کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739644 | 1046883 | 2005 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hypochlorous acid-mediated mitochondrial dysfunction and apoptosis in human hepatoma HepG2 and human fetal liver cells: role of mitochondrial permeability transition
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کلمات کلیدی
PBS3-(4,5-dimethyl-2-yl)-2,5-diphenyltetrazolium bromideEarle's buffered salt solutionHFLMitochondria permeability transitionCyDTMRMCyclophilin DEBSSBKACCCPΔΨmMPTANTTCAGSHGC-MS - کروماتوگرافی گازی-طیف سنج جرمیMTT - MTTBongkrekic acid - اسید بونکروکیکtrichloroacetic acid - اسید ترشکلراکتیکhypochlorous acid - اسید هیپوکلریدهinflammation - التهاب( توروم) CSA - ایالات مؤتلفهٔ آمریکاadenine nucleotide translocase - ترانسکوز نوکلئوتید آدنینApoptosis - خزان یاختهایFree radicals - رادیکال آزادCell toxicity - سمیت سلولیcyclosporin A - سیکلوسپورین Agas chromatography–mass spectrometry - طیف سنجی جرم کروماتوگرافی گازPhosphatidylserine - فسفاتیدیلسرینtetramethylrhodamine methyl ester - متیل استر تترامتیل رودامینPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریMitochondrial membrane potential - پتانسیل غشای میتوکندریPropidium iodide - پروتئین یدیدreduced glutathione - کاهش گلوتاتیونLiver - کبدHuman fetal liver - کبد جنین انسانcarbonyl cyanide m-chlorophenylhydrazone - کربنیل سیانید m-chlorophenylhydrazonehigh-pressure liquid chromatography - کروماتوگرافی مایع با فشار بالاHPLC - کروماتوگرافی مایعی کارا
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Liver cirrhosis is often preceded by overt signs of hepatitis, including parenchymal cell inflammation and infiltration of polymorphonuclear (PMN) leukocytes. Activated PMNs release both reactive oxygen species and reactive halogen species, including hypochlorous acid (HOCl), which are known to be significantly cytotoxic due to their oxidizing potential. Because the role of mitochondria in the hepatotoxicity attributed to HOCl has not been elucidated, we investigated the effects of HOCl on mitochondrial function in the human hepatoma HepG2 cell line, human fetal liver cells, and isolated rat liver mitochondria. We show here that HOCl induced mitochondrial dysfunction, and apoptosis was dependent on the induction of the mitochondrial permeability transition (MPT), because HOCl induced mitochondrial swelling and collapse of the mitochondrial membrane potential with the concomitant release of cytochrome c. These biochemical events were inhibited by the classical MPT inhibitor cyclosporin A (CSA). Cell death induced by HOCl exhibited several classical hallmarks of apoptosis, including annexin V labeling, caspase activation, chromatin condensation, and cell body shrinkage. The induction of apoptosis by HOCl was further supported by the finding that CSA and caspase inhibitors prevented cell death. For the first time, these results show that HOCl activates the MPT, which leads to the induction of apoptosis and provides a novel insight into the mechanisms of HOCl-mediated cell death at sites of chronic inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 38, Issue 12, 15 June 2005, Pages 1571-1584
Journal: Free Radical Biology and Medicine - Volume 38, Issue 12, 15 June 2005, Pages 1571-1584
نویسندگان
Matthew Whiteman, Peter Rose, Jia Ling Siau, Nam Sang Cheung, Gek San Tan, Barry Halliwell, Jeffrey S. Armstrong,