Adverse Effects of SYP-3343 on Zebrafish Development Via ROS-Mediated Mitochondrial Dysfunction

For a newly-invented and highly-efficiency strobilurin fungicide, pyraoxystrobin (SYP-3343) has been recognized as a highly poisonous toxin for a variety of aquatic organisms. Nevertheless, the multi-organ developmental toxicity of SYP-3343 and its potential mechanism have not been well-documented. The results showed that SYP-3343 was relatively stable and maintained within the range of 20% in 24 h and the LC50 value of SYP-3343 to embryos at 72 hpf was 17.13 ppb. The zebrafish embryotoxicity induced by SYP-3343 is demonstrated by repressive embryo incubation, enhancive mortality rate, abnormal heart rate, malformed morphological characteristic, and motor function injury. SYP-3343 triggered pathological changes in cardiac and hepatic morphology. SYP-3343 induced cell cycle arrest, increased mitochondrial membrane potential, and reactive oxygen species production as well as cellular apoptosis of zebrafish primary cells, which can be mitigated using antioxidant N-acetyl-L-cysteine. SYP-3343 substantially caused oxidative tissue damage. In addition, SYP-3343 exposure was sufficient to dramatically change total protein and the activities of alkaline phosphatase, succinate dehydrogenase, and mitochondrial electron transport chain complex â…¢. SYP-3343 substantially altered the mRNA levels of heart development-, mitochondrial function-, and apoptosis-related genes in zebrafish embryos. These results indicated that SYP-3343 induced apoptosis via reactive oxygen species-initiated mitochondrial dysfunction in zebrafish embryos.