[在人类正常肝细胞中由短链化帕拉芬诱导的代谢干扰]
Yun Luo1, Ning-Bo Geng2, Shuang-Shuang Chen2
1College of Medicine, Linyi University, Linyi 276005, China.
Se pu = Chinese journal of chromatography
|February 20, 2024
概括
短链甲 (SCCP) 破坏人类肝细胞的新陈代谢,特别是脂质和核酸通路. 较高的SCCP剂量会导致更大的代谢损伤,包括生物膜破坏和减少能量生产.
科学领域:
- 环境科学 环境科学
- 毒理学 毒理学 毒理学
- 代谢学 代谢学 代谢学
背景情况:
- 短链甲 (SCCP) 是持久性有机污染物 (POP),由于其持久性,生物积累和毒性,它们对人类健康存在重大风险.
- 在环境和人体样本中广泛检测到SCCP,需要对其特定的毒理机制进行研究.
研究的目的:
- 在暴露于不同剂量的SCCP后,研究人类正常肝细胞 (L02) 的代谢变化.
- 确定受SCCP暴露影响的关键代谢途径,并了解剂量依赖的影响.
主要方法:
- 利用代谢学技术分析暴露于低,中等和高剂量的SCCP的L02细胞中的细胞变化.
- 使用主要成分分析 (PCA) 和代谢效应水平指数 (MELI) 进行数据分析.
- 使用MS/MS,HMDB和商业标准识别和注释差异化代谢物 (DMs).
主要成果:
- 所有的SCCP剂量都在L02细胞中引起了显著的代谢干扰,观察到剂量依赖的效应.
- 确定了72种不同的代谢物,其中脂质代谢,脂肪酸β-氧化和核酸代谢是最受影响的途径.
- 暴露于SCCP导致生物膜损伤 (改变的脂和脂),抑制脂肪酸β-氧化,扰乱核酸代谢,由增加的低素水平表明.
结论:
- SCCP会对人类肝细胞产生显著的代谢干扰,影响脂质,脂肪酸和核酸代谢.
- 观察到的代谢干扰表明潜在的不良健康影响,包括缺氧,氧化应激和突变发生.
- 代谢学是一个有价值的工具,用于了解新兴的POPs (如SCCPs) 的毒理机制.
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