Developmental toxicity caused by sanguinarine in zebrafish embryos via regulating oxidative stress, apoptosis and wnt pathways.

[Display omitted] • Sanguinarine induces developmental toxicity in zebrafish embryos/larvae. • Sanguinarine has adverse effects on the developing heart, liver and nervous system in zebrafish embryos/larvae. • Sanguinarine can increase ROS level and then induce apoptosis in zebrafish embryos. • The Nrf2 and Wnt pathways were inhibited and involved in the developmental toxicity induced by sanguinarine. Sanguinarine, derived from the root of Sanguinaria canadensis , have multiple biological activities, such as antimicrobial, insecticidal, antitumor, anti-inflammatory and anti-angiogenesis effect, but little is known about its toxicity on normal embryonic development. Here, we study the developmental toxicity using zebrafish model. Notably, sanguinarine caused a significant increase of the malformation rate and decrease of hatching rates and body length of zebrafish embryos. Sanguinarine also impaired the normal development of heart, liver and nerve system of zebrafish embryos. Further, the ROS level and MDA concentrations were remarkably increased, while the activity of T-SOD was decreased. In addition, obvious increase of apoptosis were observed by AO staining or TUNEL assay. Further studies showed that the oxidative stress-, apoptosis-related genes were changed, while genes of nrf2 and wnt pathways were inhibited by sangunarine. To sum up, our study will be helpful to understand the adverse effect of sanguinarine on embryonic development and the underlying molecular mechanism. [ABSTRACT FROM AUTHOR]