Concentration-dependent transcriptome of zebrafish larvae for environmental bisphenol S assessment

• Published in: Ecotoxicology and environmental safety Vol. 223; p. 112574
• Main Authors: Yang, Feng, Zhao, Ziyu, Zhang, Haiji, Zhou, Liping, Tao, Liang, Wang, Qin
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 15.10.2021; Elsevier
• Subjects: Bisphenol S; RNA-seq; Toxicity assays; WGCNA; Zebrafish larvae; Zebrafish larvae; Toxicity assays; RNA-seq; WGCNA; Bisphenol S
• ISSN: 0147-6513; 1090-2414
• DOI: 10.1016/j.ecoenv.2021.112574

The widespread use of bisphenol S (BPS) as an alternative to bisphenol A has captured attention due to its potential toxicity to aquatic organisms. In the present study, the zebrafish was used as a model to evaluate the toxicity of BPS and determine the underlying mechanisms. The environmental concentration-dependent (0, 0.1, 1, 10, 100, and 1000 μg/L BPS) transcriptome approach was employed in combination with toxicity assays to address the problem. Based on a weighted correlation network analysis, we speculated that excess reactive oxygen species (ROS) may initiate cellular events in BPS-exposed zebrafish, leading to multiple toxic effects. Furthermore, we used pathway enrichment analysis to identify key pathways (MAPK signalling pathway and metabolic pathways) that link the molecular mechanisms with different toxic effects. In addition, we performed protein-protein network and shortest path analyses to identify six hub genes (erbb2, rrm2, rps27a, his2h3c, cdk1, and mcm5) and their interactions. Moreover, we suggest that BPS may interact with erbb2 by molecular docking. Thus, the BPS-erbb2 interaction may activate the MAPK signalling and metabolic pathways, resulting in ROS production and then caused multiple toxic effects in zebrafish. This study provides information for characterising the mechanisms of BPS exposure in aquatic environments. •Integrating the large-scale transcriptomics data and toxicity endpoints by BPS.•The toxicity of BPS is mainly the formation of ROS leading to oxidative stress.•The key pathways of BPS exposure were MAPK signalling pathway and Metabiotic pathways.•BPS might interact with errb2