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In order to provide the scientific basis for the environmental risk assessment of cycloxaprid and 6-Cl-PMNI (intermediate of cycloxaprid), the degradation properties of 6-Cl-PMNI in aerobic, anaerobic and/or sterile soil, as well as in water with different pH values at different temperature were explored under laboratory conditions using HPLC for its kinetics study and UPLC-MS/MS for the identification of its metabolites/degradation products. Fortification study showed that the recoveries of 71.4–100.5% with the maximum coefficient variation (CV) of 7.47% were obtained. The linear range was 0.1–10 mg/L with the good linearity of R 2 = 0.9990. For standard, the method LOD (limit of detection) and LOQ (limit of quantification) was 0.03 mg/L and 0.1 mg/L, respectively. Results demonstrated the good performance of the developed method. Kinetics study indicated that the degradation half-lives (t 0.5 ) in pH 3-pH 10 buffers varied from 111.8 d to 288.8 d at 25 °C but rapidly shortened to 1.6–25.7 d at 70 °C. Good negative linear ships (R 2 ≥ 0.8423) between half life and temperature were found. 6-Cl-PMNI could be readily degraded in non-sterile soil (t 0.5 0.8–7.5 d) while slowly degraded in sterile soil (t 0.5 64.8–91.2 d). Three hydrolytic products and one metabolite of 6-Cl-PMNI in aerobic soil were identified. The C C olefinic bond reacted with H 2 O by Markovnikov Additive Reaction and the split of C–Cl were mainly proposed as the possible reaction pathway for 6-Cl-PMNI degradation in water and in soil, respectively. [ABSTRACT FROM AUTHOR]

Tebuconazole is widely used as fungicide and has frequently been detected at elevated concentrations in environmental media. To characterize the potential toxicity of tebuconazole on vertebrate and humans. Using zebrafish as a vertebrate model, the toxic effects in liver that produced by low-toxic concentrations of tebuconazole were assessed in adult zebrafish. We further focused on tebuconazole-induced toxicity and its possible mechanism in larval zebrafish using a hepatotoxicity assay. The induction of oxidative stress in adult fish was evaluated by superoxide dismutase (T-SOD), catalase (CAT), peroxidase (POD), glutathione S-transferase (GST) activity, and the increased aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio. Significantly increased enzyme activity was observed in the liver of male and female fish at both exposure and depuration stage. Exposure to maximum non-lethal (MNLC) concentration of tebuconazole from 72 to 120 h post-fertilization (hpf) affected the liver size and yolk retention in larval zebrafish. Decreased fluorescence intensity was observed in larval Tg(Apo14:GFP) zebrafish, indicating liver degeneration after tebuconazole treated. Histopathological examination confirmed the alterations in liver histoarchitecture in exposed zebrafish. Significant 1.28-fold and 1.65-fold increases in reactive oxygen species levels were observed in juveniles exposed to MNLC and lethal concentration 10 (LC 10) group, respectively. The acridine orange staining assay showed that apoptotic cells occurred in the liver regions. These results indicated that tebuconazole exposure resulted in impacts on the ecological risk in fish and vertebrate. Overall, the present study suggested further research in needed to better understand the tebuconazole-induced toxicity mechanism that associated with oxidative stress. Image 1 • Tebuconazole induced hepatotoxicity in both adult and larval zebrafish. • Tg(Apo14: GFP) zebrafish was used for hepatotoxicity assay. • Histopathological results showed alterations in liver histoarchitecture after exposure. • ROS-mediated pathway might induce apoptosis in zebrafish after tebuconazole exposure. [ABSTRACT FROM AUTHOR]