کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739330 | 1046871 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Beryllium-stimulated reactive oxygen species and macrophage apoptosis
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کلمات کلیدی
MnTBAPBALDcfCBDDCFH-DA2′,7′-dichlorofluorescein - 2 '، 7'-dichlorofluorescein2′,7′-dichlorofluorescein diacetate - 2 '، 7'-dichlorofluorescein diacetateROS - ROSHydrogen peroxide - آب اکسیژنهethidium bromide - اتیدیوم برومایدinflammation - التهاب( توروم) beryllium - بریلیوم Chronic Beryllium Disease - بیماری بریلیم مزمنApoptosis - خزان یاختهایDihydroethidine - دی هیدروتیدینFree radicals - رادیکال آزادbronchoalveolar lavage - لارو برونکلو آلوئولارMacrophage - ماکروفاژ H2O2 - هیدروژن پراکسیدDHE - وReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Beryllium (Be), the etiologic agent of chronic beryllium disease, is a toxic metal that induces apoptosis in human alveolar macrophages. We tested the hypothesis that Be stimulates the formation of reactive oxygen species (ROS) which plays a role in Be-induced macrophage apoptosis. Mouse macrophages were exposed to 100 μM BeSO4 in the absence and presence of the catalytic antioxidant MnTBAP (100 μM). Apoptosis was measured as the percentage of TUNEL+ and caspase-8+ cells. ROS production was measured by flow cytometry using the fluorescence probes, dihydroethidine (DHE) and dichlorofluorescein diacetate (DCFH-DA). Be-exposed macrophages had increased TUNEL+ cells (15 ± 1% versus controls 1 ± 0.2%, P < 0.05) and increased caspase-8+ cells (18.7 ± 2% versus controls 1.8 ± 0.4%, P < 0.05). Be-induced caspase-8 activation, and a 4-fold increase in ROS formation, was ameliorated by exposure to MnTBAP. Hydrogen peroxide (30 μM) exposure potentiated Be-induced caspase-8 activation, and was also attenuated by MnTBAP. Our data are the first to demonstrate that Be stimulates macrophage ROS formation which plays an important role in Be-induced macrophage apoptosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 38, Issue 7, 1 April 2005, Pages 928-937
Journal: Free Radical Biology and Medicine - Volume 38, Issue 7, 1 April 2005, Pages 928-937
نویسندگان
Richard T. Sawyer, David R. Dobis, Mark Goldstein, Leonard Velsor, Lisa A. Maier, Andrew P. Fontenot, Lori Silveira, Lee S. Newman, Brian J. Day,