Exposure to trietazine causes cardiovascular and liver damage and impairs neurodevelopment through oxidative stress and inflammatory mechanisms in zebrafish and transgenic lines

초록

Trietazine is an s -triazine–based herbicide commonly applied in agricultural systems, but its stability in aquatic environments has prompted growing concern about unintended effects on non-target organisms. To assess its developmental toxicity and clarify associated mechanisms, we used both wild-type zebrafish embryos and multiple organ-specific transgenic lines as in vivo models of early vertebrate development. The embryos were continuously exposed to trietazine from 8 to 96 h post-fertilization, resulting in clear dose-dependent developmental defects, including shortened body length, reduced ocular size, and frequent pericardial and yolk sac edema, indicative of moderate to high embryotoxicity across the tested concentrations. In parallel, trietazine markedly enhanced intracellular reactive oxygen species levels and induced transcriptional activation of genes involved in inflammatory signaling and programmed cell death, supporting a central role for oxidative stress–driven apoptosis in its developmental toxicity. To delineate organ-level toxicity, we examined a panel of transgenic zebrafish lines. Embryos expressing cmlc2 :dsRED and gata1a :dsRED exhibited pronounced cardiac malformations and impaired blood flow, while altered vascular organization was detected in the flk1 :mCherry line. Disruption of cardiovascular development was further supported by aberrant expression patterns of the cardiac regulatory genes nkx2.5 and vmhc , as revealed by whole-mount in situ hybridization. Additionally, neurodevelopmental deficits and liver malformations were observed in olig2 :dsRED, huC :EGFP, and fabp10a :dsRED embryos, demonstrating multi-organ developmental toxicity involving the nervous system and liver. Taken together, these results demonstrate that trietazine interferes with normal embryonic development across multiple organ systems by promoting oxidative stress–dependent inflammatory and apoptotic responses in both wild-type and transgenic zebrafish models. Our findings highlight the potential ecological hazards associated with trietazine contamination in aquatic ecosystems and provide mechanistic insight into the level and spectrum of its developmental toxicity. © 2026 Elsevier Inc.

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