ABSTRACT
OBJECTIVE: Reactive oxygen species (ROS) are involved in a variety of biological phenomena and serve both deleterious and beneficial roles. ROS quantification and assessment of reaction networks are desirable but difficult because of their short half-life and high reactivity. Here, we describe a pro-oxidative model in a single human lung carcinoma SPC-A-1 cell that was created by application of extracellular H2O2 stimuli. METHODS: Modified microfluidics and imaging techniques were used to determine O2 â¢- levels and construct an O2 â¢- reaction network. To elucidate the consequences of increased O2 â¢- input, the mitochondria were given a central role in the oxidative stress mode, by manipulating mitochondria-interrelated cytosolic Ca2+ levels, mitochondrial Ca2+ uptake, auto-amplification of intracellular ROS and the intrinsic apoptotic pathway. RESULTS AND CONCLUSIONS: Results from a modified microchip demonstrated that 1 mmol/L H2O2 induced a rapid increase in cellular O2 â¢- levels (>27 vs. >406 amol in 20 min), leading to increased cellular oxidizing power (evaluated by ROS levels) and decreased reducing power (evaluated by glutathione (GSH) levels). In addition, we examined the dynamics of cytosolic Ca2+ and mitochondrial Ca2+ by confocal laser scanning microscopy and confirmed that Ca2+ stores in the endoplasmic reticulum were the primary source of H2O2-induced cytosolic Ca2+ bursts. It is clear that mitochondria have pivotal roles in determining how exogenous oxidative stress affects cell fate. The stress response involves the transfer of Ca2+ signals between organelles, ROS auto-amplification, mitochondrial dysfunction, and a caspase-dependent apoptotic pathway.
Subject(s)
Hydrogen Peroxide/chemistry , Mitochondria/metabolism , Oxidative Stress , Reactive Oxygen Species/metabolism , Superoxides/chemistry , Apoptosis , Calcium/metabolism , Calcium Signaling , Caspases/metabolism , Cell Line, Tumor , Cell Lineage , Cytosol/metabolism , Glutathione/metabolism , Humans , Oxidation-Reduction , Signal TransductionABSTRACT
BACKGROUND: Esophagectomy after pneumonectomy has been rarely reported, mainly due to the technical difficulty in performing this surgical approach. Conventional intubation to the contralateral respiratory passage is technically challenging, while the homolateral respiratory tract is absent, making oxygenation impossible. METHODS: To overcome this problem, we used venoarterial (VA) extracorporeal membrane oxygenation (ECMO) which can help achieve gas exchange despite the collapsed lung and provide a clear unobstructed surgical field for esophagectomy. RESULTS: We obtained satisfactory outcomes with VA ECMO in our treated patient. CONCLUSIONS: This technique may be an excellent option for the treatment of complex situations such as esophagectomy after pneumonectomy.
