2018Environmental PollutionOpen access

The use of gene expression to unravel the single and mixture toxicity of abamectin and difenoconazole on survival and reproduction of the springtail Folsomia candida

Lívia Pitombeira de Figueirêdo, Michiel A. Daam, Giulia Mainardi, Janine Mariën, Evaldo Luiz Gaeta Espíndola, Cornelis A.M. van Gestel, Dick Roelofs

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Abstract

Pesticides risk assessments have traditionally focused on the effects on standard parameters, such as mortality, reproduction and development.However, one of the first signs of adverse effects that occur in organisms exposed to stress conditions is an alteration in their genomic expression, which is specific to the type of stress, sensitive to very low contaminant concentrations and responsive in a few hours.The aim of the present study was to evaluate the single and binary mixture toxicity of commercial products of abamectin (Kraft ® 36 EC) and difenoconazole (Score ® 250 EC) to Folsomia candida.Laboratory toxicity tests were conducted to access the effects of these pesticides on springtail survival, reproduction and gene expression.The reproduction assays gave EC 50 and EC 10 values, respectively, of 6.3 and 1.4 mg a.s./ kg dry soil for abamectin; 1.0 and 0.12 mg a.s./kg dry soil for Kraft ® 36 EC; and 54 and 23 mg a.s./kg dry soil for Score ® 250 EC.Technical difenoconazole did not have any effect at the concentrations tested.No significant differences in gene expression were found between the abamectin concentrations tested (EC 10 and EC 50 ) and the solvent control.Exposure to Kraft ® 36 EC, however, significantly induced Cyp6 expression at the EC 50 level, while VgR was significantly downregulated at both the EC 10 and EC 50 .Exposure to the simple pesticide mixture of Kraft ® 36 EC þ Score ® 250 EC caused significant up regulation of ABC transporter, and significant down regulation of VgR relative to the controls.GABA receptor also showed significant down-regulation between the EC 10 and EC 50 mixture treatments.Results of the present study demonstrate that pesticide-induced gene expression effects precede and occur at lower concentrations than organism-level responses.Integrating "omic" endpoints in traditional bioassays may thus be a promising way forward in pesticide toxicity evaluations.

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Pesticides risk assessments have traditionally focused on the effects on standard parameters, such as mortality, reproduction and development.However, one of the first signs of adverse effects that occur in organisms exposed to stress conditions is an alteration in their genomic expression, which is specific to the type of stress, sensitive to very low contaminant concentrations and responsive in a few hours.The aim of the present study was to evaluate the single and binary mixture toxicity of commercial products of abamectin (Kraft ® 36 EC) and difenoconazole (Score ® 250 EC) to Folsomia candida.Laboratory toxicity tests were conducted to access the effects of these pesticides on springtail survival, reproduction and gene expression.The reproduction assays gave EC 50 and EC 10 values, respectively, of 6.3 and 1.4 mg a.s./ kg dry soil for abamectin; 1.0 and 0.12 mg a.s./kg dry soil for Kraft ® 36 EC; and 54 and 23 mg a.s./kg dry soil for Score ® 250 EC.Technical difenoconazole did not have any effect at the concentrations tested.No significant differences in gene expression were found between the abamectin concentrations tested (EC 10 and EC 50 ) and the solvent control.Exposure to Kraft ® 36 EC, however, significantly induced Cyp6 expression at the EC 50 level, while VgR was significantly downregulated at both the EC 10 and EC 50 .Exposure to the simple pesticide mixture of Kraft ® 36 EC þ Score ® 250 EC caused significant up regulation of ABC transporter, and significant down regulation of VgR relative to the controls.GABA receptor also showed significant down-regulation between the EC 10 and EC 50 mixture treatments.Results of the present study demonstrate that pesticide-induced gene expression effects precede and occur at lower concentrations than organism-level responses.Integrating "omic" endpoints in traditional bioassays may thus be a promising way forward in pesticide toxicity evaluations.

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Available abstract

Pesticides risk assessments have traditionally focused on the effects on standard parameters, such as mortality, reproduction and development.However, one of the first signs of adverse effects that occur in organisms exposed to stress conditions is an alteration in their genomic expression, which is specific to the type of stress, sensitive to very low contaminant concentrations and responsive in a few hours.The aim of the present study was to evaluate the single and binary mixture toxicity of commercial products of abamectin (Kraft ® 36 EC) and difenoconazole (Score ® 250 EC) to Folsomia candida.Laboratory toxicity tests were conducted to access the effects of these pesticides on springtail survival, reproduction and gene expression.The reproduction assays gave EC 50 and EC 10 values, respectively, of 6.3 and 1.4 mg a.s./ kg dry soil for abamectin; 1.0 and 0.12 mg a.s./kg dry soil for Kraft ® 36 EC; and 54 and 23 mg a.s./kg dry soil for Score ® 250 EC.Technical difenoconazole did not have any effect at the concentrations tested.No significant differences in gene expression were found between the abamectin concentrations tested (EC 10 and EC 50 ) and the solvent control.Exposure to Kraft ® 36 EC, however, significantly induced Cyp6 expression at the EC 50 level, while VgR was significantly downregulated at both the EC 10 and EC 50 .Exposure to the simple pesticide mixture of Kraft ® 36 EC þ Score ® 250 EC caused significant up regulation of ABC transporter, and significant down regulation of VgR relative to the controls.GABA receptor also showed significant down-regulation between the EC 10 and EC 50 mixture treatments.Results of the present study demonstrate that pesticide-induced gene expression effects precede and occur at lower concentrations than organism-level responses.Integrating "omic" endpoints in traditional bioassays may thus be a promising way forward in pesticide toxicity evaluations.

Key concepts: Springtail, Abamectin, EC50, Toxicity, Biology, Ecotoxicology, Pesticide, Toxicology

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The use of gene expression to unravel the single and mixture toxicity of abamectin and difenoconazole on survival and reproduction of the springtail Folsomia candida — Research Paper | ScholarLens