PUBLICATION
Exposure of Parental Zebrafish to Difenoconazole throughout Their Life Cycle May Lead to Developmental Toxicity in the F1 Generation through Epigenetic Changes in Gametes, Impaired Nutrient Supply from the Ovum, and Maternal Transfer of Difenoconazole
- Authors
- Chen, X., Zheng, J., Wang, C., Teng, M., Jiang, J., Wu, F.
- ID
- ZDB-PUB-250329-3
- Date
- 2025
- Source
- Environmental science & technology : (Journal)
- Registered Authors
- Keywords
- difenoconazole, epigenetics, maternal transfer, offspring development, zebrafish
- MeSH Terms
-
- Ovum/drug effects
- Dioxolanes*/toxicity
- Triazoles*/toxicity
- Water Pollutants, Chemical/toxicity
- Zebrafish*
- Fungicides, Industrial/toxicity
- Animals
- Male
- Germ Cells/drug effects
- Female
- Epigenesis, Genetic/drug effects
- PubMed
- 40153714 Full text @ Env. Sci. Tech.
Citation
Chen, X., Zheng, J., Wang, C., Teng, M., Jiang, J., Wu, F. (2025) Exposure of Parental Zebrafish to Difenoconazole throughout Their Life Cycle May Lead to Developmental Toxicity in the F1 Generation through Epigenetic Changes in Gametes, Impaired Nutrient Supply from the Ovum, and Maternal Transfer of Difenoconazole. Environmental science & technology. :.
Abstract
Difenoconazole is a widely used agricultural fungicide that has been frequently detected in aquatic environments. Given its stable presence in aquatic environments, long-term exposure of wild fish may pose a risk to offspring embryonic development. This study demonstrated that exposure of zebrafish to environmental concentrations of difenoconazole throughout their life cycle resulted in abnormal development of offspring embryos/larvae, including decreased heart rate, delayed hatching, increased malformation rate, shortened body length, and increased mortality. These changes were significantly correlated with the affected apoptosis, autophagy, energy metabolism and MAPK signaling pathways in F1 generation. This transgenerational toxic effect results from epigenetic alterations in gametes, impaired nutrient supply from the ovum, and maternal transfer of difenoconazole. After exposure to difenoconazole, the development of female fish offspring was affected more than that of male fish offspring, which was mainly caused by the impaired nutrient supply from the ovum and the maternal transfer of difenoconazole. Because this transgenerational developmental toxicity was observed at environmental levels, difenoconazole may pose a threat to the survival of wild larvae and therefore a risk to wild fish populations.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping