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 (including hsp70, grp78, hsp90, and grp94), inflammatory genes (including p65-nf kappa b, il-1 beta, and cox2a), and lipid synthetic genes (including srebp1, fas, acc, and ppar-gamma) in 3 dpf embryos was significantly increased, which was also partially observed in the intestinal cell line form Pampus 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.

Automated summary

The toxicity of triflumizole (TFZ) was investigated in zebrafish to understand its potential risks in the aquatic environment. The study found that TFZ exposure affected the development of zebrafish and resulted in disturbances in oxidative stress, heat shock response, inflammation, and lipid synthesis. These findings provide important insights into the potential risks of TFZ to the aquatic ecosystem.