Journal
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 30, Issue 42, Pages 95338-95347Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s11356-023-28940-9
Keywords
Springtails; Neonicotinoids; Biomarkers; Glutathione-S-transferase; Diethyl maleate
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Neonicotinoid insecticides have negative effects on non-target soil invertebrates, but gene expression biomarkers could be used to measure exposure and toxicity. The expression of Glutathione S-Transferase 3 (GST3) has been proposed as a biomarker, but its reliability and its response to different neonicotinoids and metabolic inhibitors are unclear. In this study, springtails were exposed to neonicotinoids and a GST metabolic inhibitor, and the effects on fecundity and gene expression were measured. The results suggest that GST3 is not a reliable indicator of neonicotinoid exposure, and the toxicity of different neonicotinoids is mediated by probable GST enzymatic inhibition. Further research is needed to investigate biomarker reliability under different metabolic conditions.
Neonicotinoid insecticides are harmful to non-target soil invertebrates, which are crucial for sustainable agriculture. Gene expression biomarkers could provide economic and high-throughput metrics of neonicotinoid exposure and toxicity to non-target invertebrates. Thereby, biomarkers can help guide remediation efforts or policy enforcement. Gene expression of Glutathione S-Transferase 3 (GST3) has previously been proposed as a biomarker for the neonicotinoid imidacloprid in the soil ecotoxicological model species Folsomia candida (Collembola). However, it remains unclear how reliably gene expression of neonicotinoid biomarkers, such as GST3, can indicate the exposure to the broader neonicotinoid family under putative GST enzymatic inhibition. In this work, we exposed springtails to two neonicotinoids, thiacloprid and imidacloprid, alongside diethyl maleate (DEM), a known GST metabolic inhibitor that imposes oxidative stress. First, we determined the influence of DEM on neonicotinoid toxicity to springtail fecundity. Second, we surveyed the gene expression of four biomarkers, including GST3, under mutual exposure to neonicotinoids and DEM. We observed no effect of DEM on springtail fecundity. Moreover, the expression of GST3 was only influenced by DEM under mutual exposure with thiacloprid but not with imidacloprid. The results indicate that GST3 is not a robust indicator of neonicotinoid exposure and that probable GST enzymatic inhibition mediates the toxicity of imidacloprid and thiacloprid differentially. Future research should investigate biomarker reliability under shifting metabolic conditions such as provided by DEM exposure.
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