作为潜在的环境肥胖原体,1,6-二氧甲会诱导斑马鱼的脂质积累和肝脏发育缺陷
Weitao Hu1, Wenbin Yuan1, Ziang Wang1
1Jiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Jiangxi Key Laboratory of Development Biology of Organs and Epigenetics, Key Laboratory of Jiangxi Province for Biological Invasion and Biosecurity, School of Life Science, Clinical Research Center of Jinggangshan University, Jinggangshan University, Ji'an 343009, China.
Ecotoxicology and environmental safety
|January 28, 2026
概括
暴露于1,6-二氧纳甲烯 (1,6-DHN) 会通过引起氧化应激,代谢问题和亡来损害斑马鱼的肝脏发育. 这种染料中间体可能会作为环境肥胖原体,造成生态和健康风险.
科学领域:
- 环境毒理学环境毒理学
- 发展生物学 发展生物学
- 代谢学 代谢学 代谢学
背景情况:
- 1,6-二氧化纳 (1,6-DHN) 是一种染料中间体和多环芳香碳化合物代谢物.
- 它的内分泌干扰潜力和毒理作用,特别是对肝脏发育的影响,尚不清楚.
研究的目的:
- 为了研究1,6-DHN对斑马鱼幼虫肝脏发育的影响.
- 阐明1,6-DHN诱导的肝毒性背后的分子机制.
主要方法:
- 斑马鱼幼虫暴露于1,6-DHN.
- 评估了肝脏的生长,脂质和糖原的积累以及反应性氧物种 (ROS) 的产生.
- 转录组分析确定了受影响的信号通路.
- 研究了与亡相关的基因表达和p53的作用.
主要成果:
- 1,6-DHN暴露抑制了肝脏生长,并导致异常的脂质/糖原积累.
- 观察到ROS产量增加和脂质过氧化.
- 破坏PPAR信号通路的基因表达导致了代谢失调.
- 升调p53和bax诱导肝细胞亡,与p53敲击部分缓解毒性.
结论:
- 1,6-DHN通过氧化应激,脂质代谢中断和亡来损害斑马鱼的肝脏发育.
- p53通路在1,6-DHN诱导的肝毒性中发挥着关键作用.
- 1,6-DHN可能作为环境肥胖原体起作用,需要对其生态和人类健康风险进行进一步调查.
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