Disruption of mitochondrial homeostasis and apoptosis by oryzalin exposure in zebrafish embryos

Abstract

Dinitroaniline compounds are important industrial chemicals widely used in dye manufacturing and pre-emergence pesticide production. They disrupt microtubule formation, leading to a higher proportion of cells arrested at metaphase during development. The potential toxicity of oryzalin, a dinitroaniline compound and a commonly used herbicide, toward nontarget organisms remains poorly understood. This study evaluated the developmental toxicity of oryzalin using zebrafish embryos as an in vivo model, given their rapid organogenesis and sensitivity to chemical exposure during early development. To investigate the toxic effects of oryzalin, we conducted developmental toxicity assessments using zebrafish embryos. Interestingly, low-dose exposure to oryzalin caused severe developmental abnormalities, significantly impairing the survival and growth of the embryos. Fluorescent imaging of multiple transgenic zebrafish lines (fli1a;eGFP and l-fabp;dsRed) revealed that oryzalin exposure disrupted liver organogenesis and vascular network formation. Furthermore, transcriptional alterations in essential genes associated with early developmental stages further supported the observed abnormalities. Mitochondrial dysfunction triggered by oryzalin was found to promote oxidative stress and apoptosis. These findings suggest that dinitroaniline compounds, such as oryzalin, may pose developmental toxicity risks to vertebrates, highlighting the need for caution in their extensive use.