Pyridaben induced cardiotoxicity during the looping stages of zebrafish (Danio rerio) embryos.

Pyridaben is a widely used acaricide in agriculture and reaches a high concentration (97 μg/L) in paddy water for a short time when pyridaben was applied to rice. However, its toxicity to aquatic organisms is still poorly understood. Therefore, we assessed the pyridaben cardiotoxicity to aquatic organisms using the zebrafish (Danio rerio) model. We found that pyridaben is highly toxic to aquatic organisms, and LC50 of pyridaben for zebrafish at 72 hpf was 100.6 μg/L. Pyridaben caused severe cardiac malformations and functional abnormalities. Morphologic abnormity included severe pericardial edema, cardiomegaly, decreased cardiomyocytes, thinning of the myocardial layer, linear heart, and increased the distance between sinus venous and bulbus arteriosus (SV-BA). Functional failure included arrhythmia, heart failure, and reduced pumping efficiency. The genes involved in heart development, WNT signaling, BMP signaling, ATPase, and cardiac troponin C were abnormally expressed in the pyridaben treatment group. Exposure to pyridaben increased oxidative stress and induced cell apoptosis. The above causes may lead to cardiac toxicity. The results suggest that pyridaben exposure induced elevated oxidative stress through the WNT signaling pathway, which in turn led to apoptosis in the heart and cardiotoxicity. Besides, pyridaben exposure at the critical stage of cardiac looping (24-36 hpf) resulted in the greatest cardiotoxicity. The chorion reduced the entry of pyridaben and protected zebrafish embryos, resulting in cardiotoxicity second only to the stage of cardiac looping. The study should provide valuable information that pyridaben exposure causes cardiotoxicity in zebrafish embryos and have potential health risks for other aquatic organisms and humans.