Developmental Toxicity and Mechanistic Insights into the Novel Fungicide Fluindapyr in Zebrafish Embryos.
L, Q., M, Z., J, J., K, H., Y, Z., X, H., Z, C., G, C., & S, L. (2026). Developmental Toxicity and Mechanistic Insights into the Novel Fungicide Fluindapyr in Zebrafish Embryos.. Journal of agricultural and food chemistry. https://doi.org/10.1021/acs.jafc.6c02355
L Q, M Z, J J, K H, Y Z, X H, et al. Developmental Toxicity and Mechanistic Insights into the Novel Fungicide Fluindapyr in Zebrafish Embryos.. Journal of agricultural and food chemistry. 2026; doi: 10.1021/acs.jafc.6c02355
L Q, M Z, J J, et al. Developmental Toxicity and Mechanistic Insights into the Novel Fungicide Fluindapyr in Zebrafish Embryos.[J]. Journal of agricultural and food chemistry. 2026. DOI: 10.1021/acs.jafc.6c02355.
@article{l2026,
author = {Qian L and Zhang M and Jiang J and He K and Zhang Y and Huang X and Che Z and Chen G and Liu S},
title = {Developmental Toxicity and Mechanistic Insights into the Novel Fungicide Fluindapyr in Zebrafish Embryos.},
journal = {Journal of agricultural and food chemistry},
year = {2026},
doi = {10.1021/acs.jafc.6c02355},
note = {PMID: 42616441},
}
TY - JOUR AU - Qian L AU - Zhang M AU - Jiang J AU - He K AU - Zhang Y AU - Huang X AU - Che Z AU - Chen G AU - Liu S TI - Developmental Toxicity and Mechanistic Insights into the Novel Fungicide Fluindapyr in Zebrafish Embryos. T2 - Journal of agricultural and food chemistry PY - 2026 DO - 10.1021/acs.jafc.6c02355 AN - PMID:42616441 ER -
Succinate dehydrogenase inhibitor (SDHI) fungicides pose potential risks to nontarget aquatic organisms. Fluindapyr, a newly registered SDHI fungicide, is likely to enter aquatic environments, yet its toxicity remains largely unexplored. Here, zebrafish (Danio rerio) embryos were used to assess their developmental toxicity and underlying mechanisms. Fluindapyr exhibited high toxicity, with a 96 h LC50 of 0.36 mg/L, and induced multiple developmental defects including edema, growth retardation, reduced locomotion, and bradycardia. Transcriptomic analysis revealed that differentially expressed genes were enriched in pathways related to cardiac muscle contraction and adrenergic signaling, indicating cardiac dysfunction as the primary target. Molecular docking further showed the strong binding of fluindapyr to the L-type calcium channel CaV1.2, suggesting a potential involvement of calcium signaling. Additionally, reduced ATP levels and the suppression of glycolysis-related genes indicated impaired energy metabolism. At higher concentrations, immune- and inflammation-related pathways were activated. These findings highlight cardiotoxicity and energy disruption as key mechanisms underlying fluindapyr-induced developmental toxicity.