کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739529 | 1046878 | 2005 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Fatty acid-mediated intracellular iron translocation: A synergistic mechanism of oxidative injury
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کلمات کلیدی
deferoxamine mesylateFFAnDNAHUVECSAFCTBARSDCFDAJC-1TFRDFXDIOC6PBSMMPBSA - BSAMitochondria DNA - DNA میتوکندریاNuclear DNA - DNA هسته ایMTT - MTTROS - ROSbovine serum albumin - آلبومین سرم گاوPolyunsaturated fatty acids - اسید چرب اشباع نشدهPUFA - اسید چرب چند غیراشباعFree fatty acids - اسیدهای چرب آِزادLipid oxidation - اکسیداسیون لیپیدیOxidative stress - تنش اکسیداتیوApoptosis - خزان یاختهایmtDNA - دیانای میتوکندریاییFree radical - رادیکالهای آزاد SOD - سدCancer - سرطانHuman umbilical vein endothelial cells - سلول های اندوتلیالی ورید ناف انسانSuperoxide dismutase - سوکسوکس دیسموتازPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریthiobarbituric acid-reactive substances - مواد واکنش پذیر اسید تیوباربیتوریکMitochondria - میتوکندریاIron overload - هموکروماتوزPalmitic acid - پالمیتیک اسیدMitochondria membrane potential - پتانسیل غشای میتوکندریاReactive oxygen species - گونههای فعال اکسیژنtransferrin receptor - گیرنده انتقالین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Fatty acid has been reported to be associated with cardiovascular diseases and cancer, but the possible mechanism remains unclear. Here, we reported a novel mechanism for the permissive role of fatty acid on iron intracellular translocation and subsequent oxidative injury. In vitro study from endothelial cells showed that iron alone had little effect, whereas in combination with PA (palmitic acid), iron-mediated toxicity was markedly potentiated, as reflected in mitochondrial dysfunction, cell death, apoptosis, and DNA mutation. We also showed that PA not only facilitated iron translocation into cells through a transferrin-receptor (TfR)-independent mechanism, but also translocated iron into mitochondria; the subsequent intracellular iron overload resulted in reactive oxygen species (ROS) overgeneration and lipid oxidation. Further investigation revealed that PA-facilitated iron translocation is due to Fe/PA-mediated extracellular oxidative stress and the subsequent membrane damage with increased membrane permeability. Fe/PA-mediated toxic effects were reduced in Ï0 cells lacking mitochondrial DNA or by antioxidant enzyme SOD, especially mitochondrially localized MnSOD, suggesting a permissive role of PA for iron deposition on the vascular wall and its subsequent toxicity via mitochondrial oxidative stress. This observation was confirmed in vivo in mice, wherein higher vascular iron deposition and accompanying superoxide release were observed in the presence of a high-fat diet with iron administration.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 39, Issue 10, 15 November 2005, Pages 1385-1398
Journal: Free Radical Biology and Medicine - Volume 39, Issue 10, 15 November 2005, Pages 1385-1398
نویسندگان
Dachun Yao, Weibin Shi, Yulan Gou, Xinrong Zhou, Tak Yee Aw, Yikai Zhou, Zhengxiang Liu,