کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9002488 | 1118588 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
BCL-xL overexpression effectively protects against tetrafluoroethylcysteine-induced intramitochondrial damage and cell death
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کلمات کلیدی
VDACBax translocationFBSBcl-xLTFECGAPDHintATF3AmCTNFHspBSS3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate - 3 - [(3-کلامیدوپروپیل) دی متیل آمونیو] -1-پروپان سولفونات3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyl tetrazolium bromide7-amino-4-methylcoumarin - 7-آمینو-4-متیل کومارینMTT - MTTpiperazine-N,N′-bis(2-ethanesulfonic acid) - piperazine-N، N'-bis (2-ethanesulfonic acid)α-ketoglutarate dehydrogenase - α-کتوگلووترات دهیدروژنازfetal bovine serum - سرم جنین گاوCytotoxicity - سمیت سلولیtumor necrosis factor - فاکتور نکروز تومورActivating transcription factor-3 - فعال کردن عامل رونویسی 3Pipes - لوله هایbuffered saline solution - محلول نمک بافرNecrosis - نکروز یا بافتمردگیHeat shock protein - پروتئین شوک حرارتCHAPS - چاپسvoltage-dependent anion-selective channel - کانال انتخابی آنیونی وابسته به ولتاژglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژنازiodonitrotetrazolium chloride - یدونیت تترتازولیم کلرید
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: BCL-xL overexpression effectively protects against tetrafluoroethylcysteine-induced intramitochondrial damage and cell death BCL-xL overexpression effectively protects against tetrafluoroethylcysteine-induced intramitochondrial damage and cell death](/preview/png/9002488.png)
چکیده انگلیسی
S-(1,1,2,2-Tetrafluoroethyl)-l-cysteine (TFEC), a major metabolite of the industrial gas tetrafluoroethylene, has been shown to mediate nephrotoxicity by necrosis. TFEC-induced cell death is associated with an early covalent modification of specific intramitochondrial proteins; including aconitase, α-ketoglutarate dehydrogenase (KGDH) subunits, HSP60 and HSP70. Previous studies have indicated that the TAMH line accurately models TFEC-induced in vivo cell death with dose- and time-dependent inhibitions of both KGDH and aconitase activities. Here, we show that the molecular pathway leading to TFEC-mediated cell death is associated with an early cytosolic to mitochondrial translocation of BAX, a pro-apoptotic member of the BCL-2 family. Immunoblot analyses indicated movement of BAX (21 kDa) to the mitochondrial fraction after exposure to a cytotoxic concentration of TFEC (250 μM). Subsequent cytochrome c release from mitochondria was also demonstrated, but only a modest increase in caspase activities was observed, suggesting a degeneration of early apoptotic signals into secondary necrosis. Significantly, TAMH cells overexpressing BCL-xL preserved cell viability even to supratoxicological concentrations of TFEC (â¤600 μM), and this cytoprotection was associated with decreased HSP70i upregulation, indicating suppression of TFEC-induced proteotoxicity. Hence, TFEC-induced necrotic cell death in the TAMH cell line is mediated by BAX and antagonized by the anti-apoptotic BCL-2 family member, BCL-xL.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 69, Issue 1, 1 January 2005, Pages 147-157
Journal: Biochemical Pharmacology - Volume 69, Issue 1, 1 January 2005, Pages 147-157
نویسندگان
Han K. Ho, Zhong-Hua Hu, Shie-Pon Tzung, David M. Hockenbery, Nelson Fausto, Sidney D. Nelson, Sam A. Bruschi,