Developmental toxicity induced by chelerythrine in zebrafish embryos via activating oxidative stress and apoptosis pathways

Chelerythrine (CHE), a natural benzophenanthridine alkaloid, possesses various biological and pharmacological activities, such as antimicrobial, antitumor and anti-inflammatory effects. However, its adverse side effect has not been fully elucidated. Therefore, this study was designed to investigate the developmental toxicity of CHE in zebrafish. We found that CHE could lead to a notably increase of the mortality and malformation rate, while lead to reduction of the hatching rate and body length. CHE also could affect the normal developing processes of the heart, liver and phagocytes in zebrafish. Furthermore, the reactive oxygen species (ROS) and apoptosis levels were notably increased. In addition, the mRNA expressions of genes (bax, caspase-9, p53, SOD1, KEAP1, TNF-& alpha;, STAT3 and NF-KB) were significantly increased, while the bcl2 and nrf2 were notably inhibited by CHE. These results indicated that the elevation of ROS and apoptosis were involved in the developmental toxicity induced by CHE. In conclusion, CHE exhibits a developmental toxicity in zebrafish, which helps to understand the potential toxic effect of CHE.

Automated summary

This study investigates the developmental toxicity of Chelerythrine in zebrafish and finds that it leads to a significant increase in mortality and malformation rate, as well as a reduction in hatching rate and body length. Chelerythrine also affects the normal development processes of the heart, liver, and phagocytes in zebrafish, and increases levels of reactive oxygen species (ROS) and apoptosis.