Although imidacloprid has been shown to present potential risks to non-target invertebrates and vertebrates, researches exploring this risk from the perspective of the underground ecosystem remains incomplete. In this study, we determined that the presence of imidacloprid significantly reduced the abundance and diversity of soil nematodes in maize rhizospheric soil. Furthermore, imidacloprid also exerted negative effects on the body length, reproduction, locomotion, lipid accumulation, lipofuscin accumulation, and acetylcholinesterase activity in the model organism Caenorhabditis elegans. These toxic phenotypes are correlated with the upregulation of fat-2, fat-6, hsp-16.41, and hsp-16.2, along with the downregulation of ace-1, ace-2, and ace-3. In response to these toxic effects of imidacloprid, nematodes also developed corresponding adaptive mechanisms. UPLC-MS/MS analysis revealed that nematodes could convert imidacloprid to imidacloprid-guanidine and imidacloprid-urea to reduce the toxicity of imidacloprid. Moreover, C. elegans and Meloidogyne incognita exhibited repellent behavior towards imidacloprid-treated area, even the concentration of imidacloprid is only 0.4 μg/mL. This study revealed the interaction between imidacloprid and nematodes, providing a basis for understanding the potential risks of non-target soil nematodes after application of imidacloprid in sustainable agriculture and the resistance mechanism of nematodes to nematocidal pesticide.
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