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.

Fosthiazate 是一种广泛使用的有机磷杀线虫剂，存在于土壤中并控制土壤根结线虫。然而，它是否对蚯蚓等非目标土壤生物有毒性作用尚不清楚。因此，在本研究中，以 Eisenia fetida 为模式生物进行了为期 28 天的 fosthiazate 暴露实验。结果表明，磷噻氮酯胁迫导致活性氧（ROS）的过量产生，丙二醛（MDA）和8-羟基-2-脱氧鸟苷（8-OHdG）水平升高，超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性降低，表明磷硫唑酯诱导了Fetida的氧化应激和DNA损伤.乙酰胆碱酯酶 （AChE） 活性显著降低，其相关功能基因的表达也发生改变，表明 fosthiazate 损害了 E. fetida 的神经系统，AlphaFold2 建模和分子对接模拟进一步证实了这一点。此外，京都基因与基因组百科全书 （KEGG） 富集分析表明，磷硫氮酸盐暴露可能诱导 E. fetida 细胞凋亡、炎症和病毒感染，从而对生物体产生不利影响。本研究为磷硫唑酯的生态毒性提供了参考数据。