PUBLICATION
A transcriptomics-based analysis of toxicity mechanisms of zebrafish embryos and larvae following parental Bisphenol A exposure
- Authors
- Huang, W., Zheng, S., Wang, X., Cai, Z., Xiao, J., Liu, C., Wu, K.
- ID
- ZDB-PUB-200825-16
- Date
- 2020
- Source
- Ecotoxicology and environmental safety 205: 111165 (Journal)
- Registered Authors
- Keywords
- Bisphenol A, Embryos, Larvae, Toxicity pathways, Transcriptomics, Zebrafish
- MeSH Terms
-
- Animals
- Benzhydryl Compounds/toxicity*
- Embryo, Nonmammalian/drug effects*
- Embryo, Nonmammalian/metabolism
- Embryonic Development/drug effects*
- Embryonic Development/genetics
- Epigenesis, Genetic/drug effects
- Gene Expression Profiling
- Larva/drug effects*
- Larva/genetics
- Phenols/toxicity*
- Sequence Analysis, RNA
- Transcriptome/drug effects*
- Water Pollutants, Chemical/toxicity*
- Zebrafish/genetics*
- Zebrafish/metabolism
- PubMed
- 32836160 Full text @ Ecotoxicol. Environ. Saf.
- CTD
- 32836160
Citation
Huang, W., Zheng, S., Wang, X., Cai, Z., Xiao, J., Liu, C., Wu, K. (2020) A transcriptomics-based analysis of toxicity mechanisms of zebrafish embryos and larvae following parental Bisphenol A exposure. Ecotoxicology and environmental safety. 205:111165.
Abstract
Background Bisphenol A (BPA) is a well-known xenobiotic endocrine disrupting chemical, with estrogenic activity and many other potential biological effects. Although multiple toxicities have been reported for BPA, molecular mechanisms underlying the transgenerational toxic effects of BPA are still underestimated.
Methods Parental F0 fish were exposed to 1.0 μM BPA or control (0.1% DMSO, v/v) for 7 days. Eggs (F1) were collected and kept in control medium until 4.5 or 120 h post fertilization (hpf). RNA sequencing (RNA-seq) was conducted on embryos and larvae, to discover differentially expressed genes (DEGs), and then KEGG pathway, GO enrichment and GSEA were performed to interpret functional ontology. Histopathology was performed to explore the morphological and structural alterations in liver tissues of zebrafish larvae (120 hpf) after parental BPA exposure.
Results Parental BPA exposure induced global transcriptomic changes in zebrafish embryos and larvae. For embryos, epigenetic regulation genes were decidedly affected, highlighted epigenotoxicity might involve in the transgenerational effects during embryogenesis and early development. By further investigation on its delayed effects, our RNA-Seq data of larvae suggested ROS metabolic process, apoptosis, p53 and MAPK signaling pathway were concentrated, indicating defensive cellular processes still involved in protecting against BPA toxicity. Furthermore, parental BPA-treated larvae manifested hepatic injury by histopathological analysis.
Conclusions Parental BPA exposure led to global transcriptomic changes involved in epigenetic regulation, oxidative stress, apoptosis and DNA damage of offspring. These findings advanced the field of the parental-mediated subsequent generational toxic effects of BPA.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping