Dinitramine (DN), an herbicide in the dinitroaniline family, is used in agricultural areas to prevent unwanted plant growth. Dinitroaniline herbicides inhibit cell division by preventing microtubulin synthesis. They are strongly absorbed by the soil and can contaminate groundwater; however, the mode of action of these herbicides in non-target organisms remains unclear. In this study, we examined the developmental toxicity of DN in zebrafish embryos exposed to 1.6, 3.2, and 6.4 mg/L DN, compared to embryos exposed to DMSO (control) for 96 h. Visual assessments using transgenic zebrafish (fli1:eGFP) indicated abnormal cardiac development with enlarged ventricles and atria, decreased heartbeats, and impaired cardiac function. Along with cardiac development, vessel formation and angiogenesis were suppressed through activation of the inflammatory response. In addition, exposure to 6.4 mg/L DN for 96 h induced cell death, with upregulation of genes related to apoptosis. Our results showed that DN induced morphological changes and triggered an inflammatory response and apoptotic cell death that can impair embryonic growth and survival, providing an important mechanism of DN in aquatic organisms.
Keywords: Cardiotoxicity; apoptosis; dinitramine; inflammation; zebrafish embryos.
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