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

Livia Pitombeira de Figueirêdo, Michiel A Daam, Giulia Mainardi, Janine Mariën, Evaldo L G Espíndola, Cornelis A M van Gestel, Dick Roelofs

Research output: Contribution to JournalArticleAcademicpeer-review

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 EC50 and EC10 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 (EC10 and EC50) and the solvent control. Exposure to Kraft® 36 EC, however, significantly induced Cyp6 expression at the EC50 level, while VgR was significantly downregulated at both the EC10 and EC50. Exposure to the simple pesticide mixture of Kraft® 36 EC + 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 EC10 and EC50 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.

Original languageEnglish
Pages (from-to)342-350
Number of pages9
JournalEnvironmental Pollution
Volume244
Early online date16 Oct 2018
DOIs
Publication statusPublished - Jan 2019

Fingerprint

abamectin
Candida
Pesticides
Gene expression
Reproduction
Toxicity
Gene Expression
Soil
Down-Regulation
Soils
Toxicity Tests
GABA Receptors
ATP-Binding Cassette Transporters
Bioassay
Binary mixtures
Biological Assay
Risk assessment
Assays
Up-Regulation
difenoconazole

Keywords

  • ABC transporter
  • Cyp6
  • GABA receptor
  • Pesticides
  • Vitellogenin receptor

Cite this

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title = "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",
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{\circledR} 36 EC) and difenoconazole (Score{\circledR} 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 EC50 and EC10 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{\circledR} 36 EC; and 54 and 23 mg a.s./kg dry soil for Score{\circledR} 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 (EC10 and EC50) and the solvent control. Exposure to Kraft{\circledR} 36 EC, however, significantly induced Cyp6 expression at the EC50 level, while VgR was significantly downregulated at both the EC10 and EC50. Exposure to the simple pesticide mixture of Kraft{\circledR} 36 EC + Score{\circledR} 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 EC10 and EC50 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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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. / Pitombeira de Figueirêdo, Livia; Daam, Michiel A; Mainardi, Giulia; Mariën, Janine; Espíndola, Evaldo L G; van Gestel, Cornelis A M; Roelofs, Dick.

In: Environmental Pollution, Vol. 244, 01.2019, p. 342-350.

Research output: Contribution to JournalArticleAcademicpeer-review

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AU - Pitombeira de Figueirêdo, Livia

AU - Daam, Michiel A

AU - Mainardi, Giulia

AU - Mariën, Janine

AU - Espíndola, Evaldo L G

AU - van Gestel, Cornelis A M

AU - Roelofs, Dick

N1 - Copyright © 2018 Elsevier Ltd. All rights reserved.

PY - 2019/1

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N2 - 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 EC50 and EC10 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 (EC10 and EC50) and the solvent control. Exposure to Kraft® 36 EC, however, significantly induced Cyp6 expression at the EC50 level, while VgR was significantly downregulated at both the EC10 and EC50. Exposure to the simple pesticide mixture of Kraft® 36 EC + 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 EC10 and EC50 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.

AB - 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 EC50 and EC10 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 (EC10 and EC50) and the solvent control. Exposure to Kraft® 36 EC, however, significantly induced Cyp6 expression at the EC50 level, while VgR was significantly downregulated at both the EC10 and EC50. Exposure to the simple pesticide mixture of Kraft® 36 EC + 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 EC10 and EC50 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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