Buprofezin causes early developmental toxicity of zebrafish (Danio rerio) embryos: morphological, physiological and biochemical responses

Buprofezin (BPFN), a pesticide used to control crop pests and diseases, causes potential harm to aquatic animals and the environment by leaching into aquatic ecosystems. However, there are limited studies on the toxicity of BPFN to aquatic organisms. Using zebrafish embryos, we integrated flow cytometry, qRT-PCR, RNA-seq and other techniques to assess BPFN's developmental toxicity. Additionally, IBRv2 index and Mantel test correlation were applied to comprehensively evaluate the developmental toxicity of BPFN. The results showed that BPFN induced cytotoxicity, including increased reactive oxygen species levels, mitochondrial membrane potential depolarization, and apoptosis, which further resulted in developmental toxicity of zebrafish embryos such as delayed hatching, reduced survival rate, and severe morphological deformities. BPFN also affected the number and distribution of immune cells, resulting in immunotoxicity, and disrupted the endogenous antioxidant system by altering the activities of catalase, superoxide dismutase, and glutathione S-transferase and contents of malondialdehyde and glutathione. Gene expression analysis revealed that BPFN induced changes in the expression of genes associated with oxidative stress, apoptosis, inflammation, swim bladder development, and eye development. In the comprehensive evaluation, BPFN showed the strongest developmental toxic effect in the 20 μM BPFN-treated group at 48 hpf, and there was the significant correlation between embryonic development, oxidative stress, apoptosis, and inflammatory response. The rescue experiment confirmed that astaxanthin can alleviate the embryonic developmental toxicity caused by BPFN to a certain extent. In summary, BPFN induced early developmental toxicity in zebrafish embryos, which might be associated with mitochondria-mediated apoptosis pathway induced by oxidative stress.