@article {274,
	title = {Multigenerational effects of disperse blue 79 at environmentally relevant concentrations on zebrafish (Danio rerio) fecundity: An integrated approach.},
	journal = {J Hazard Mater},
	volume = {478},
	year = {2024},
	month = {2024 Oct 05},
	pages = {135442},
	abstract = {<p>The brominated azo dye (BAD) Disperse Blue (DB79) is a widespread environmental pollutant. The long-term toxicological effects of DB79 and the mechanisms thereof must be understood to allow assessment of the risks of DB79 pollution. A dual-omics approach employing in silico analysis, bioinformatics, and in vitro bioassays was used to investigate the transgenerational (F-F) toxicity of DB79 in zebrafish at environmentally relevant concentrations and identify molecular initiating events and key events associated with DB79-induced fertility disorders. Exposure to 500\&nbsp;{\textmu}g/L DB79 decreased fecundity in the F and F generations by \&gt;\&nbsp;30\&nbsp;\% and increased the condition factor of the F generation 1.24-fold. PPARα/RXR and PXR ligand binding activation were found to be critical molecular initiating events associated with the decrease in fecundity. Several key events (changes in fatty acid oxidation and uptake, lipoprotein metabolism, and xenobiotic metabolism and transport) involved in lipid dysregulation and xenobiotic disposition were found to be induced by DB79 through bioinformatic annotation using dual-omics data. The biomolecular underpinnings of decreased transgenerational fertility in zebrafish attributable to BAD exposure were elucidated and novel biomolecular targets in the adverse outcome pathway framework were identified. These results will inform future studies and facilitate the development of mitigation strategies.</p>},
	keywords = {Animals, Azo Compounds, Female, Fertility, Male, Pregnane X Receptor, Water Pollutants, Chemical, Zebrafish},
	issn = {1873-3336},
	doi = {10.1016/j.jhazmat.2024.135442},
	author = {Wang, Chao and Gu, Wen and Zhang, Shaoping and Li, Li and Kong, Jian and Zhi, Hong and Liu, Juan and Wang, Mengmeng and Miao, Ke and Li, Qi and Yu, Jie and Wang, Runming and He, Runming and Zhang, Shuyi and Deng, Fuchang and Duan, Shuling and Zhang, Qiannan and Liu, Zhenming and Yang, Hui and Jia, Xudong and Peng, Hui and Tang, Song}
}
@article {235,
	title = {Multi-omics reveals 2-bromo-4,6-dinitroaniline (BDNA)-induced hepatotoxicity and the role of the gut-liver axis in rats.},
	journal = {J Hazard Mater},
	volume = {457},
	year = {2023},
	month = {2023 Jun 03},
	pages = {131760},
	abstract = {<p>2-Bromo-4, 6-dinitroaniline (BDNA) is a widespread azo-dye-related hazardous pollutant. However, its reported adverse effects are limited to mutagenicity, genotoxicity, endocrine disruption, and reproductive toxicity. We systematically assessed the hepatotoxicity of BDNA exposure via pathological and biochemical examinations and explored the underlying mechanisms via integrative multi-omics analyses of the transcriptome, metabolome, and microbiome in rats. After 28 days of oral administration, compared with the control group, 100\&nbsp;mg/kg BDNA significantly triggered hepatotoxicity, upregulated toxicity indicators (e.g., HSI, ALT, and ARG1), and induced systemic inflammation (e.g., G-CSF, MIP-2, RANTES, and VEGF), dyslipidemia (e.g., TC and TG), and bile acid (BA) synthesis (e.g., CA, GCA, and GDCA). Transcriptomic and metabolomic analyses revealed broad perturbations in gene transcripts and metabolites involved in the representative pathways of liver inflammation (e.g., Hmox1, Spi1, L-methionine, valproic acid, and choline), steatosis (e.g., Nr0b2, Cyp1a1, Cyp1a2, Dusp1, Plin3, arachidonic acid, linoleic acid, and palmitic acid), and cholestasis (e.g., FXR/Nr1h4, Cdkn1a, Cyp7a1, and bilirubin). Microbiome analysis revealed reduced relative abundances of beneficial gut microbial taxa (e.g., Ruminococcaceae and Akkermansia muciniphila), which further contributed to the inflammatory response, lipid accumulation, and BA synthesis in the enterohepatic circulation. The observed effect concentrations here were comparable to the highly contaminated wastewaters, showcasing BDNA{\textquoteright}s hepatotoxic effects at environmentally relevant concentrations. These results shed light on the biomolecular mechanism and important role of the gut-liver axis underpinning BDNA-induced cholestatic liver disorders in vivo.</p>},
	issn = {1873-3336},
	doi = {10.1016/j.jhazmat.2023.131760},
	author = {Deng, Fuchang and Qin, Guangqiu and Chen, Yuanyuan and Zhang, Xu and Zhu, Mu and Hou, Min and Yao, Qiao and Gu, Wen and Wang, Chao and Yang, Hui and Jia, Xudong and Wu, Chongming and Peng, Hui and Du, Huamao and Tang, Song}
}
