Developmental toxicity of prometryn induces mitochondrial dysfunction, oxidative stress, and failure of organogenesis in zebrafish (Danio rerio)

Prometryn, 2-methylthio-4,6-bis(isopropylamino)-1,3,5-triazine, is a selective thiomethyl triazine herbicide widely used to control unwanted weeds and harmful insects by inhibiting electron transport in target organisms. Despite having various advantages, herbicides pose as a major threat to the environment and human health due to persistent contamination, bioaccumulation, and damage to non-target organisms. In this study, the developmental toxicity of 5, 10, and 20 mg/L prometryn in zebrafish (Danio rerio) embryos was evaluated and compared to that of the solvent control for 96 h. Several transgenic zebrafish models (fli1a:eGFP, flk1:eGFP, olig2:dsRed and L-fabp:dsRed) were visually assessed to detect fluorescently tagged genes. Results showed that prometryn shortened body length, and induced yolk sac, heart edema, abnormal heart rate, and loss of viability. Fluorescence microscopy revealed that prometryn exposure caused defects in organ development, reactive oxygen species accumulation, and apoptotic cell death. Mitochondrial bioenergetics were also evaluated to determine the effect of prometryn on the electron transport chain activity and metabolic alterations. Prometryn was found to interfere with mitochondrial function, ultimately inhibiting energy metabolism and embryonic development. Collectively, our findings suggest that prometryn is a potential contaminate for non-target sites and organisms, especially aquatic, and emphasize the need to consider the toxic effects of prometryn.