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可以缓解诱导的氧化应激,内网膜应激和L8824细胞的亡
Tingting Zhang1, Siyuan Sun1, Ana Gavrilović2
1College of Fisheries, Huazhong Agricultural University, Wuhan 430070, China.
Ecotoxicology and environmental safety
|August 11, 2023
概括
(Se) 通过减少氧化应激,内网膜应激和亡,保护Ctenopharyngodon idella肝细胞免受 (Cd) 毒性影响. Se增强抗氧化能力并维持平衡,抵消Cd诱导的损害.
科学领域:
- 环境毒理学环境毒理学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- (Cd) 是一种有毒的工业污染物,会导致器官损伤和亡.
- (Se) 对Cd有毒性的保护作用.
- 了解Se在鱼肝细胞中的保护机制至关重要.
研究的目的:
- 为了研究在Ctenopharyngodon idella肝 (L8824) 细胞中对诱导的损伤的保护机制.
- 阐明Se在减轻Cd诱导的氧化应激,内质网膜应激和亡中的作用.
主要方法:
- 在用化进行预化后,L8824细胞暴露在CdCl2的不同度下.
- 评估了细胞活力,ROS水平,抗氧化酶活性,线粒体膜潜力,ERS标志物,细胞内和亡.
- 分析了与Keap1-Nrf2通路和亡相关的基因表达.
主要成果:
- 暴露在Cd下降了细胞活力,增加了ROS,降低了抗氧化酶活性,并诱导了亡.
- 补充Se改善了这些影响,增强了细胞增殖,并恢复了抗氧化酶活性.
- Se缓解了Cd诱导的内等质网膜应激和亡,并有助于维持细胞内平衡.
结论:
- 会在L8824细胞中诱导氧化应激,内分泌网膜应激,线粒体损伤和亡.
- 通过抑制ERS,维持平衡,增强抗氧化能力,表现出显著的保护作用.
- 补充降低了Keap1/Nrf2通路的调节,为鱼类的Cd毒性提供了一种保护策略.
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