Fluopyram (FO), a widely used succinate dehydrogenase inhibitor (SDHI) fungicide, poses a potential risk to aquatic ecosystems due to its mitochondrial toxicity in non-target organisms. This study investigated its toxic effects on zebrafish (Danio rerio). Embryos (n = 30 per concentration) were exposed to FO (0, 0.375, 0.75, 1.5 mg/L) for 96 h, resulting in concentration-dependent developmental toxicity, including increased malformations, reduced heart rate, and inhibited swimming behavior. Adult zebrafish were chronically exposed to lower concentrations (0, 0.01, 0.1, 1.0 mg/L; n = 20 per concentration per replicate) for 28 days. Biochemical analyses across both life stages revealed that FO significantly inhibited succinate dehydrogenase (SDH) activity and mitochondrial complex II, reduced ATP levels, and induced oxidative stress. Integrated transcriptomic and metabolomic analyses showed that FO profoundly perturbed specific metabolic pathways, primarily glutathione metabolism, cytochrome P450-mediated detoxification, and core nutrient metabolism pathways involving carbohydrates, lipids, and amino acids. In adults, chronic exposure induced significant hepatotoxicity, evidenced by histopathological damage, altered liver enzyme activities (GPT/GOT), and activation of autophagy and PPAR/FoxO signaling pathways. Our results demonstrate that FO induces multifaceted toxicity in zebrafish, from developmental defects to hepatic metabolic dysfunction, primarily driven by mitochondrial impairment and oxidative stress. This study provides crucial mechanistic hazard data and insights for the ecological risk assessment of SDHI fungicides.
Wang et al. (Mon,) studied this question.