کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10758150 | 1050404 | 2013 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Oxidative stress potentially enhances FcεRI-mediated leukotriene C4 release dependent on the late-phase increase of intracellular glutathione in mast cells
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کلمات کلیدی
GSHGSSGBSOFcεRIL-buthionine-S,R-sulfoximineOxidative stress - تنش اکسیداتیوLeukotriene C4 - لوکوترین C4Leukotriene - لکوترینMast cell - ماستسلGlutathione - گلوتاتیونoxidized glutathione - گلوتاتیون اکسید شدهhigh-affinity IgE receptor - گیرنده IgE باکتریProstaglandin E2 receptor - گیرنده پروستاگلاندین E2
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Cysteinyl leukotrienes (cysLTs), which include leukotriene C4 (LTC4), are the predominant class of LTs synthesized by mast cells. CysLTs can induce many of the abnormalities seen in asthma. LTC4 is generated by the conjugation of LTA4 with reduced glutathione (GSH) by LTC4 synthase. During screening of the effects of prostanoids on high-affinity IgE receptor (FcεRI)-mediated LTC4 release from mast cells, we realized that some prostanoids, including ONO-AE1-259-01 and ONO-AE-248, inhibited LTC4 release, which was associated with a decrease in the amount of intracellular total GSH. We ascertained that l-buthionine-S,R-sulfoximine (BSO), a selective inhibitor of glutamate-cysteine ligase, inhibited LTC4 release. In addition, cell-permeable GSH, the glutathione reduced form ethyl ester (GSH-OEt), enhanced LTC4 release in accordance with the change in intracellular total GSH. Depletion of intracellular total GSH induced by ONO-AE-248 or BSO enhanced FcεRI-mediated LTB4 release in contrast to LTC4. Oxidative stress contributes to many pathological conditions including asthma. GSH is a major soluble antioxidant and a cofactor for several detoxifying enzymes including GSH peroxidase. Exposure of mast cells to hydrogen peroxide (H2O2) or diamide to mimic oxidative stress unexpectedly increased rather than decreased the intracellular reduced GSH content as well as total GSH in the late phase (i.e., 24 or 48 h after exposure), which was accompanied by an increase in LTC4 release. In conclusion, FcεRI-mediated LTC4 release from mast cells is mainly regulated by the amount of intracellular GSH. In some cases, oxidative stress may induce a late-phase increase in intracellular GSH, resulting in enhanced LTC4 release from mast cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 439, Issue 3, 27 September 2013, Pages 357-362
Journal: Biochemical and Biophysical Research Communications - Volume 439, Issue 3, 27 September 2013, Pages 357-362
نویسندگان
Kaori Seki, Takeshi Hisada, Tadayoshi Kawata, Yosuke Kamide, Kunio Dobashi, Masanobu Yamada, Masatomo Mori, Fumikazu Okajima, Tamotsu Ishizuka,