کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1909112 | 1046701 | 2012 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mercury and selenium interaction in vivo: Effects on thioredoxin reductase and glutathione peroxidase
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کلمات کلیدی
GPXCysLC50GSSGMeHgp38ASK1HGTGSHHg0SECBSA - BSAHg2+ - Hg2 +ROS - ROSsEH - SEHbovine serum albumin - آلبومین سرم گاوCysteine residue - باقی مانده سستیونMercury vapor - بخار جیوهinductively coupled plasma mass spectrometry - طیفسنجی جرمی پلاسمای جفتشده القاییICP-MS - طیفسنجی جرمی پلاسمای جفتشده القاییMethylmercury - متیل کرکریreduced glutathione - کاهش گلوتاتیونTotal mercury - کل جیوهapoptosis signal-regulating kinase 1 - کیناز تنظیم کننده سیگنال آپوپتوز 1Thiol group - گروه تیولoxidized glutathione - گلوتاتیون اکسید شدهglutathione reductase - گلوتاتیون ردوکتازglutathione peroxidase - گلوتاتیون پراکسیدازReactive 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: Mercury and selenium interaction in vivo: Effects on thioredoxin reductase and glutathione peroxidase Mercury and selenium interaction in vivo: Effects on thioredoxin reductase and glutathione peroxidase](/preview/png/1909112.png)
چکیده انگلیسی
Mercury compounds exert toxic effects via interaction with many vital enzymes involved in antioxidant regulation, such as selenoenzymes thioredoxin reductase (TrxR) and glutathione peroxidase (GPx). Selenium supplementation can reactivate the mercury-inhibited TrxR and recover the cell viability in vitro. To gain an insight on how selenium supplementation affects mercury toxicity in vertebrates, we investigated the effects of selenium on the mercury accumulation and TrxR and GPx activities in a fish model. Juvenile zebra-seabreams were exposed either to methylmercury (MeHg) or inorganic mercury (Hg2+) in the presence or absence of sodium selenite (Se) for 28Â days followed by 14Â days of depuration. Mercury accumulation was found to be 10-fold higher under MeHg exposure than under Hg2+ exposure. Selenium supplementation caused a half decrease of the accumulation of MeHg but did not influence Hg2+ accumulation. Exposure to both mercurials led to a decrease of the activity of TrxR (<Â 50% of control) in all organs. Se supplementation coincident with Hg2+ exposure protected the thioredoxin system in fish liver. However, supplementation of Se during the depuration phase had no effects. The activity of GPx was only affected in the brain of fishes upon the exposure to MeHg and coexposure to MeHg and Se. Selenium supplementation has a limited capacity to prevent mercury effects in brain and kidney. These results demonstrate that Se supplementation plays a protective role in a tissue-specific manner and also highlight the importance of TrxR as a main target for mercurials in vivo.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 52, Issue 4, 15 February 2012, Pages 781-793
Journal: Free Radical Biology and Medicine - Volume 52, Issue 4, 15 February 2012, Pages 781-793
نویسندگان
Vasco Branco, João Canário, Jun Lu, Arne Holmgren, Cristina Carvalho,