Sevoflurane-induced oxidative stress and cellular injury in human peripheral polymorphonuclear neutrophils.
Food Chem Toxicol. 2006 Mar 29; [Epub ahead of print]
Sevoflurane-induced oxidative stress and cellular injury in human peripheral polymorphonuclear neutrophils.
‘Wong CH, Liu TZ, Chye SM, Lu FJ, Liu YC, Lin ZC, Chen CH.
Department of Anesthesiology, Chang Gung Memorial Hospital at ChiaYi, and ChiaYi School, Chang Gung Institute of Technology, Puzih City, ChiaYi County 613, Taiwan, ROC.’
Sevoflurane is an inhalation anesthetic used for general anesthesia. Several studies have demonstrated that reactive oxygen species (ROS) exist in cardioprotection when preconditioned with sevoflurane. Moreover, sevoflurane can also directly trigger the formation of peroxynitrite. Up to now, information pertinent to the effect of sevoflurane on cellular injuries in human polymorphonuclear neutrophils (PMN) is scant. In this study, we demonstrated that sevoflurane significantly increases intracellular H(2)O(2) and/or peroxide, superoxide, and nitric oxide (NO) in PMN within 1h treatment. Intensification of intracellular glutathione (GSH) depletion in PMN has been demonstrated with the presence of sevoflurane. Inhibition of sevoflurane-mediated intracellular H(2)O(2) and/or peroxide in PMN by catalase, mannitol, dexamethasone, N-acetylcysteine (NAC) and trolox, but not superoxide dismutase (SOD) pretreatment, was observed. Among them, catalase has the best effect scavenging intracellular H(2)O(2) and/or peroxide, suggesting that H(2)O(2) is the major ROS during sevoflurane treatment. Two apoptotic critical factors-lowering of the mitochondrial transmembrane potential (DeltaPsi(m)) and activation of caspase 3/7-were significantly increased after 1h of sevoflurane treatment. Apoptosis of PMN were determined by comet assay and flow cytometric analysis of annexin V-FITV protein binding to the cell surface. Exposure of PMN to sevoflurane markedly increased apoptosis in a dose-dependent manner. In summary, these results are important for demonstrating the oxidative stress and cellular injury on sevoflurane-treated human PMN.
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