Spiromesifen conferred abnormal development in zebrafish embryos by inducing embryonic cytotoxicity via causing oxidative stress

Spiromesifen (SPF) is widely used in agriculture to protect against herbivorous mites, whose residues may harmful to the environment. However, the toxicity assessment of SPF is insufficient. Here, we investigated the toxicological effects of SPF using zebrafish embryos as an animal model. The results showed that SPF exposure solutions at 10, 20, 30, and 40 mu M caused cytotoxicity in zebrafish embryos such as reactive oxygen species (ROS) accumulation, mitochondrial membrane potential decrease, cell division arrest, and apoptosis, which further led to developmental toxicity in zebrafish embryos including delayed hatching, decreased survival rate and spontaneous curling rate, and severe morphological deformities. SPF also induced apoptosis via changes the expressions of apoptosis-related marker genes, caused immunotoxicity by reducing the number of macro-phages and the activity of AKP/ALP and increasing inflammatory factors, and disturbed endogenous antioxidant systems via changes SOD, CAT, and GST activities as well as MDA and GSH contents. Therefore, the potential mechanism that caused embryonic developmental toxicity appeared to be related to the generation of oxidative stress by an elevation in ROS and changes in apoptosis-, immune-, antioxidant-related markers. The antioxidant system and inflammatory response simultaneously participated in and resisted the threat of SPF to prevent tissue damage. Taken together, spiromesifen induced oxidative stress to contribute to developmental toxicity zebrafish embryos by inducing embryonic cytotoxicity. Our study provides new insight into the toxicity assessment of SPF to non-target organisms.