重金属暴露导致的脂代谢失调
Shaheer Ahmad1, Sierra Single1, Yuelong Liu1
1Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL 35294-0006, USA.
Antioxidants (Basel, Switzerland)
|August 29, 2024
概括
高度的重金属如,和会破坏脂平衡,并诱导肺细胞的氧化应激,导致呼吸系统疾病,如喘.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 肺部医学 肺部医学
背景情况:
- 暴露于重金属 (HM) 与炎症和细胞死亡有关,恶化了喘等呼吸道疾病.
- 吸入的细颗粒物 (PM$_{2.5}$) 与肺细胞中的HM沉积物结合,但局部高度的影响尚未研究.
研究的目的:
- 调查局部高度的酸 (NaAsO),化 (MnCl) 和化 (CdCl) 对脂平衡和氧化应激的影响.
- 探索脂代谢和氧化应激在调解细胞对喘相关的HM暴露反应中的作用.
主要方法:
- 使用了体外细胞模型和体外3D人肺组织模型.
- 评估了脂酶代谢的酶调节剂 (救援,回收,新合成).
- 进行了脂组分析,空间转录组学和定量实时PCR.
主要成果:
- 通过特定的HM观察到脂代谢酶的差异调节.
- 暴露于HM增加了抗亡性脂和减少了亲亡性脂,这表明救援和de novo合成途径的激活.
- 在肺组织中,CdCl2和NaAsO2的暴露分别特别激活了救援和de novo合成途径. 在肺上皮细胞和组织中识别了HM诱导的氧化应激特征.
结论:
- 局部高度的特定HM破坏了脂平衡,并在肺细胞中诱导氧化应激.
- 这些干扰脂代谢和诱导氧化应激是HM诱导的肺损伤的关键机制,并可能导致喘病原性.
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