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对二夸特诱导的氧化应激及其对器官特异性毒性影响的单细胞分析

Zhimin Chen¹, Guo Lin², Keng Ye¹

¹Department of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China; Research Center for Metabolic Chronic Kidney Disease, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China; Department of Nephrology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou 350212, China.

Ecotoxicology and environmental safety

|May 6, 2025

概括

迪卡特除草剂中毒会通过创建氧化应激环境而导致多器官损伤. 这导致细胞死亡和炎症,突显了对迪奎特 (DQ) 毒性的早期干预的需要.

科学领域:

毒理学毒理学毒理学
分子生物学分子生物学
基因组学就是基因组学.

背景情况:

迪奎特 (DQ) 是一种广泛使用的除草剂,在不当使用时可能导致严重的多器官损伤.
由于DQ引起的多器官损伤的确切机制仍然不完全理解.

研究的目的:

为了阐明底层的分子机制和细胞反应,迪卡特诱导的多器官损伤.
为了创建一个全面的单细胞地图,关于器官对迪卡特中毒的反应.

主要方法:

单细胞/单核RNA测序 (scRNA-seq/snRNA-seq) 在迪卡特暴露后的多个时间点在小鼠肺部,肝脏和脏上进行.
创建了一个多器官单细胞地图,分析了超过27万个细胞.

主要成果:

迪卡特暴露诱导了内皮细胞和副皮细胞的氧化应激微环境,其特征是活性氧化酸化和炎症.
氧化应激触发了表细胞和免疫细胞的调节细胞死亡,放大了炎症和氧化环境.
帕伦基马和免疫细胞中的代谢重编程导致能量代谢发生变化,肝脏排毒减少,免疫细胞激活发生变化,组织损伤恶化.
没有发现显著的纤维化,这表明损伤主要是由急性氧化和炎症过程驱动的.

结论:

迪卡特诱导的氧化应激微环境是多器官损伤的核心.
了解这些分子机制对于开发及时干预迪卡特毒性至关重要.
这项研究提供了一个详细的分子地图,在单细胞水平上对Diquat对多个器官的影响.

关键词:

迪克瓦特 (Diquat) 是一种代谢重编程是一种代谢重编程.氧化应激微环境中的氧化应激.调节的细胞死亡.单细胞测序是一种单细胞测序.

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