双S暴露了淡水,Procambarus clarkii的肠道微生物群和代谢学上的变化
Changchang Pu1, Yuanyi Liu1, Jianshuang Ma1
1College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, Henan, People's Republic of China.
Aquatic toxicology (Amsterdam, Netherlands)
|May 21, 2024
概括
双S (BPS) 暴露会破坏鱼肠道细菌和新陈代谢,导致肝损伤. 即使是低水平的BPS (10μg/L) 也会引起氧化应激,并改变微生物群落,影响水生生态系统.
科学领域:
- 环境毒理学环境毒理学
- 甲动物生物学 甲动物生物学
- 微生物组研究 微生物组研究
背景情况:
- 双S (BPS) 是一种内分泌干扰化学物质 (EDC),与器官损伤有关.
- 在甲类动物中急性BPS毒性的机制仍未得到充分研究.
- BPS在水生环境中普遍存在,对淡水动物群构成风险.
研究的目的:
- 研究BPS暴露对淡水 (Procambarus clarkii) 的肠道微生物群和代谢物的影响.
- 阐明BPS诱导的肝损伤和的氧化应激背后的机制.
主要方法:
- 淡水暴露于BPS的度为10微克/升和100微克/升.
- 使用16S rRNA基因测序来分析肠道微生物社区结构.
- 液体染色学-并联质谱学 (LC-MS/MS) 用于分析肝中代谢物.
主要成果:
- 暴露于BPS显著降低了抗氧化酶活性 (CAT,SOD),这表明通过抑制Nrf2-Keap1通路的氧化应激.
- 观察到肠道微生物群失生症,潜在的致病细菌增加,如Citrobacter和Hafnia-Obesumbacterium.
- 肝内醇和白血 (LT) 水平的降低与10μg/L BPS的脂质积累和损伤有关.
结论:
- 超过10μg/L的BPS度会破坏淡水的肠道微生物群和肝的代谢.
- BPS通过氧化应激和代谢障碍诱导急性毒性,影响甲动物的健康.
- 这些发现突显了BPS在环境相关度下对水生无脊椎动物的生态风险.
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