在脂质氧化过程中,两种不同的机制参与了膜透
Min Xie1, Eveline H W Koch1, Cornelis A van Walree2
1Membrane Biochemistry & Biophysics, Bijvoet Center for Biomolecular Research, Department of Chemistry, Utrecht University, Utrecht, the Netherlands.
Biophysical journal
|October 31, 2023
概括
脂质氧化通过两个机制损害细胞膜:通过截断的氧化脂的快速透,以及依赖于脂质不和的较慢损伤. 哺乳动物膜中的多不和脂质可能会促进长期的氧化损伤.
科学领域:
- 生物物理学的生物物理.
- 细胞生物学 细胞生物学
- 氧化压力是一种氧化压力.
背景情况:
- 脂质氧化是氧化应激的一个关键过程,它改变了细胞膜的特性和功能.
- 氧化损伤与膜生物物理性质之间的关系尚不清楚.
- 反应性氧和物种 (RONS) 在各种病理生理条件下诱导脂质氧化.
研究的目的:
- 量化脂质氧化和确定生物物理膜参数.
- 研究由RONS引起的膜通透的机制.
- 探索脂质不和在氧化膜损伤中的作用.
主要方法:
- 使用了具有不同脂质不和度的模型膜.
- 采用冷等离子体作为RONS的来源.
- 量化脂质氧化和测量生物物理膜参数.
主要成果:
- 确定了两种不同的脂质氧化诱导的膜透机制.
- 第一个机制,独立于脂质不和,涉及截断的氧化脂和短暂的RONS.
- 第二个机制依赖于脂质不和,发生在更长的潜伏期后,涉及脂质氧气添加物.
结论:
- 膜的氧化损伤是复杂的,并且取决于环境.
- 哺乳动物膜中的多不和脂质不会增加即时的RONS敏感性,但可能会导致长期损伤.
- 从膜中释放的氧化脂质可能充当信号分子.
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