کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5559316 | 1561569 | 2017 | 44 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Superoxide-hydrogen peroxide genetic imbalance modulates differentially the oxidative metabolism on human peripheral blood mononuclear cells exposed to seleno-L-methionine
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کلمات کلیدی
PBMCPBSSECTrxRDTNBSPS2ALACATTBARSGPXtRNAFe2+ - Fe2 +O2•− - O2 • -OH• - OH •alanine - آلانینferrous iron - آهن آهنtransfer ribonucleic acid - انتقال ریبونوکلئیک اسیدthioredoxin reductase - تریودوکسین ردوکتازthymine - تیمینSeMet - خودشانsuperoxide radical - رادیکال سوپراکسیدHydroxyl radical - رادیکال هیدروکسیلval - ساعتSOD - سدselenophosphate - سلنفسفاتseleno-l-methionine - سلنو-ال-متیونینSelenoproteins - سلنوپروتئین هاSelenium - سلنیومImmune cell - سلول ایمنیperipheral blood mononuclear cells - سلول های تک هسته ای خون محیطیSuperoxide dismutase - سوکسوکس دیسموتازPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریthiobarbituric acid reactive substances - مواد واکنش پذیر اسید تیوباربیتوریکNitric oxide - نیتریک اکسیدValine - والینPropidium iodide - پروتئین یدید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
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چکیده انگلیسی
Superoxide-hydrogen peroxide (S-HP) imbalance genetically caused by a gene polymorphism in the human manganese superoxide dismutase enzyme (Val16Ala-MnSOD) is associated with several diseases. Into mitochondria, MnSOD catalyses superoxide radical producing HP and oxygen. Ala-MnSOD genotype presents a high MnSOD efficiency and generates the highest HP concentrations that has been associated with the risk of several cancer types. Cellular selenoenzymes glutathione peroxidase and thioredoxin reductase (TrxR) and catalase (CAT) are essential to HP removal produced in excess in cells. Since, synthesis and activities of selenoenzymes are selenium dependent, we hypothesized that AA-MnSOD cells could have an improvement on antioxidant status undergoing Seleno-L-methionine (SeMet) treatment. This study performed an in vitro protocol to evaluate the response of peripheral blood mononuclear cells (PBMC) carriers of different Val16Ala-MnSOD genotypes exposed to SeMet. SeMet effects on cell viability, apoptosis induction and modulation of oxidative variables were determined using spectrophotometric, flow cytometry, fluorimetric and immunoassays. Gene modulation of antioxidant enzymes was also performed by qRT-PCR. From an initial protocol using heterozygous (AV) cells was determined that 1nM SeMet presented a cytoprotective effect. However, whereas this concentration did not change AA viability, in VV cells it was cytotoxic by increasing necrosis events. SeMet induced higher selenoenzymes levels in AA and VV cells and decreased oxidative markers levels including DNA damage. The results suggest a pharmacogenetic positive response of SeMet effect on AA-cells. Future studies in vivo could be essential to evaluate the potential clinical impact of S-HP imbalance after use of foods or supplements containing SeMet.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemico-Biological Interactions - Volume 273, 1 August 2017, Pages 18-27
Journal: Chemico-Biological Interactions - Volume 273, 1 August 2017, Pages 18-27
نویسندگان
Karen Lilian Schott, Charles Elias Assmann, Fernanda Barbisan, Verônica Farina Azzolin, Beatriz Bonadiman, Marta Maria Medeiros Frescura Duarte, Alencar Kolinski Machado, Ivana Beatrice Mânica da Cruz,