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Oxidative stress and mitochondrial damage induced by a novel pesticide fluopimomide in Caenorhabditis elegans

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Abstract

Fluopimomide is a novel pesticide intensively used in agricultural pest control; however, its excessive use may have toxicological effects on non-target organisms. In this study, Caenorhabditis elegans was used to evaluate the toxic effects of fluopimomide and its possible mechanisms. The effects of fluopimomide on the growth, pharyngeal pumping, and antioxidant systems of C. elegans were determined. Furthermore, the gene expression levels associated with mitochondria in the nematodes were also investigated. Results indicated that fluopimomide at 0.2, 1.0, and 5.0 mg/L notably (p < 0.001) decreased body length, pharyngeal pumping, and body bends in the nematodes compared to the untreated control. Additionally, fluopimomide at 0.2, 1.0, and 5.0 mg/L notably (p < 0.05) increased the content of malondialdehyde by 3.30-, 21.24-, and 33.57-fold, respectively, while fluopimomide at 1.0 and 5.0 mg/L significantly (p < 0.001) increased the levels of reactive oxygen species (ROS) by 49.14% and 77.06% compared to the untreated control. In contrast, fluopimomide at 1.0 and 5.0 mg/L notably reduced the activities of target enzyme succinate dehydrogenase and at 5.0 mg/L reduced the activities of antioxidant enzyme superoxide dismutase. Further evidence revealed that fluopimomide at 1.0 and 5.0 mg/L significantly inhibited oxygen consumption and at 0.2, 1.0, and 5.0 mg/L significantly inhibited ATP level in comparison to the untreated control. The expression of genes related to the mitochondrial electron transport chain mev-1 and isp-1 was significantly downregulated. ROS levels in the mev-1 and isp-1 mutants after fluopimomide treatments did not change significantly compared with the untreated mutants, suggesting that mev-1 and isp-1 may play critical roles in the toxicity induced by fluopimomide. Overall, the results demonstrate that oxidative stress and mitochondrial damage may be involved in toxicity of fluopimomide in C. elegans.

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The datasets used and/or analyzed during the current study are available from authors on a reasonable request.

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Funding

This work was supported by Shandong Provincial Natural Science Foundation (ZR2021MC065), Shandong Innovation Capability Enhancement Project for Technological Small and Medium sized Enterprises (2023TSGC0613), Shandong Province Modern Agricultural Technology System Peanut Innovation Team, China (SDAIT-04-08), and National Natural Science Foundation of China (31601661).

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KQ and XJ conceived and designed the research. HL, GF, LB, and WL conducted the experiments and analyzed data. All authors contributed to discussion of the results. KQ and SZ supervised the research, and reviewed and revised the manuscript. KQ wrote the paper. All authors read this manuscript and approved its submission.

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Correspondence to Kang Qiao.

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This article does not contain any studies with human participants or animals performed by any of the authors. Informed consent was obtained from all individual participants included in the study.

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The authors declare no competing interests.

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Liu, H., Fu, G., Li, W. et al. Oxidative stress and mitochondrial damage induced by a novel pesticide fluopimomide in Caenorhabditis elegans. Environ Sci Pollut Res 30, 91794–91802 (2023). https://doi.org/10.1007/s11356-023-28893-z

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  • DOI: https://doi.org/10.1007/s11356-023-28893-z

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