Zhang_2025_Pestic.Biochem.Physiol_209_106345

Dinotefuran, a third-generation neonicotinoid insecticide, is widely used in agriculture production due to its excellent insecticidal efficacy. Considering its persistence and high toxicity in soil, it is essential to evaluate its low-dose toxic effects on non-target soil organisms such as the springtail (Folsomia candida). The results revealed that the 7-day half lethal concentration (7d-LC(50)) of dinotefuran contact toxicity to springtails was 0.029 microg cm(-2). Its chronic toxicity in 4 soil types was ranked as: red soil (0.021 mg kg(-1)) > fluvo-aquic soil (0.040 mg kg(-1)) > artificial soil (0.049 mg kg(-1)) > black soil (0.085 mg kg(-1)). Soil organic matter (SOC), pH, and total nitrogen (TN) were identified as critical factors affecting dinotefuran toxicity. Biochemical assay results showed that environmental concentrations (0.2-1.6 mg kg(-1)) of dinotefuran induced oxidative stress and oxidative damage in springtails. Oxidative stress-related enzymes (including superoxide dismutase (SOD) and catalase (CAT)) and detoxification enzymes were subjected to initial activation at low dinotefuran concentrations, inhibition and re-activation at high concentration. Target enzyme acetylcholinesterase (AChE), malondialdehyde (MDA) content, and total protein content were inhibited with prolonged exposure time and increasing concentrations of dinotefuran. Molecular docking analysis showed that dinotefuran bound to the active sites of related enzymes, thus disrupting their structure and functions, eventually resulting in damages to physiological functions of springtails. In summary, this study deciphers the dinotefuran toxicological mechanism on soil springtails at environmental concentrations. Our findings lay theoretical basis for further assessing its pollution risk and managing its application.