PUBLICATION
Life cycle exposure to propiconazole reduces fecundity by disrupting the steroidogenic pathway and altering DNA methylation in zebrafish (Danio rerio)
- Authors
- Teng, M., Chen, X., Wang, C., Song, M., Zhang, J., Bi, S., Wang, C.
- ID
- ZDB-PUB-191223-21
- Date
- 2019
- Source
- Environment International 135: 105384 (Journal)
- Registered Authors
- Keywords
- DNA methylation, Endocrine disruption, Offspring development, Propiconazole, Reproduction
- MeSH Terms
-
- Animals
- DNA Methylation*
- Ecosystem
- Fertility
- Gonads
- Male
- Reproduction
- Triazoles
- Vitellogenins
- Water Pollutants, Chemical
- Zebrafish*
- PubMed
- 31862640 Full text @ Environ. Int.
Citation
Teng, M., Chen, X., Wang, C., Song, M., Zhang, J., Bi, S., Wang, C. (2019) Life cycle exposure to propiconazole reduces fecundity by disrupting the steroidogenic pathway and altering DNA methylation in zebrafish (Danio rerio). Environment International. 135:105384.
Abstract
Propiconazole is fungicide widely used in agriculture, which may enter aquatic ecosystems and affect organisms. In this study, zebrafish (Danio rerio) were exposed to environmentally relevant levels of propiconazole throughout the life cycle, from embryo to sexually mature adults, and the effects on growth, reproduction, and offspring viability were investigated. To investigate the mechanisms of propiconazole action, the sex steroid hormones and the expression of genes related to the hypothalamus-pituitary-gonad-liver (HPGL) axis and DNA methylation were examined. Growth decreased in the parental zebrafish (F0) after exposure to propiconazole for 120 days. In males, increases in the levels of 17β-estradiol and vitellogenin were observed. The alterations in sex steroid hormones were regulated by the expression of genes involved with the HPGL axis. The decreases in fecundity and fertilization of the F0 was induced by the global DNA methylation, and then may result in the abnormal development of the F1. Therefore, propiconazole disrupted the steroidogenic pathway and caused changes in global DNA methylation that induced reproductive toxicity.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping