Developmental toxicity of chlorpropham induces pathological changes and vascular irregularities in zebrafish embryos.

Chlorpropham is used to prevent sprouting in stored agricultural products. It functions through mitosis inhibition or microtubule assembly inhibition in target organisms including plants, protozoa, and fungi. Although the toxicity ranges of chlorpropham in different organisms are known, specific studies on the environmental contamination and the harmful effects of chlorpropham has not been elucidated. In the present study, we demonstrated that toxicity assays of chlorpropham using zebrafish embryos showed pathological morphology alteration with half the embryos undergoing embryonic death. Fluorescent dye was used in live embryos to identify whether oxidative stress and apoptosis mediated developmental malformation. Specific genes related to apoptosis, ccnd1, ccne1, and cdk6, belonging to cell cycle regulation were downregulated on exposure to sublethal concentrations of chlorpropham. Moreover, vascular morphogenesis, which contributes to the cardiovascular circulatory system, was disrupted by chlorpropham along with decreased expression of specific regulators (flt1, kdr, and vegfaa). These data suggest that environmentally preserved chlorpropham is a potential pollutant in non-target species, especially in aquatic organisms, and emphasizes the need for caution regarding the ecotoxicity of chlorpropham.