Acute toxicity effects of rice paddy bactericide bismerthiazol on zebrafish (Danio rerio) embryos

Bismerthiazol is an extensively utilized agricultural bactericide in paddy fields. However, its toxicity to aquatic animals remains poorly understood. Through acute exposure of zebrafish ( Danio rerio) embryos, we determined that the 72 h half-lethal concentration (LC 50 ) of bismerthiazol was 7.38 mg/L, and 3 mg/L bismerthiazol induced systemic developmental abnormalities. Further studies showed that low concentrations (25 ng/L, 50 ng/L) of bismerthiazol selectively impaired notochord and muscle development in embryos and reduced their motility. Additionally, bismerthiazol exposure upregulated the Sonic hedgehog (SHH) signaling pathway and myogenic gene expression. It also increased reactive oxygen species (ROS) levels while decreasing the enzymatic activity of catalase (CAT), glutathione (GSH), and superoxide dismutase (SOD). Notably, the antioxidant N -acetylcysteine (NAC) rescued the bismerthiazol-induced notochord and muscle defects. In summary, our findings demonstrate that acute bismerthiazol exposure causes developmental toxicity in aquatic organisms by inducing oxidative stress, highlighting its potential ecological risk. Bismerthiazol is an extensively utilized agricultural bactericide in paddy fields. However, its toxicity to aquatic animals remains poorly understood. Through acute exposure of zebrafish ( Danio rerio) embryos, we determined that the 72-h half-lethal concentration (LC 50 ) of bismerthiazol was 7.38 mg/L, and 3 mg/L bismerthiazol induced systemic developmental abnormalities. Further studies showed that low concentrations (25 ng/L, 50 ng/L) of bismerthiazol selectively impaired notochord and muscle development in embryos and reduced their motility. Additionally, bismerthiazol exposure upregulated the Sonic hedgehog (SHH) signaling pathway and myogenic gene expression. It also increased reactive oxygen species (ROS) levels while decreasing the enzymatic activity of catalase (CAT), glutathione (GSH), and superoxide dismutase (SOD). Notably, the antioxidant N -acetylcysteine (NAC) rescued the bismerthiazol-induced notochord and muscle defects. In summary, our findings demonstrate that acute bismerthiazol exposure causes developmental toxicity in aquatic organisms by inducing oxidative stress, highlighting its potential ecological risk. • High concentration of bismerthiazol induces systemic developmental abnormalities in zebrafish embryos. • Low concentration of bismerthiazol selectively inhibits zebrafish notochord and muscle development. • Low concentration of bismerthiazol elevates the expression of SHH signaling and myogenic genes in zebrafish embryos. • Bismerthiazol induces developmental toxicity in zebrafish embryos through the oxidative stress pathway.