-methyl by enhancing the oxidative activation of dimethoate into omethoate, and disulfoton and demeton-S-methyl into their sulfoxide analogs with increased anticholinesterase activity. In contrast, atrazine reduced the toxicity of omethoate possibly by enhancing the oxidative Metabolic Detoxification since omethoate does not require oxidative activation.

Jahangir Khajehali - One of the best experts on this subject based on the ideXlab platform.

  • incidence and characterization of resistance to pyrethroid and organophosphorus insecticides in thrips tabaci thysanoptera thripidae in onion fields in isfahan iran
    Pesticide Biochemistry and Physiology, 2016
    Co-Authors: A Nazemi, Jahangir Khajehali, T G Van Leeuwen
    Abstract:

    Onion thrips, Thrips tabaci Lindeman, is the main pest of onion-growing fields in Isfahan and is mainly controlled by frequently spraying several insecticides. To investigate the resistance status and mechanisms, the susceptibility of ten field populations collected from Isfahan onion-growing regions were tested to several currently used pesticides. Resistance to the tested insecticides was observed in most populations when compared with the susceptible reference population. Enhanced Detoxification, implicated by the use of inhibitors of major Metabolic Detoxification enzymes, was observed in the populations resistant to profenofos and chlorpyrifos. In the deltamethrin resistant populations, the amino acid substitution T929I was detected in the voltage gated sodium channel, which is known to confer pyrethroid resistance. These data are a first step towards more efficient resistance management tactics through early detection of resistant onion thrips in Iran.

  • genetic and biochemical analysis of a laboratory selected spirodiclofen resistant strain of tetranychus urticae koch acari tetranychidae
    Pest Management Science, 2009
    Co-Authors: Steven Van Pottelberge, Thomas Van Leeuwen, Jahangir Khajehali, Luc Tirry
    Abstract:

    BACKGROUND: Spirodiclofen is a selective, non-systemic acaricide from the new chemical class of tetronic acid derivatives. In order to develop strategies to minimise resistance in the field, a laboratory-selected spirodiclofen-resistant strain of the two-spotted spider mite, Tetranychus urticae Koch, was used to determine genetic, toxicological, biochemical and cross-resistance data. RESULTS: Selecting for spirodiclofen resistance in the laboratory yielded a strain (SR-VP) with a resistance ratio of 274, determined on the larval stage. The egg stage remained far more susceptible. No cross-resistance was found against other established acaricides, except for spiromesifen. Based on synergist experiments and enzyme assays, it appeared that especially P450 monooxygenases, but also esterases and glutathione-S-transferases, could be involved in the Metabolic Detoxification of spirodiclofen. Genetic analysis showed that the resistance is inherited as an intermediate trait under control of more than one gene. CONCLUSIONS: Resistance to spirodiclofen exceeded by far the recommended field rate. A good acaricide resistance management programme is necessary to prevent fast resistance build-up in the field. Spirodiclofen can be used in alternation with most established acaricides, except for other tetronic acid derivatives. Without selection pressure, resistance tends to be unstable and can decrease in the presence of susceptible individuals owing to the intermediate, polygenic inheritance mode.

  • Effects of spirodiclofen on reproduction in a susceptible and resistant strain of Tetranychus urticae (Acari: Tetranychidae)
    Experimental and Applied Acarology, 2009
    Co-Authors: Steven Van Pottelberge, Thomas Van Leeuwen, Jahangir Khajehali, Luc Tirry
    Abstract:

    In this study the reproductive capacity of a laboratory-selected spirodiclofen resistant strain was investigated after treatment with spirodiclofen. Firstly, females were exposed to different concentrations of spirodiclofen (200 and 1,000 mg/l) during 6, 12 or 24 h. In contrast to the susceptible parental strain, the fecundity and fertility of resistant mites was not affected by treatment with these concentrations after any time of exposure tested. Secondly, pre-treatment of the resistant females with the synergists PBO or DEF could increase the inhibitory effect of spirodiclofen on reproduction, demonstrating the possible involvement of monooxygenases and esterases in Metabolic Detoxification of the acaricide. Because spirodiclofen interferes with lipid biosynthesis, total lipid content was measured in female adults. There were no significant differences between treated and non-treated female adults, both in the susceptible and resistant strain. However, the total lipid content in the resistant females was significantly higher than in susceptible females. Our data shows that the detection of spirodiclofen resistance should not be limited to mortality bioassays with eggs or larvae, but should be combined with inhibitory studies on female fertility and fecundity.

Fang Zhu - One of the best experts on this subject based on the ideXlab platform.

  • rna interference of nadph cytochrome p450 reductase increases susceptibilities to multiple acaricides in tetranychus urticae
    Pesticide Biochemistry and Physiology, 2020
    Co-Authors: Adekunle W. Adesanya, Mark D. Lavine, Laura Corley Lavine, Antonio Cardenas, Douglas B Walsh, Fang Zhu
    Abstract:

    The two-spotted spider mite, Tetranychus urticae, is a polyphagous pest feeding on over 1100 plant species, including numerous highly valued economic crops. The control of T. urticae largely depends on the use of acaricides, which leads to pervasive development of acaricide resistance. Cytochrome P450-mediated Metabolic Detoxification is one of the major mechanisms of acaricide resistance in T. urticae. NADPH-cytochrome P450 reductase (CPR) plays as a crucial co-factor protein that donates electron(s) to microsomal cytochrome P450s to complete their catalytic cycle. This study seeks to understand the involvement of CPR/P450 in acaricide resistance in T. urticae. The full-length cDNA sequence of T. urticae's CPR (TuCPR) was cloned and characterized. TuCPR was ubiquitously transcribed in different life stages of T. urticae and the highest transcription was observed in the nymph and adult stages. TuCPR was constitutively over-expressed in six acaricide resistant populations compared to a susceptible one. TuCPR transcriptional expression was also induced by multiple acaricides in a time-dependent manner. Down-regulation of TuCPR via RNA interference (RNAi) in T. urticae led to reduced enzymatic activities of TuCPR and cytochrome P450s, as well as a reduction of resistance to multiple acaricides, abamectin, bifenthrin, and fenpyroximate. The outcome of this study highlights CPR as a potential novel target for eco-friendly control of T. urticae and other related plant-feeding pests.

  • rna interference of nadph cytochrome p450 reductase increases susceptibilities to multiple acaricides in tetranychus urticae
    bioRxiv, 2019
    Co-Authors: Adekunle W. Adesanya, Mark D. Lavine, Laura Corley Lavine, Antonio Cardenas, Douglas B Walsh, Fang Zhu
    Abstract:

    The two-spotted spider mite, Tetranychus urticae, is a polyphagous pest feeding on over 1,100 plant species, including numerous highly valued economic crops. The control of T. urticae largely depends on the use of acaricides, which leads to pervasive development of acaricide resistance. Cytochrome P450-mediated Metabolic Detoxification is one of the major mechanisms of acaricide resistance in T. urticae. NADPH-cytochrome P450 reductase (CPR) plays as a crucial co-factor protein that donates electron(s) to microsomal cytochrome P450s to complete their catalytic cycle. This study seeks to understand the involvement of CPR in acaricide resistance in urticae. The full-length cDNA sequence of T. urticaes CPR (TuCPR) was cloned and characterized. TuCPR was ubiquitously transcribed in different life stages of T. urticae and the highest transcription was observed in the nymph and adult stages. TuCPR was constitutively over-expressed in six acaricide resistant populations compared to a susceptible one. TuCPR transcriptional expression was also induced by multiple acaricides in a time-dependent manner. Down-regulation of TuCPR via RNA interference (RNAi) in T. urticae led to reduced enzymatic activities of TuCPR and cytochrome P450s, as well as a significant reduction of resistance to multiple acaricides, abamectin, bifenthrin, and fenpyroximate. The outcome of this study highlights CPR as a potential novel target for eco-friendly control of T. urticae and other related plant-feeding pests.nnHighlightsO_LIPipernoyl butoxide significantly reduced abamectin, bifenthrin, and fenpyroximate resistance in T. urticae populationsnC_LIO_LIT. urticaes cytochrome P450 reductase (TuCPR) was cloned, sequenced and phylogenetically analyzednC_LIO_LIAbamectin, bifenthrin and fenpyroximate treatment induced TuCPR gene expressionnC_LIO_LISilencing of TuCPR in T. urticae caused a reduction in acaricide resistancenC_LI

  • Multiple acaricide resistance and underlying mechanisms in Tetranychus urticae on hops
    Journal of Pest Science, 2018
    Co-Authors: Adekunle W. Adesanya, Mark D. Lavine, Laura Corley Lavine, Douglas B Walsh, Mariany A. Morales, Fang Zhu
    Abstract:

    The polyphagous pest Tetranychus urticae feeds on over 1100 plant species including highly valued economic crops such as hops (Humulus lupulus). In the key hop production region of the Pacific Northwest of the USA, T. urticae is one of the major arthropod pests. Over the years, T. urticae control has been dominated by the application of various acaricides. However, T. urticae quickly adapts to these acaricides by developing resistance. Here, we determined resistance ratios of T. urticae populations in hops to three acaricides: etoxazole, fenpyroximate, and spirodiclofen. The mechanisms underlying resistance to these and three other acaricides were investigated in 37 field-collected T. urticae populations using a comprehensive diagnostic approach. Our data showed that T. urticae populations exhibited complex adaptation patterns to acaricides. Resistance to abamectin, fenpyroximate, and spirodiclofen by enhanced target Metabolic Detoxification gene(s) was identified in 100%, 50%, and 20% of populations tested, respectively. Resistance to bifenthrin, bifenazate, and etoxazole by target site insensitivity was pervasive among tested populations. Our study provides new information in understanding the complexity of T. urticae adaptation to multiple acaricides, which will help in designing sustainable pest control strategies for T. urticae on hops and other economically valuable crops.