Triflumizole Induces Developmental Toxicity, Liver Damage, Oxidative Stress, Heat Shock Response, Inflammation, and Lipid Synthesis in Zebrafish
Triflumizole (TFZ) toxicity must be investigated in the aquatic environment to understand the potential risks to aquatic species. Accordingly, the adverse effects of TFZ exposure in zebrafish were investigated. Results demonstrate that, after TFZ exposure, the lethal concentration 50 (LC50) in 3 d post-fertilization (dpf) embryos and 6 dpf larvae were 4.872 and 2.580 mg/L, respectively. The development (including pericardium edema, yolk sac retention, and liver degeneration) was apparently affected in 3 dpf embryos. Furthermore, the alanine aminotransferase (ALT) activity, superoxide dismutase (SOD) activity, catalase (CAT) activity, and malondialdehyde (MDA) content in 6 dpf larvae were significantly increased. Additionally, the expression of heat shock response genes (includinghsp70,grp78,hsp90, andgrp94), inflammatory genes (includingp65-nfκb,il-1β, andcox2a), and lipid synthetic genes (includingsrebp1,fas,acc, andppar-γ) in 3 dpf embryos was significantly increased, which was also partially observed in the intestinal cell line formPampus argenteus. Taken together, TFZ could affect the development of zebrafish, accompanied by disturbances of oxidative stress, heat shock response, inflammation, and lipid synthesis. Our findings provide an original insight into the potential risks of TFZ to the aquatic ecosystem.Keywords:triflumizole;zebrafish;oxidative stress;heat shock response;inflammation;lipid synthesis
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