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在过氧引起的氧化应激后对挥发性有机化合物的HS-GC-MS分析:一个验证研究
Thijs A Lilien1,2, Dominic W Fenn3,4, Paul Brinkman4
1Department of Paediatric Intensive Care Medicine, Emma Children's Hospital, Amsterdam UMC Location University of Amsterdam, Meibergdreef 9, Amsterdam, The Netherlands. t.a.lilien@amsterdamumc.nl.
这项研究发现,高氧暴露不会增加肺细胞中的挥发性有机化合物 (VOC),与氧化应激相关的常见VOC与患者的氧气暴露无关. 这些发现质疑它们作为生物标志物的使用.
科学领域:
- 生物化学 生物化学
- 肺部医学 肺部医学
- 生物标志物发现发现
背景情况:
- 呼出的挥发性有机化合物 (VOC) 与过氧和氧化应激有关.
- 对于已识别的VOCs的确切起源和异质性存在担忧.
- 需要进行翻译性研究,以验证VOC作为高氧化引起的氧化应激的标志物.
研究的目的:
- 为了研究高氧暴露的肺上皮细胞中与氧化应激相关的VOCs的变化.
- 评估之前提出的VOCs作为过氧诱导氧化应激标记物的有效性.
主要方法:
- A549膜上皮细胞暴露于高氧,室内空气 (对照组) 或过氧化 (阳性对照组).
- 用气色谱-质谱法 (GC-MS) 分析了头部空间的VOC.
- 一项临床队列分析评估了重症患者中VOC与氧气暴露的相关性.
主要成果:
- 过氧暴露并没有增加向的VOCs;decane水平显著下降.
- 不针对性分析显示,没有新的高氧化物相关的VOC.
- 六,八和十在区分高氧暴露患者时没有诊断价值.
结论:
- 肺上皮细胞的过氧没有提高可识别的VOCs.
- 以前提出的氧化应激VOC与患者的氧气暴露无关.
- 拟议的VOC生物标志物的病理生理起源比单纯的细胞水平上高氧化诱导的氧化应激更复杂.
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