在MDCK细胞中,Tl (I) 和Tl (III) 诱导网膜应激
Emanuel Morel Gómez1, Cecilia I Casali2, María Del Carmen Fernández2
1Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Ciencias Biológicas, Cátedra de Biología Celular y Molecular, Buenos Aires, Argentina.
Environmental toxicology and pharmacology
|June 22, 2023
概括
暴露会阻止MDCK细胞的增殖,但保持活力. 它会诱导细胞内网膜应激和亡,这表明增殖障碍的机制.
科学领域:
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
- 生物化学 生物化学
背景情况:
- 是一种有毒的重金属.
- 了解的细胞作用对于毒理学和细胞生物学至关重要.
研究的目的:
- 研究 (I) 和 (III) 对马丁-达比犬 (MDCK) 细胞活力和增殖的影响.
- 阐明毒性背后的细胞机制,包括自,内质网膜 (ER) 应激和亡.
主要方法:
- 增殖的MDCK细胞暴露于.
- 细胞活力和增殖的评估.
- 对自标记物的分析 (SQSTM-1,LC3β,贝克林-1).
- 测量ER压力标志物 (ATF-6,IRE-1,XBP-1) 的测量.
- 细胞形态学的超结构分析.
- 对特定蛋白质表达的评估 (PHB,β-tubulin).
主要成果:
- 塔抑制了细胞增殖,同时保持了高细胞活力 (>95%).
- 自标志物发生了变化,48小时后SQSTM-1和贝克林-1表达增加.
- 在24小时内观察到显著的ER压力,由增加的ATF-6和IRE-1和XBP-1拼接表明.
- 超结构异常,包括ER扩大和细胞质真空化,在48小时后被发现.
- 增加的PHB和降低的β-tubulin表达表明潜在的帕帕托斯诱导.
结论:
- 暴露会在MDCK细胞中诱导内等质网膜应激.
- 可能会促进亡,导致增殖障碍.
- 这些发现提供了关于的细胞毒性机制的见解.
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