Tralopyril is an emerging marine antifouling agent with potential toxic effects on non-target aquatic organisms. To evaluate the toxicity of tralopyril, to turbot (Scophthalmus maximus), we assessed biomarkers, including oxidative stress, neurotoxicity, and osmotic homeostasis regulation enzymes, after a 7-day exposure to tralopyril (5 μg/L, 15 μg/L, 30 μg/L). Superoxide dismutase activity was significantly decreased at 30 μg/L, and Ca2+-Mg2+-ATPase activity in the gills was significantly increased at 15 μg/L and 30 μg/L. No statistically significant differences in the responses of acetylcholinesterase and nitric oxide were detected. In addition, 15 μg/L and 30 μg/L tralopyril induced hyperthyroidism, reflected by significantly increased of T3 levels. The expression levels of hypothalamus-pituitary-thyroid axis-related genes were also upregulated. The molecular docking results showed that the thyroid system disruption was not caused by competitive binding to the receptor. In addition, the integrated biomarker response index showed that 15 μg/L tralopyril had the greatest effect on turbot. In general, tralopyril caused oxidative damage, affected energy metabolism, and interfered with the endocrine system. These findings could provide reference data for assessing the ecological risk of tralopyril in marine environments.
Keywords: Integrated biomarker responses; Marine fish; Molecular docking; Physiological stress; Tralopyril.
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