Disruption of mitochondrial bioenergetics and redox balance by tetraconazole underlies physiological and behavioral impairments in zebrafish

초록

Tetraconazole, a triazole fungicide, is widely used in agriculture and is frequently detected in aquatic environments, where it may affect non‑target organisms. However, its developmental toxicity and the underlying mechanisms of action remain poorly understood. In this study, the effects of tetraconazole on zebrafish embryonic development were investigated based on physiological and behavioral changes as well as associated toxicological pathways. Tetraconazole exposure induced morphological abnormalities and mitochondrial dysfunction, as evidenced by decreased mitochondrial respiration, increased reactive oxygen species production, and reduced expression of antioxidant enzyme genes sod1, cat, gpx1a , and gpx1b . Furthermore, acridine orange and TUNEL staining revealed elevated apoptosis, which was supported by dysregulated expression of bcl2l1, bax , and casp9 . In parallel, tetraconazole modulated Erk and Akt signaling and induced multiorgan toxicity, as demonstrated in transgenic reporter lines for the cardiovascular ( cmlc2:dsRED and fli1a:EGFP ), nervous ( olig2:dsRED, gfap:EGFP , and gad1b:EGFP ), and metabolic organs ( fabp10a:dsRED, elastase:EGFP , and insulin:EGFP ), revealing defects in cardiac function, neurobehavior, vascular development, and hepatopancreatic differentiation. Collectively, these findings indicate that tetraconazole functions as a potent developmental toxicant in zebrafish embryos by inducing mitochondrial dysfunction‒mediated oxidative stress and interfering with physiological and behavioral processes, ultimately disrupting Erk/Akt-dependent signaling networks and leading to widespread organ-level abnormalities. © 2026 Elsevier B.V.

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