کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738550 | 1046714 | 2011 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Depletion of cytosolic or mitochondrial thioredoxin increases CYP2E1-induced oxidative stress via an ASK-1-JNK1 pathway in HepG2 cells
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کلمات کلیدی
ASK-1TNFαTrx-1Jnk4-HNE4-hydroxynonenalCYP2E1c-Jun NH2-terminal kinaseBSOPDI3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyl tetrazolium bromideMAPK - MAPKMTT - MTTROS - ROSOxidative stress - تنش اکسیداتیوtumor necrosis factor α - تومور نکروز عامل αthioredoxin - تیرودوکسینDihydroethidine - دی هیدروتیدینHepG2 cells - سلولهای HepG2Cell toxicity - سمیت سلولیcytochrome P4502E1 - سیتوکروم P4502E1endoplasmic reticulum - شبکه آندوپلاسمی DHE - وmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenApoptosis signal-regulating kinase-1 - کیناز-1 تنظیم کننده سیگنال آپوپتوزGlutathione ethyl ester - گلوتاتیون اتیل استرReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Depletion of cytosolic or mitochondrial thioredoxin increases CYP2E1-induced oxidative stress via an ASK-1-JNK1 pathway in HepG2 cells Depletion of cytosolic or mitochondrial thioredoxin increases CYP2E1-induced oxidative stress via an ASK-1-JNK1 pathway in HepG2 cells](/preview/png/10738550.png)
چکیده انگلیسی
Thioredoxin is an important reducing molecule in biological systems. Increasing CYP2E1 activity induces oxidative stress and cell toxicity. However, whether thioredoxin protects cells against CYP2E1-induced oxidative stress and toxicity is unknown. SiRNA were used to knockdown either cytosolic (TRX-1) or mitochondrial thioredoxin (TRX-2) in HepG2 cells expressing CYP2E1 (E47 cells) or without expressing CYP2E1 (C34 cells). Cell viability decreased 40-60% in E47 but not C34 cells with 80-90% knockdown of either TRX-1 or TRX-2. Depletion of either thioredoxin also potentiated the toxicity produced either by a glutathione synthesis inhibitor or by TNFα in E47 cells. Generation of reactive oxygen species and 4-HNE protein adducts increased in E47 but not C34 cells with either thioredoxin knockdown. GSH was decreased and adding GSH completely blocked E47 cell death induced by either thioredoxin knockdown. Lowering TRX-1 or TRX-2 in E47 cells caused an early activation of ASK-1, followed by phosphorylation of JNK1 after 48 h of siRNA treatment. A JNK inhibitor caused a partial recovery of E47 cell viability after thioredoxin knockdown. In conclusion, knockdown of TRX-1 or TRX-2 sensitizes cells to CYP2E1-induced oxidant stress partially via ASK-1 and JNK1 signaling pathways. Both TRX-1 and TRX-2 are important for defense against CYP2E1-induced oxidative stress.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 51, Issue 1, 1 July 2011, Pages 185-196
Journal: Free Radical Biology and Medicine - Volume 51, Issue 1, 1 July 2011, Pages 185-196
نویسندگان
Lili Yang, Defeng Wu, Xiaodong Wang, Arthur I. Cederbaum,