暴露于U(VI) 对肺上皮细胞BEAS-2B细胞的生物学影响
Mingxia Zhang1, Han Zhou2, Lei Liu3
1College of Life Sciences, Anhui Normal University, Wuhu 241000, China; Anhui Province Key Laboratory of Medical Physics and Technology, Institute of Health & Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei 230031, China.
Chemosphere
|October 3, 2024
概括
(VI) 暴露会导致肺上皮细胞受到显著损伤,包括DNA损伤和抑制增殖. 这项研究详细介绍了由毒性破坏的分子通路.
科学领域:
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- (VI) 是一种具有已知的健康风险的环境毒素.
- 肺上皮细胞是吸入毒素的主要目标.
- 了解对细胞的影响对于风险评估至关重要.
研究的目的:
- 研究 (VI) 对肺上皮细胞的生物作用.
- 阐明引起的细胞毒性背后的分子机制.
- 为了确定受U (VI) 暴露影响的关键信号通路.
主要方法:
- 对细胞活力的MTT测定.
- 免疫光和流细胞测量用于细胞应激和DNA损伤.
- 西方涂抹用于分析蛋白质表达和信号通路 (MAPK,PI3K/AKT/GSK-3β/β-catenin).
主要成果:
- U(VI) 暴露诱导了氧化应激,炎症,并激活了MAPK通路.
- 观察到显著的细胞膜损伤和DNA损伤.
- 通过破坏PI3K/AKT/GSK-3β/β-catenin通路并降低CyclinD1表达,U(VI) 抑制了细胞的增殖和迁移.
- 细胞周期延迟,线粒体损伤和能量代谢降低被注意到.
结论:
- (VI) 对肺上皮细胞产生显著的细胞毒性作用.
- 分子干扰包括氧化应激,DNA损伤和细胞循环调节的改变.
- PI3K/AKT/GSK-3β/β-catenin通路是肺细胞中U(VI) 毒性的关键目标.
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