缺氧会降低细胞中线粒体ROS的产生
Bijoya Sen1, Bérengère Benoit1, Martin D Brand1
1Buck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, 94945, USA.
Free radical biology & medicine
|August 15, 2024
概括
急性缺氧降低了细胞中的反应性氧物种 (ROS) 生产,这与之前的报道相反. 这一发现表明细胞质过氧化 (H2O2),而不是线粒体ROS,对于稳定HIF1α至关重要.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生物化学
- 缺氧研究 缺氧研究
背景情况:
- 据报道,在急性缺氧期间,线粒体的活性氧物种 (ROS) 生产通常会增加.
- 在细胞对低氧反应,特别是HIF1α稳定中的ROS的作用仍然不完全理解.
研究的目的:
- 重新检查急性缺氧对细胞ROS产生的影响.
- 研究不同ROS产生的部位对缺氧诱导反应的贡献,包括HIF1α稳定.
主要方法:
- 综合超红/马过氧化酶试验和二二化素试验,以测量过氧化 (H2O2) 的释放.
- 从线粒体复合物I (部位IQ),复合物III (部位IIIQo) 和细胞质NADH氧化酶 (NOX) 的ROS产生的评估.
- HIF1α 记者细胞系,以评估 ROS 生产对 HIF1α 表达的影响.
主要成果:
- 急性缺氧减少了HEK293细胞的H2O2释放,而H2O2降解能力没有变化.
- 从线粒体位点IQ,IIIQo和细胞质NOX的ROS生产率同样被急性缺氧降低.
- 从IQ,IIIQo站点抑制ROS生产,或NOX降低了HIF1α表达,类似于之前对IIIQo站点的发现.
结论:
- 线粒体ROS产量的增加不会驱动HIF1α对急性缺氧的反应.
- 来自网站IQ,IIIQo和NOX的细胞质H2O2对于其他信号的HIF1α稳定是必要的.
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