| الوصف: |
Neonicotinoid insecticides are harmful to non-target soil invertebrates, which are crucial for sustainable agriculture. Gene expression biomarkers could provide economical and high-throughput metrics of neonicotinoid exposure and toxicity to non-target invertebrates and could help guide remediation efforts or policy enforcement. Gene expression of Glutathione S-Transferase 3 (GST3), which negates oxidative stress, has previously been proposed as a biomarker for the neonicotinoid imidacloprid in the soil ecotoxicological model species Folsomia candida (Collembola). It remains unclear, however, how reliably gene expression of neonicotinoid biomarkers, such as GST3, can indicate the exposure to the broader neonicotinoid family under varying oxidative stress conditions. 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 regimes 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 oxidative stress mediates the toxicity of imidacloprid and thiacloprid differentially. Due to influence of DEM on biomarker expression, future research should investigate biomarker reliability under increased oxidative stress conditions as provided by DEM exposure. |
