暴露于赫克萨布罗摩环多德干 (HBCD) 诱导过早的丸衰老通过NCOA4 / Fe2 + / ROS调解
Deyi Wu1, Yuebing Kong1, Ruoting Zhang1
1College of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China.
International immunopharmacology
|July 27, 2024
概括
暴露于hexabromocyclododecane (HBCD) 会通过诱导氧化应激和炎症,导致小鼠和小鼠细胞的丸过早衰老. 这种衰老是由通过NCOA4介导的铁食引起的铁含量升高所驱动的,突出了关键的NCOA4/Fe2+/ROS通路.
科学领域:
- 环境毒理学环境毒理学
- 生殖毒理学 生殖毒理学
- 细胞衰老 细胞衰老
背景情况:
- 赫克萨布罗摩环多德干 (HBCD) 是一种在人类和动物血液中检测到的环境污染物.
- 暴露于HBCD可能导致组织损伤,器官功能障碍和细胞毒性.
- HBCD对丸衰老的影响需要进一步调查.
研究的目的:
- 在体内和体外研究HBCD对丸过早衰老的影响.
- 阐明 HBCD 诱导的丸衰老背后的分子机制.
- 为了确定关键的分子驱动因素和涉及HBCD毒性的途径.
主要方法:
- 在体内研究使用C57小鼠暴露于HBCD20周.
- 在实验室研究中,使用暴露于HBCD的小鼠精子细胞GC-1spg细胞.
- 测量与衰老相关的标志物 (p16,p21),氧化应激和炎症.
- 评估细胞衰老标志物和铁水平.
- 对NCOA4介导的费里丁和ROS生成的研究.
主要成果:
- 在小鼠中,HBCD暴露导致丸过早衰老,由增加的p16和p21表达体现出来.
- HBCD导致丸组织的氧化应激和炎症.
- 在GC-1spg细胞中,HBCD诱导过早衰老.
- 铁 (Fe2+) 被确定为HBCD诱导衰老的关键驱动因素.
- 铁含量升高是NCOA4介导的铁食导致的.
- 由HBCD诱导的衰老是由NCOA4/Fe2+/ROS信号通路介导的.
结论:
- 暴露于HBCD会导致丸过早衰老和细胞衰老.
- 在HBCD诱导的生殖毒性中,NCOA4/Fe2+/ROS信号通路至关重要.
- 这项研究为了解HBCD的生殖毒理学提供了基础.
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