Glover R E, Mile B, Rowlands C C, Jackson S K
Department of Medical Microbiology, University of Wales, College of Medicine, Cardiff, UK.
Biochim Biophys Acta. 1996 Jan 10;1310(1):5-9. doi: 10.1016/0167-4889(95)00171-9.
The rate of oxygen consumption in the human acute monocytic leukemia-derived cell line, Mono Mac 6, in response to lipopolysaccharide (LPS) in vitro was measured by electron paramagnetic resonance spectroscopy using an oxygen-sensitive spin-label, 4-oxo-2,2,6,6-tetramethylpiperidine-d16-1-oxyl (15N-PDT). Lipopolysaccharide impaired oxygen consumption in a dose-dependent manner which was shown to be mediated by mitochondrial dysfunction and could be augmented by pretreatment of the cells with interferon-gamma. Treatment of the cells with anti-CD14 monoclonal antibody failed to inhibit the LPS-induced effects on cellular respiration. These results suggest that LPS can directly reduce normal cellular oxygen consumption possibly via a CD14-independent pathway. This alteration of mitochondrial function by LPS may be responsible for the observed cell damage during sepsis.
利用氧敏感自旋标记物4-氧代-2,2,6,6-四甲基哌啶-d16-1-氧基(15N-PDT),通过电子顺磁共振波谱法测定人急性单核细胞白血病衍生细胞系Mono Mac 6在体外对脂多糖(LPS)反应时的耗氧率。脂多糖以剂量依赖方式损害耗氧,这被证明是由线粒体功能障碍介导的,并且可以通过用γ干扰素预处理细胞来增强。用抗CD14单克隆抗体处理细胞未能抑制LPS对细胞呼吸的诱导作用。这些结果表明,LPS可能通过不依赖CD14的途径直接降低正常细胞的耗氧。LPS对线粒体功能的这种改变可能是脓毒症期间观察到的细胞损伤的原因。