کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2587065 | 1130916 | 2006 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Sevoflurane-induced oxidative stress and cellular injury in human peripheral polymorphonuclear neutrophils
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کلمات کلیدی
dichlorofluoresceinS-nitroso-N-acetylpenicillamineDAF-2PMNCCCPDCFH-DAGSHDcfSevoflurane - سووفلوران4,5-diaminofluorescein - 4،5-دیامین فلوئورسینROS - ROSOxidative stress - تنش اکسیداتیوApoptosis - خزان یاختهایSNAP - ضربه محکم و ناگهانیPolymorphonuclear neutrophils - نوتروفیل های پلیمورون هسته ایNitric oxide - نیتریک اکسیدHydroethidine - هیدروتیدینMitochondrial transmembrane potential - پتانسیل ترانزیتی میتوکندریPropidium iodide - پروتئین یدیدcarbonyl cyanide m-chlorophenylhydrazone - کربنیل سیانید m-chlorophenylhydrazoneGlutathione - گلوتاتیونReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
دانش تغذیه
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Sevoflurane-induced oxidative stress and cellular injury in human peripheral polymorphonuclear neutrophils Sevoflurane-induced oxidative stress and cellular injury in human peripheral polymorphonuclear neutrophils](/preview/png/2587065.png)
چکیده انگلیسی
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 H2O2 and/or peroxide, superoxide, and nitric oxide (NO) in PMN within 1 h treatment. Intensification of intracellular glutathione (GSH) depletion in PMN has been demonstrated with the presence of sevoflurane. Inhibition of sevoflurane-mediated intracellular H2O2 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 H2O2 and/or peroxide, suggesting that H2O2 is the major ROS during sevoflurane treatment. Two apoptotic critical factors-lowering of the mitochondrial transmembrane potential (ÎΨm) and activation of caspase 3/7-were significantly increased after 1 h 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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Food and Chemical Toxicology - Volume 44, Issue 8, August 2006, Pages 1399-1407
Journal: Food and Chemical Toxicology - Volume 44, Issue 8, August 2006, Pages 1399-1407
نویسندگان
Chung Hang Wong, Tsan-Zon Liu, Soi-Moi Chye, Fung-Jou Lu, Ya-Chen Liu, Zhao-Cen Lin, Ching-Hsein Chen,