Fosthiazate is a widely used organophosphorus nematicide that resides in the soil and controls soil root-knot nematodes. However, whether it has toxic effects on non-target soil organisms such as earthworms is unclear. Therefore, in this study, a 28-day experiment of fosthiazate exposure was conducted using the Eisenia fetida as the model organism. The results showed that fosthiazate stress caused excessive production of reactive oxygen species (ROS), increased the levels of malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine (8-OHdG), and decreased the activities of superoxide dismutase (SOD) and catalase (CAT), suggesting that fosthiazate induced oxidative stress and DNA damage in E. fetida. Acetylcholinesterase (AChE) activity was significantly reduced, and the expression of its related functional genes was also altered, demonstrating that fosthiazate damaged the nervous system of E. fetida, which was further confirmed by AlphaFold2 modeling and molecular docking simulations. Furthermore, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that fosthiazate exposure may induce apoptosis, inflammation, and viral infection in E. fetida, which adversely affect the organism. This study provides reference data for the ecotoxicity of fosthiazate.
Keywords: AlphaFold2 models; Molecular docking; Neurotoxicity; Oxidative stress; Transcriptomics.
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