MnO2纳米颗粒通过依赖mtROS的Hsf1Ser326酸化引发肝脏脂毒性和髓性
Tao Zhao1, Hua Zheng1, Jie-Jie Xu1
1Hubei Hongshan Laboratory, Fishery College, Huazhong Agricultural University, Wuhan, 430070, China.
Free radical biology & medicine
|December 4, 2023
概括
过度的二氧化纳米颗粒 (MnO2 NPs) 破坏肝脏脂质代谢,导致脂毒性,并通过线粒体氧化应激和hsf1酸化激活线粒体.
科学领域:
- 生物化学 生化学
- 毒理学 毒理学 毒理学
- 纳米医学是一种纳米医学.
背景情况:
- (Mn) 对于脊椎动物的新陈代谢至关重要.
- 二氧化纳米粒子 (MnO2NP) 为生物应用提供了独特的特性.
- MnO2 NPs对新陈代谢的不良影响仍然在很大程度上是未知的.
研究的目的:
- 调查食MnO2NP对脊椎动物肝脂代谢的影响.
- 阐明MnO2 NP诱导的肝毒性背后的机制.
主要方法:
- 对肝脏和线粒体含量的分析.
- 评估肝脏脂肪生成,脂解和脂肪酸β-氧化.
- 评估线粒体的氧化应激,功能,动态和线粒体衰变.
- 研究mtROS激活的hsf1酸化及其在MnO2NP毒性中的作用.
主要成果:
- 过度的MnO2NP增加了肝脏的Mn,促进了脂毒性和脂生成,并抑制了脂解和脂肪酸氧化.
- MnO2 NPs诱导了线粒体的氧化应激,损害了线粒体功能,破坏了动力学,并激活了线粒体.
- 在Ser326中通过mtROS激活的Hsf1酸化中介MnO2 NP诱导的脂毒性和线粒细胞衰变.
结论:
- 饮食中的MnO2NP会破坏肝脂代谢,并诱导肝毒性.
- 线粒体功能障碍,氧化应激和hsf1酸化是关键机制.
- 结果提供了对脊椎动物纳米粒子毒性和肝毒性的见解.
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