4.6 Article

Integration of Transcriptomics and Metabolomics for Evaluating Changes in the Liver of Zebrafish Exposed to a Sublethal Dose of Cyantraniliprole

Journal

WATER
Volume 15, Issue 3, Pages -

Publisher

MDPI
DOI: 10.3390/w15030521

Keywords

cyantraniliprole; zebrafish; toxicity; transcriptomics; metabolomics

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This study evaluated the influence of cyantraniliprole on zebrafish and provided data for assessing its risk in water. The results showed that sublethal concentrations of cyantraniliprole affected the transcription and metabolism of zebrafish liver, leading to liver damage.
Diamide insecticides are a class of insecticides with high efficiency, a broad spectrum, and environmental and ecological safety. However, their effect on the environment cannot be ignored, especially the chronic environmental effects of sublethal doses. In this study, we evaluated the influence of cyantraniliprole on zebrafish and provided data for evaluating the risk of cyantraniliprole in water. An acute toxicity test was used to obtain LC50, while 1/10 LC50 was selected to study the toxicity of the sublethal dose of cyantraniliprole on the transcription and metabolism of zebrafish liver. Our results showed that after exposure to a sublethal dose of cyantraniliprole for 30 days, the expression of various functional genes (elovl6, cpt1ab, eci1, fabp6, etc.) was abnormal and the content of various metabolites (Taurine, 1-Acyl-sn-glycero-3-phosphocholine, phosphatidylserine, betaine, sarcosine, etc.) was altered. In addition, transcriptional and metabolic correlation analysis revealed that sublethal doses of cyanobacteria could affect the fatty acid metabolism-related pathways of zebrafish liver (fatty acid elongation, metabolism, and degradation), as well as the PPAR pathway related to fat and the ABC pathway related to drug metabolism and transport. In conclusion, sublethal doses of cyantraniliprole caused abnormal liver metabolism in zebrafish by affecting fatty acid metabolism, up-regulating the PPAR pathway and down-regulating related genes and metabolites in the ABC pathway, which eventually led to liver damage.

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