Abstract

Zebrafish have been shown to experience cardiotoxicity when exposed to typical plasticizer di (2-ethylhexyl) phthalate (DEHP), yet the possible chemical pathways underlying this have not yet been completely understood. It has been shown that DEHP activates the important protein AhR, which causes developmental defects in other species. However, it is unknown if AhR signaling pathway also plays a role in DEHP-mediated cardiac developmental toxicity in zebrafish. Initially, it was suggested by molecular docking simulations that DEHP might have AhR agonistic activity. This paper examined the alterations in cardiac-related indices at the individual, protein, and gene levels in zebrafish stressed by DEHP in order to further support this hypothesis. The findings demonstrated that DEHP caused oxidative stress, elevated CYP1A1 activity, cardiac developmental abnormalities, and notable alterations in the expression levels of AhR, Wnt/β-catenin, and Nrf2-Keap1 signaling pathway proteins and genes.