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In this study, goldfish (<i>Carassius auratus</i>) were exposed to 0 (control group) and 0.81 mg/L TCCA for four consecutive days. The liver transcriptome, the molecular indices of oxidative stress, and gills histopathology were investigated. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that energy metabolism-related pathways such as glycolysis/gluconeogenesis were significantly enriched, suggesting their perturbation in the liver of goldfish. Additionally, TCCA exposure also caused pathological damage in gills, which compromised physiological function and decreased oxygen intake capacity of gills, thus leading to the enhancement of anaerobic metabolism. This finding was confirmed by the significant upregulation of lactate dehydrogenase in the liver of goldfish. Moreover, many phase I and phase II metabolic enzymes might be activated to alleviate TCCA-induced toxicity in goldfish, and glutathione S-transferases (GSTs) and cytochrome P450s (CYPs) play a crucial role in the metabolism of TCCA in the liver of goldfish. Furthermore, the antioxidant enzyme analysis showed that TCCA exposure induced oxidative damage in the liver and partially impaired the antioxidant defense system of goldfish, evidenced by decreased superoxide dismutase (SOD) and catalase (CAT), and increased malondialdehyde (MDA) level. In summary, this study will improve our understanding of the molecular mechanisms of the TCCA-induced toxicity in goldfish.