Effects of cortisone in zebrafish (Danio rerio): Insights into gut microbiota interactions and molecular mechanisms underlying DNA damage and apoptosis.

Journal of hazardous materials Pub Date : 2024-10-05 Epub Date: 2024-08-20 DOI:10.1016/j.jhazmat.2024.135576
Jiefeng Tan, Lihua Yang, Meixin Ye, Yuxin Geng, Yanfang Guo, Hong Zou, Liping Hou
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Abstract

Cortisone can enter aquatic ecosystems and pose a risk to organisms therein. However, few studies have explored the effects of cortisone on the gut microbiota of aquatic organisms. Here, we exposed zebrafish (Danio rerio) to cortisone at environmentally relevant concentrations (5.0, 50.0, or 500.0 ng L-1) for 60 days to explore its toxicological effects and their association with gut microbiota changes. The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling assay revealed that exposure to 50 ng L-1 cortisone significantly increased the intestinal cell apoptosis rate, 8-hydroxydeoxyguanosine contents, and caspase-3 and caspase-8 activities. Moreover, the transcriptome analysis results demonstrated a notable downregulation in the expression of most differentially expressed genes associated with apoptosis pathways, as well as changes in DNA replication, oxidative stress, and drug metabolism pathways; these results indicated the occurrence of cortisone-induced stress response in zebrafish. Molecular docking analysis revealed that cortisone can bind to caspase-3 through hydrogen bonds and hydrophobic interactions but that no such interactions occur between cortisone and caspase-8. Thus, cortisone may induce oxidative DNA damage and apoptosis by activating caspase-3. Finally, the 16S rRNA sequencing results demonstrated that cortisone significantly affected microbial community structures and functions in the intestinal ecosystem. These changes may indicate gut microbiota response to cortisone-induced intestinal damage and inflammation. In conclusion, the current results clarify the mechanisms underlying intestinal response to cortisone exposure and provide a basis for evaluating the health risks of cortisone in animals.

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可的松对斑马鱼(Danio rerio)的影响:洞察肠道微生物群相互作用以及 DNA 损伤和细胞凋亡的分子机制。
可的松可进入水生生态系统并对其中的生物造成危害。然而,很少有研究探讨可的松对水生生物肠道微生物群的影响。在此,我们将斑马鱼(Danio rerio)暴露于环境相关浓度(5.0、50.0 或 500.0 ng L-1)的可的松中 60 天,以探讨其毒性效应及其与肠道微生物群变化的关联。末端脱氧核苷酸转移酶介导的dUTP-生物素缺口端标记实验显示,暴露于50 ng L-1可的松可显著增加肠道细胞凋亡率、8-羟基脱氧鸟苷含量以及caspase-3和caspase-8活性。此外,转录组分析结果表明,与细胞凋亡通路相关的大多数差异表达基因的表达明显下调,DNA 复制、氧化应激和药物代谢通路也发生了变化;这些结果表明斑马鱼发生了可的松诱导的应激反应。分子对接分析表明,可的松能通过氢键和疏水作用与caspase-3结合,但可的松与caspase-8之间没有这种作用。因此,可的松可能通过激活 caspase-3 来诱导 DNA 氧化损伤和细胞凋亡。最后,16S rRNA 测序结果表明,可的松对肠道生态系统中的微生物群落结构和功能有显著影响。这些变化可能表明肠道微生物群对可的松诱导的肠道损伤和炎症的反应。总之,目前的研究结果阐明了肠道对可的松暴露的反应机制,并为评估可的松对动物的健康风险提供了依据。
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