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碳黑CB-EDA纳米颗粒在巨细胞中:氧化应激途径的变化和亡信号的变化

Joice Margareth de Almeida Rodolpho¹, Krissia Franco de Godoy¹, Patricia Brassolatti¹

¹Laboratório de Inflamação e Doenças Infecciosas, Departamento de Morfologia e Patologia, Universidade Federal de São Carlos, São Carlos 13565-905, Brazil.

|June 28, 2023

概括

黑碳纳米颗粒与乙烯基胺 (CB-EDA) 功能化,诱导J774.A1巨细胞的亡. 这是通过氧化应激,炎症和线粒体功能障碍发生的,导致细胞死亡.

科学领域:

纳米技术纳米技术
细胞生物学细胞生物学
毒理学毒理学毒理学

背景情况:

黑碳纳米粒子 (BCNP) 是具有潜在健康影响的环境污染物.
BCNP 的功能化可以改变它们的生物相互作用和毒性.
J774.A1小鼠巨细胞是研究细胞对纳米材料反应的相关模型.

研究的目的:

在J774.A1巨上研究乙烯基胺功能化黑碳纳米粒子 (CB-EDA) 的细胞毒性.
阐明CB-EDA诱导的细胞死亡背后的机制.
分析暴露于CB-EDA的巨细胞中的氧化和炎症概况.

主要方法:

暴露J774.A1细胞在CB-EDA的不同度和时间点.
使用LDH测定对细胞活性的评估.
测量氧化应激标志物 (ROS,氧化).
对促炎性细胞因子释放的分析 (IL-6,IL-12,TNF).
评估线粒体完整性和caspase-3激活.

主要成果:

在J774.A1细胞中,CB-EDA证明了时间和剂量依赖的细胞毒性.
通过增加的氧化应激 (氧化,ROS) 和氧化还原失衡,CB-EDA的细胞形成引发了亡.
暴露于CB-EDA导致膜完整性受损,增加LDH释放,以及促炎性细胞因子分泌.
线粒体完整性受到损害,细胞活力下降,与caspase-3通路激活相关.

结论:

通过氧化应激,炎症和线粒体损伤,CB-EDA诱导J774.A1巨细胞的亡.
这些发现突显了功能化黑碳纳米粒子对细胞的潜在毒性.
了解这些机制对于评估与BCNP暴露相关的健康风险至关重要.

关键词:

细胞 J774A.1 的细胞.灭症 (apoptosis) 是一种死亡的过程.碳黑纳米粒子碳黑纳米粒子氧化应激是一种氧化应激.有活性氧物种的反应性氧物种.细胞活力细胞的活力.

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