Transcriptomic analysis of the toxic effects and potential mechanisms of fenvalerate on the liver of Odontobutis potamophila

This study explored the toxic effects of short-term exposure (96 h) to fenvalerate (FEN) at environmental concentrations (C0.5: 0.5 µg/L) and application concentrations (C2: 2 µg/L) on the liver of Odontobutis potamophila and analyzed the potential toxicity mechanisms. The results showed that FEN exposure caused tissue damage and oxidative stress in O. potamophila liver in a concentration-dependent manner. Transcriptomic analysis revealed 2083 differentially expressed genes (DEGs) between control (CK) and C0.5 treatments and 2595 DEGs between CK and C2 treatments. Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed significant DEG enrichment in pathways such as serotonergic synapse, estrogen signaling, retrograde endocannabinoid signaling, etc. in C0.5, and in pathways such as oxidative phosphorylation, glutathione metabolism, retrograde endocannabinoid signaling, etc. in C2. Gene Ontology enrichment analysis showed significant DEGs enrichment in pathways such as DNA integration, obsolete oxidation-reduction process, regulation of DNA-templated transcription, etc. in C0.5, and in pathways such as obsolete oxidation-reduction process, translation, structural constituent of ribosome, etc. in C2. Investigation of genes related to liver mitochondrial function, including expression of cytochrome b (CYTB), cytochrome c oxidase subunit II (COX2), cytochrome c oxidase subunit III (COX3), and NADH dehydrogenase subunit 1 (ND1), demonstrated that CYTB and ND1 were significantly downregulated (P < 0.05) in a concentration-dependent manner, while COX2 and COX3 were significantly upregulated (P < 0.05) in C0.5 and C2, indicating that FEN could damage mitochondrial function in O. potamophila liver. In summary, this study revealed that the toxic effects of FEN on the liver of O. potamophila manifested as causing oxidative stress, resulting in tissue damage and mitochondrial dysfunction, and its key pathway of action is retrograde endocannabinoid signaling pathway. This results provide a theoretical basis for research on the toxic effects of FEN on aquatic organisms, and assessed the environmental risks of FEN exposure.