Toxic effects of broflanilide exposure on development of zebrafish (Danio rerio) embryos and its potential cardiotoxicity mechanism.

Diamide insecticides are a threat to aquatic organisms but the toxicity of broflanilide remains largely undefined. In this study, to clarify the risk of broflanilide to aquatic organisms and explore its possible mechanism, lethal and sub-lethal exposure of zebrafish embryos were performed. The acute toxicity LC50 (50% lethal concentration) (96 h) of broflanilide to zebrafish embryos and larvae were 3.72 mg/L and 1.28 mg/L, respectively. It also caused toxic symptoms including reduced heart rate, pericardial edema, yolk sac edema and shortened larval body length at ≥ 0.2 mg/L. Understanding the cellular and molecular changes underlying developmental toxicity in early stages of zebrafish may be very important to further improvement of this study. Here, we found cell apoptosis in embryonic heart, significant up-regulation in expression of genes associated with apoptosis and increased activity of caspase-9. In particular, we detected the levels of genes and TBX5 (T-box protein 5) related to cardiac development, which were significantly increased in this study and may be contribution to the cardiotoxicity of embryos. In general, our results identified the aquatic toxicity of broflanilide to the early stage of zebrafish and provide insights into the underlying mechanism in developmental toxicity especially cardiotoxicity of embryos.