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.