کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739251 | 1046869 | 2005 | 17 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mitochondria superoxide dismutase mimetic inhibits peroxide-induced oxidative damage and apoptosis: Role of mitochondrial superoxide
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کلمات کلیدی
DCFH-DAIREIRPMG-132BAECCyt Cglucose/glucose oxidaseCSSDPBSDcfLACDMEMFBS13-HODE - 13-HEAD2′,7′-dichlorodihydrofluorescein diacetate - 2 '، 7'-dichlorodihydrofluorescein diacetate2′,7′-dichlorofluorescein - 2 '، 7'-dichlorofluoresceinDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده Dulbeccoiron-regulatory protein - آهن پروتئینی نظارتی13-hydroxyoctadecadienoic acid - اسید 13-هیدروکسیکوکاتاد داودیوئیکElectron paramagnetic resonance - تشدید پارامغناطیس الکترونEPR - تشدید پارامغناطیس الکترونfetal bovine serum - سرم جنین گاوBovine aortic endothelial cells - سلولهای اندوتلیال آئورت گاوcytochrome c - سیتوکروم سیiron-responsive element - عنصر پاسخ دهنده آهنDulbecco's phosphate-buffered saline - فسفات باسیل نمک Dulbecco
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
The purpose of this study was to test the hypothesis whether Mito-carboxy proxyl (Mito-CP), a mitochondria-targeted nitroxide, inhibits peroxide-induced oxidative stress and apoptosis in bovine aortic endothelial cells (BAEC). Glucose/glucose oxidase (Glu/GO)-induced oxidative stress was monitored by dichlorodihydrofluorescein oxidation catalyzed by intracellular H2O2 and transferrin receptor-mediated iron transported into cells. Pretreatment of BAECs with Mito-CP significantly diminished H2O2- and lipid peroxide-induced intracellular formation of dichlorofluorescene and protein oxidation. Electron paramagnetic resonance (EPR) studies confirmed the selective accumulation of Mito-CP into the mitochondria. Mito-CP inhibited the cytochrome c release and caspase-3 activation in cells treated with peroxides. Mito-CP inhibited both H2O2- and lipid peroxide-induced inactivation of complex I and aconitase, overexpression of transferrin receptor (TfR), and mitochondrial uptake of 55Fe, while restoring the mitochondrial membrane potential and proteasomal activity. In contrast, the “untargeted” carboxy proxyl (CP) nitroxide probe did not protect the cells from peroxide-induced oxidative stress and apoptosis. However, both CP and Mito-CP inhibited superoxide-induced cytochrome c reduction to the same extent in a xanthine/xanthine oxidase system. We conclude that selective uptake of Mito-CP into the mitochondria is responsible for inhibiting peroxide-mediated Tf-Fe uptake and apoptosis and restoration of the proteasomal function.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 39, Issue 5, 1 September 2005, Pages 567-583
Journal: Free Radical Biology and Medicine - Volume 39, Issue 5, 1 September 2005, Pages 567-583
نویسندگان
Anuradha Dhanasekaran, Srigiridhar Kotamraju, Chandran Karunakaran, Shasi V. Kalivendi, Simmy Thomas, Joy Joseph, B. Kalyanaraman,