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Items 1 to 10 of about 1640
1. Angrisani A, Matrone N, Belli V, Vicidomini R, Di Maio N, Turano M, Scialò F, Netti PA, Porcellini A, Furia M: A functional connection between dyskerin and energy metabolism. Redox Biol; 2018 Apr;14:557-565

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A functional connection between dyskerin and energy metabolism.
  • The human DKC1 gene encodes dyskerin, an evolutionarily conserved nuclear protein whose overexpression represents a common trait of many types of aggressive sporadic cancers.
  • As a crucial component of the nuclear H/ACA snoRNP complexes, dyskerin is involved in a variety of essential processes, including telomere maintenance, splicing efficiency, ribosome biogenesis, snoRNAs stabilization and stress response.
  • Although multiple minor dyskerin splicing isoforms have been identified, their functions remain to be defined.
  • Considering that low-abundance splice variants could contribute to the wide functional repertoire attributed to dyskerin, possibly having more specialized tasks or playing significant roles in changing cell status, we investigated in more detail the biological roles of a truncated dyskerin isoform that lacks the C-terminal nuclear localization signal and shows a prevalent cytoplasmic localization.
  • Here we show that this dyskerin variant can boost energy metabolism and improve respiration, ultimately conferring a ROS adaptive response and a growth advantage to cells.
  • These results reveal an unexpected involvement of DKC1 in energy metabolism, highlighting a previously underscored role in the regulation of metabolic cell homeostasis.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
  • [Cites] Cell Death Dis. 2015 Mar 26;6:e1705 [25811802.001]
  • [Cites] J Biol Chem. 2005 Aug 5;280(31):28775-84 [15941719.001]
  • [Cites] Curr Biol. 2012 Jan 24;22(2):135-41 [22226745.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19494-9 [18042710.001]
  • [Cites] Br J Cancer. 2009 Oct 20;101(8):1410-6 [19755982.001]
  • [Cites] Sci Rep. 2017 Mar 23;7(1):347 [28337032.001]
  • [Cites] Mol Cell Biochem. 2014 Feb;387(1-2):261-70 [24234423.001]
  • [Cites] Mol Biol Cell. 2001 Aug;12(8):2245-56 [11514614.001]
  • [Cites] Cancer Biol Ther. 2004 Jan;3(1):110-20 [14726712.001]
  • [Cites] Free Radic Biol Med. 2012 Aug 1;53(3):447-56 [22634055.001]
  • [Cites] FEBS J. 2017 Jan;284(2):196-210 [27283924.001]
  • [Cites] Cell Cycle. 2015;14(18):2949-58 [26259964.001]
  • [Cites] Biomed Res Int. 2015;2015:206849 [26060813.001]
  • [Cites] Biochem Cell Biol. 2013 Dec;91(6):506-12 [24219293.001]
  • [Cites] Curr Protoc Cytom. 2001 May;Chapter 7:Unit 7.5 [18770732.001]
  • [Cites] Nat Genet. 1998 May;19(1):32-8 [9590285.001]
  • [Cites] Oncogene. 2013 Feb 7;32(6):724-35 [22430214.001]
  • [Cites] Trends Cell Biol. 2015 May;25(5):265-75 [25542066.001]
  • [Cites] Lipids. 2017 Mar;52(3):189-205 [28205069.001]
  • [Cites] Cell Oncol. 2008;30(6):483-90 [18936525.001]
  • [Cites] Curr Pharm Des. 2014;20(41):6386-403 [24975608.001]
  • [Cites] Mol Cells. 2016 Jan;39(1):1-5 [26831451.001]
  • [Cites] Curr Biol. 2008 Jan 22;18(2):102-8 [18207745.001]
  • [Cites] Clin Cancer Res. 2007 Aug 15;13(16):4695-703 [17652624.001]
  • [Cites] J Cell Biol. 2009 Dec 28;187(7):959-66 [20038677.001]
  • [Cites] J Pathol. 2006 Sep;210(1):10-8 [16841302.001]
  • [Cites] J Biol Chem. 2011 Mar 11;286(10):8394-404 [21148313.001]
  • [Cites] Biol Chem. 2014 Jun;395(6):593-610 [24468621.001]
  • [Cites] Transl Oncol. 2013 Aug 01;6(4):447-57 [23908688.001]
  • [Cites] Trends Endocrinol Metab. 2016 Feb;27(2):105-17 [26754340.001]
  • [Cites] Free Radic Biol Med. 2015 Mar;80:183-90 [25452140.001]
  • [Cites] Mol Biol Cell. 2003 Nov;14 (11):4376-86 [12960427.001]
  • [Cites] J Cell Sci. 2012 Nov 1;125(Pt 21):4963-71 [23277535.001]
  • [Cites] Biophys J. 2002 May;82(5):2811-25 [11964266.001]
  • [Cites] J Clin Invest. 2006 Dec;116(12 ):3171-82 [17111047.001]
  • [Cites] J Exp Biol. 2017 Apr 1;220(Pt 7):1170-1180 [28356365.001]
  • [Cites] PLoS One. 2012;7(8):e43147 [22912812.001]
  • [Cites] J Cell Biol. 2009 Dec 28;187(7):1023-36 [20038678.001]
  • [Cites] FASEB J. 2000 Apr;14(5):729-39 [10744629.001]
  • [Cites] Nucleic Acids Res. 2012 Aug;40(15):e115 [22730293.001]
  • [Cites] Cancer Genet. 2011 Dec;204(12):635-45 [22285015.001]
  • [Cites] J Cell Biol. 2006 Dec 4;175(5):779-89 [17145963.001]
  • [Cites] Br J Cancer. 2016 Jun 14;114(12 ):1305-12 [27219018.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2011;2011:480-6 [22160078.001]
  • [Cites] Proc Natl Acad Sci U S A. 2014 Jun 17;111(24):E2501-9 [24889636.001]
  • [Cites] Nature. 2014 Nov 6;515(7525):143-6 [25192136.001]
  • [Cites] Sci Transl Med. 2016 Jun 8;8(342):342ra78 [27280685.001]
  • [Cites] Cell Death Dis. 2016 Jun 02;7(6):e2249 [27253413.001]
  • [Cites] Arch Biochem Biophys. 1993 Jun;303(2):474-82 [8390225.001]
  • [Cites] Endocr J. 2015;62(7):633-44 [25994039.001]
  • [Cites] Mol Cells. 2016 Jan;39(1):65-71 [26813662.001]
  • [Cites] Acta Oncol. 2008;47(8):1598-9 [18607840.001]
  • [Cites] Int J Mol Med. 2010 Mar;25(3):321-9 [20127035.001]
  • [Cites] Biochim Biophys Acta. 2011 Jun;1813(6):1144-52 [21406203.001]
  • [Cites] Eur J Hum Genet. 2015 Apr;23(4):null [25182133.001]
  • [Cites] FEBS J. 2010 Aug;277(15):3249-63 [20608977.001]
  • [Cites] Biochim Biophys Acta. 2011 Dec;1810(12):1361-8 [21820037.001]
  • [Cites] Science. 2007 Mar 30;315(5820):1850-3 [17395830.001]
  • [Cites] J Biol Chem. 2003 Mar 7;278(10):8516-25 [12496265.001]
  • [Cites] Biochim Biophys Acta. 1985 Sep 6;841(3):237-46 [4027266.001]
  • (PMID = 29132127.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; DKC1 / Energy metabolism / Mitochondria / PRDX-2 / ROS signaling
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2. Kumar MR, Farmer PJ: Chemical trapping and characterization of small oxoacids of sulfur (SOS) generated in aqueous oxidations of H<sub>2</sub>S. Redox Biol; 2018 Apr;14:485-491

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemical trapping and characterization of small oxoacids of sulfur (SOS) generated in aqueous oxidations of H<sub>2</sub>S.
  • Small oxoacids of sulfur (SOS) are elusive molecules like sulfenic acid, HSOH, and sulfinic acid, HS(O)OH, generated during the oxidation of hydrogen sulfide, H<sub>2</sub>S, in aqueous solution.
  • Unlike their alkyl homologs, there is a little data on their generation and speciation during H<sub>2</sub>S oxidation.
  • These SOS may exhibit both nucleophilic and electrophilic reactivity, which we attribute to interconversion between S(II) and S(IV) tautomers.
  • We find that SOS may be trapped in situ by derivatization with nucleophilic and electrophilic trapping agents and then characterized by high resolution LC MS.
  • In this report, we compare SOS formation from H<sub>2</sub>S oxidation by a variety of biologically relevant oxidants.
  • These SOS appear relatively long lived in aqueous solution, and thus may be involved in the observed physiological effects of H<sub>2</sub>S.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
  • [Cites] FASEB J. 2005 Jul;19(9):1196-8 [15863703.001]
  • [Cites] Biochim Biophys Acta. 2005 Dec 10;1718(1-2):67-73 [16298331.001]
  • [Cites] Eur J Pharmacol. 2010 Oct 25;645(1-3):143-50 [20674563.001]
  • [Cites] Eur J Pharmacol. 2011 Nov 16;670(1):1-6 [21925165.001]
  • [Cites] Arch Biochem Biophys. 2007 Nov 15;467(2):291-6 [17923104.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Aug 28;237(3):527-31 [9299397.001]
  • [Cites] Chemistry. 2003 Nov 21;9(22):5501-10 [14639633.001]
  • [Cites] Front Biosci (Elite Ed). 2011 Jan 01;3:736-49 [21196347.001]
  • [Cites] Proc Natl Acad Sci U S A. 2017 Jan 31;114(5):864-869 [28096368.001]
  • [Cites] Physiol Rev. 2012 Apr;92(2):791-896 [22535897.001]
  • [Cites] Redox Biol. 2017 Aug;12 :325-339 [28285261.001]
  • [Cites] Eur J Pharmacol. 2009 Jan 5;602(1):117-23 [19049805.001]
  • [Cites] Chem Res Toxicol. 2010 Oct 18;23(10):1541-3 [20845929.001]
  • [Cites] Arch Biochem Biophys. 2017 Mar 1;617:9-25 [27697462.001]
  • [Cites] Mass Spectrom Rev. 2014 Mar-Apr;33(2):126-46 [24105931.001]
  • [Cites] Br J Pharmacol. 2002 Sep;137(2):139-45 [12208769.001]
  • [Cites] J Mol Spectrosc. 1996 Dec;180(2):197-206 [8979977.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Jul 6;358(3):879-84 [17502109.001]
  • [Cites] Oxid Med Cell Longev. 2016;2016:8961951 [26839635.001]
  • [Cites] Proc Natl Acad Sci U S A. 2017 Apr 18;114(16):E3215-E3223 [28373574.001]
  • [Cites] J Phys Chem A. 2013 May 2;117(17):3608-13 [23534485.001]
  • [Cites] Life Sci. 2014 Mar 11;98(2):63-7 [24412383.001]
  • [Cites] J Phys Chem A. 2015 Apr 9;119(14):3500-17 [25763808.001]
  • [Cites] Chem Res Toxicol. 2012 Apr 16;25(4):769-93 [22263838.001]
  • [Cites] Environ Toxicol. 2012 Mar;27(3):175-84 [20607818.001]
  • [Cites] Nat Rev Drug Discov. 2007 Nov;6(11):917-35 [17948022.001]
  • [Cites] J Phys Chem A. 2012 Aug 2;116(30):8031-9 [22724673.001]
  • [Cites] J Am Chem Soc. 2016 Jul 13;138(27):8476-88 [27310035.001]
  • [Cites] ACS Chem Biol. 2017 Feb 17;12 (2):474-478 [27984696.001]
  • [Cites] Arch Biochem Biophys. 2005 Oct 15;442(2):187-95 [16168948.001]
  • [Cites] J Pharmacol Exp Ther. 2006 Jan;316(1):325-35 [16192316.001]
  • [Cites] Circulation. 2013 Jun 25;127(25):2472-4 [23704250.001]
  • [Cites] Biochim Biophys Acta. 2014 Feb;1840(2):847-75 [23748139.001]
  • [Cites] Redox Biol. 2017 Aug;12 :528-529 [28363163.001]
  • [Cites] Proc Natl Acad Sci U S A. 2014 May 27;111(21):7606-11 [24733942.001]
  • [Cites] Circulation. 2013 Jun 25;127(25):2523-34 [23704252.001]
  • [Cites] Free Radic Biol Med. 2014 Dec;77:82-94 [25229186.001]
  • [Cites] Inflamm Allergy Drug Targets. 2011 Apr;10(2):118-22 [21275899.001]
  • [Cites] EMBO J. 2001 Nov 1;20(21):6008-16 [11689441.001]
  • [Cites] Br J Pharmacol. 2010 Jun;160(4):941-57 [20590590.001]
  • (PMID = 29096321.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; And bromobimane / Dimedone / Hydrogen sulfide / Sulfenic acid / Sulfinic acid
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3. Henderson D, Huebner C, Markowitz M, Taube N, Harvanek ZM, Jakob U, Knoefler D: Do developmental temperatures affect redox level and lifespan in C. elegans through upregulation of peroxiredoxin? Redox Biol; 2018 Apr;14:386-390

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Do developmental temperatures affect redox level and lifespan in C. elegans through upregulation of peroxiredoxin?
  • Lifespan in poikilothermic organisms, such as Caenorhabditis elegans, can be substantially increased simply by decreasing growth temperature.
  • To gain insights into the mechanistic underpinnings of this effect, we investigated the effects of temperature in development and adulthood on C. elegans lifespan.
  • We found that worms exposed to 25°C during development and shifted to 15°C in adulthood exhibited an even longer lifespan than animals constantly kept at 15°C.
  • Analysis of the in vivo redox status demonstrated that at 25°C, C. elegans larvae have a more reduced redox state and higher Prdx-2 expression levels than animals raised at 15°C.
  • Worms lacking prdx-2 fail to show the additional lifespan extension upon shift from 25°C to 15°C and reveal a lifespan similar to prdx-2 worms always kept at 15°C.
  • These results suggest that transiently altering the in vivo redox state during development can have highly beneficial long-term consequences for organisms.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
  • [Cites] J Gerontol. 1956 Jul;11(3):298-300 [13332224.001]
  • [Cites] Cell Rep. 2015 Jun 9;11(9):1414-24 [26027928.001]
  • [Cites] Nat Methods. 2006 Apr;3(4):281-6 [16554833.001]
  • [Cites] PLoS Biol. 2007 Oct 2;5(10):e259 [17914900.001]
  • [Cites] Antioxid Redox Signal. 2011 Mar 15;14(6):1023-37 [20649472.001]
  • [Cites] Antioxid Redox Signal. 2013 Sep 10;19(8):779-87 [23841595.001]
  • [Cites] Mech Ageing Dev. 1977 Nov-Dec;6(6):413-29 [926867.001]
  • [Cites] Free Radic Biol Med. 2012 Mar 1;52(5):850-9 [22226831.001]
  • [Cites] Nat Methods. 2008 Jun;5(6):553-9 [18469822.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11399-403 [10500188.001]
  • [Cites] J Exp Biol. 2016 Apr 15;219(Pt 8):1090-2 [27103672.001]
  • [Cites] Mech Ageing Dev. 2011 Oct;132(10):519-21 [21893079.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19839-44 [19064914.001]
  • [Cites] Biotechnol Bioeng. 2003 Sep 30;83(7):772-9 [12889017.001]
  • [Cites] Mol Cell. 2012 Sep 14;47(5):767-76 [22819323.001]
  • [Cites] Science. 2002 Dec 20;298(5602):2398-401 [12471266.001]
  • [Cites] Antioxid Redox Signal. 2016 May 1;24(13):731-51 [26607375.001]
  • (PMID = 29055282.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Grant] United States / NIH HHS / OD / P40 OD010440; United States / NIA NIH HHS / AG / R01 AG027349; United States / NIGMS NIH HHS / GM / R35 GM122506
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Aging / C. elegans / Oxidants / Peroxiredoxin / Temperature
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4. Huang Y, Feng F, Chen ZG, Wu T, Wang ZH: Green and efficient removal of cadmium from rice flour using natural deep eutectic solvents. Food Chem; 2018 Apr 01;244:260-265

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Green and efficient removal of cadmium from rice flour using natural deep eutectic solvents.
  • Natural deep eutectic solvents (NADESs) constitute a novel class of biodegradable and inexpensive solvents.
  • In this study, twenty choline chloride- and glycerol-based NADESs were prepared and investigated as washing agents in the removal of cadmium (Cd) from rice flour for the first time.
  • Choline chloride-based NADESs demonstrated good Cd removal (51%-96%).
  • A natural, biodegradable surfactant, saponin, was mixed with the NADESs to enhance their efficiency.
  • No increase in Cd removal was observed when glycerol-based NADESs were combined with 1% saponin; however, synergistic effects between saponin and choline chloride-based NADESs were observed during the washing process and >99% Cd was removed using NADES-saponin mixtures.
  • Moreover, NADESs washing process did not affect the main chemical components or structure of rice flour.
  • The mechanism of Cd removal by NADESs and regeneration of Cd-contaminated NADESs were also explored.
  • The study presents a green and efficient way of removing Cd from contaminated rice.

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  • [Copyright] Copyright © 2017 Elsevier Ltd. All rights reserved.
  • (PMID = 29120780.001).
  • [ISSN] 0308-8146
  • [Journal-full-title] Food chemistry
  • [ISO-abbreviation] Food Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Keywords] NOTNLM ; Cadmium / Natural deep eutectic solvents / Removal / Rice flour
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5. Han SJ, Choi HS, Kim JI, Park JW, Park KM: IDH2 deficiency increases the liver susceptibility to ischemia-reperfusion injury via increased mitochondrial oxidative injury. Redox Biol; 2018 Apr;14:142-153
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IDH2 deficiency increases the liver susceptibility to ischemia-reperfusion injury via increased mitochondrial oxidative injury.
  • Mitochondrial NADP<sup>+</sup>-dependent isocitrate dehydrogenase 2 (IDH2) is a major producer of mitochondrial NADPH, required for glutathione (GSH)-associated mitochondrial antioxidant systems including glutathione peroxidase (GPx) and glutathione reductase (GR).
  • Here, we investigated the role of IDH2 in hepatic ischemia-reperfusion (HIR)-associated mitochondrial injury using Idh2-knockout (Idh2<sup>-/-</sup>) mice and wild-type (Idh2<sup>+/+</sup>) littermates.
  • Mice were subjected to either 60min of partial liver ischemia or sham-operation.
  • Some mice were administered with 2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride (mito-TEMPO, a mitochondria-targeting antioxidant).
  • HIR induced severe histological and functional damages of liver in both Idh2<sup>+/+</sup> mice and Idh2<sup>-/-</sup> mice and those damages were more severe in Idh2<sup>-/-</sup> mice than in wild-type littermates.
  • HIR induces dysfunction of IDH2, leading to the decreases of NADPH level and mitochondrial GR and GPx functions, consequently resulting in mitochondrial and cellular oxidative injury as reflected by mitochondrial cristae loss, mitochondrial fragmentation, shift in mitochondrial fission, cytochrome c release, and cell death.
  • These HIR-induced changes were greater in Idh2<sup>-/-</sup> mice than wild-type mice.
  • The mito-TEMPO supplement significantly attenuated the aforementioned changes, and these attenuations were much greater in Idh2<sup>-/-</sup> mice when compared with wild-type littermates.
  • Taken together, results have demonstrated that HIR impairs in the IDH2-NADPH-GSH mitochondrial antioxidant system, resulting in increased mitochondrial oxidative damage and dysfunction, suggesting that IDH2 plays a critical role in mitochondrial redox balance and HIR-induced impairment of IDH2 function is associated with the pathogenesis of ischemia-reperfusion-induced liver failure.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
  • [Cites] Biochim Biophys Acta. 2014 Feb;1842(2):135-43 [24240089.001]
  • [Cites] Circ Res. 2010 Jul 9;107(1):106-16 [20448215.001]
  • [Cites] Free Radic Res. 2013 Aug;47(8):555-68 [23738581.001]
  • [Cites] Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2009 Nov;25(11):1058-60 [20104683.001]
  • [Cites] Placenta. 1987 Mar-Apr;8(2):175-84 [3615376.001]
  • [Cites] Am J Physiol Renal Physiol. 2009 Aug;297(2):F461-70 [19458120.001]
  • [Cites] J Biol Chem. 2001 May 11;276(19):16168-76 [11278619.001]
  • [Cites] Nat Immunol. 2011 Mar;12 (3):222-30 [21151103.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Jul;82(14):4668-72 [3860816.001]
  • [Cites] Nat Med. 2011 Jan;17(1):71-8 [21186368.001]
  • [Cites] J Biol Chem. 2002 May 31;277(22):19396-401 [11904290.001]
  • [Cites] Sci Rep. 2017 Mar 07;7:43684 [28266555.001]
  • [Cites] Free Radic Res. 2005 Apr;39(4):441-8 [16028369.001]
  • [Cites] Dev Cell. 2001 Oct;1(4):515-25 [11703942.001]
  • [Cites] J Signal Transduct. 2012;2012:329635 [22175013.001]
  • [Cites] J Natl Cancer Inst. 2010 Jul 7;102(13):932-41 [20513808.001]
  • [Cites] Nephrol Dial Transplant. 2012 Oct;27(10):3762-70 [22555250.001]
  • [Cites] Lancet. 2008 Jan 5;371(9606):64-74 [18177777.001]
  • [Cites] Eur J Pharmacol. 2003 Mar 28;465(1-2):163-70 [12650846.001]
  • [Cites] J Surg Res. 2012 Jul;176(1):164-70 [22560539.001]
  • [Cites] Hepatology. 2017 Jun 23;:null [28646508.001]
  • [Cites] Free Radic Biol Med. 2012 Sep 1;53(5):1123-38 [22683818.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Dec 3;325(1):32-8 [15522197.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2015 Jul 15;309(2):G100-11 [26045616.001]
  • [Cites] Arch Biochem Biophys. 1981 Sep;210(2):505-16 [7305340.001]
  • [Cites] Antioxid Redox Signal. 2009 Nov;11(11):2685-700 [19558212.001]
  • [Cites] EMBO J. 2016 Feb 15;35(4):402-13 [26783364.001]
  • [Cites] Cell. 2010 Sep 17;142(6):889-901 [20850011.001]
  • [Cites] World J Gastroenterol. 2004 Jul 1;10(13):1934-8 [15222040.001]
  • [Cites] J Surg Res. 2003 May 15;111(2):240-7 [12850469.001]
  • [Cites] Methods Enzymol. 1978;52:302-10 [672633.001]
  • [Cites] Mol Pharmacol. 2006 Sep;70(3):1053-61 [16785314.001]
  • [Cites] Nephrol Dial Transplant. 2015 Sep;30(9):1497-506 [26142397.001]
  • [Cites] Biochimie. 2009 Aug;91(8):1020-8 [19500645.001]
  • [Cites] Methods Enzymol. 1981;77:373-82 [7329314.001]
  • [Cites] Transplant Proc. 2007 Jun;39(5):1332-7 [17580134.001]
  • [Cites] Curr Pathobiol Rep. 2013 Sep;1(3):null [24386614.001]
  • [Cites] Nat Protoc. 2007;2(2):287-95 [17406588.001]
  • [Cites] Toxicol Pathol. 2007 Jun;35(4):495-516 [17562483.001]
  • [Cites] J Am Soc Nephrol. 2017 Apr;28(4):1200-1215 [27821630.001]
  • [Cites] Methods Enzymol. 1985;113:548-55 [4088074.001]
  • [Cites] Gastroenterology. 2008 Oct;135(4):1344-57 [18778711.001]
  • [Cites] Antioxid Redox Signal. 2005 Jan-Feb;7(1-2):60-71 [15650396.001]
  • [Cites] Oxid Med Cell Longev. 2016;2016:2950503 [27313826.001]
  • [Cites] Acta Pharmacol Sin. 2017 May;38(5):672-687 [28216619.001]
  • (PMID = 28938192.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Apoptosis / IDH2 / Liver ischemia / Mitochondria / Oxidative stress
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6. Shi C, Cai Y, Li Y, Li Y, Hu N, Ma S, Hu S, Zhu P, Wang W, Zhou H: Yap promotes hepatocellular carcinoma metastasis and mobilization via governing cofilin/F-actin/lamellipodium axis by regulation of JNK/Bnip3/SERCA/CaMKII pathways. Redox Biol; 2018 Apr;14:59-71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Yap promotes hepatocellular carcinoma metastasis and mobilization via governing cofilin/F-actin/lamellipodium axis by regulation of JNK/Bnip3/SERCA/CaMKII pathways.
  • Despite the increasingly important role of Hippo-Yap in hepatocellular carcinoma (HCC) development and progression, little insight is available at the time regarding the specifics interaction of Yap and cancer cells migration.
  • Here, we identified the mechanism by which tumor-intrinsic Yap deletion resulted in HCC migratory inhibition.
  • Yap was greatly upregulated in HCC and its expression promoted the cells migration.
  • Functional studies found that knockdown of Yap induced JNK phosphorylation which closely bound to the Bnip3 promoter and contributed to Bnip3 expression.
  • Higher Bnip3 employed excessive mitophagy leading to mitochondrial dysfunction and ATP shortage.
  • The insufficient ATP inactivated SERCA and consequently triggered intracellular calcium overload.
  • As the consequence of calcium oscillation, Ca/calmodulin-dependent protein kinases II (CaMKII) was signaled and subsequently inhibited cofilin activity via phosphorylated modification.
  • The phosphorylated cofilin failed to manipulate F-actin polymerization and lamellipodium formation, resulting into the impairment of lamellipodium-based migration.
  • Collectively, our results identified Hippo-Yap as the tumor promoter in hepatocellular carcinoma that mediated via activation of cofilin/F-actin/lamellipodium axis by limiting JNK-Bnip3-SERCA-CaMKII pathways, with potential application to HCC therapy involving cancer metastasis.

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  • [Cites] Gastroenterology. 2017 Mar;152(4):745-761 [28043904.001]
  • [Cites] Gut. 2014 May;63(5):844-55 [24531850.001]
  • [Cites] J Pineal Res. 2016 Apr;60(3):277-90 [26732239.001]
  • [Cites] Redox Biol. 2016 Dec;10 :140-147 [27744119.001]
  • [Cites] Redox Biol. 2017 Aug;12 :833-842 [28448945.001]
  • [Cites] Clin Exp Pharmacol Physiol. 2014 Nov;41(11):940-6 [25283076.001]
  • [Cites] Cell Stress Chaperones. 2017 Jul 1;:null [28669047.001]
  • [Cites] JCI Insight. 2016 Apr 21;1(5):null [27218122.001]
  • [Cites] Curr Opin Cell Biol. 2016 Apr;39:43-52 [26896558.001]
  • [Cites] Gastroenterology. 2013 Dec;145(6):1215-29 [24140396.001]
  • [Cites] Curr Opin Cell Biol. 2015 Oct;36:23-31 [26186729.001]
  • [Cites] Mol Med Rep. 2015 Jun;11(6):4063-72 [25625935.001]
  • [Cites] Free Radic Biol Med. 2016 Jun;95:278-92 [27038735.001]
  • [Cites] Redox Biol. 2016 Aug;8:68-78 [26760912.001]
  • [Cites] J Physiol. 2017 Aug 15;595(16):5525-5544 [28627017.001]
  • [Cites] J Pineal Res. 2016 Oct;61(3):381-95 [27465521.001]
  • [Cites] J Pineal Res. 2016 Jan;60(1):55-64 [26462739.001]
  • [Cites] Nat Rev Clin Oncol. 2017 Jul 18;:null [28719584.001]
  • [Cites] Redox Biol. 2015;4:6-13 [25479550.001]
  • [Cites] Genes Cells. 2013 Jul;18(7):533-43 [23600483.001]
  • [Cites] Mol Cancer Ther. 2017 May;16(5):914-923 [28167504.001]
  • [Cites] Biotechnol J. 2008 Jun;3(6):765-80 [18512869.001]
  • [Cites] Redox Biol. 2016 Dec;10 :274-284 [27833040.001]
  • [Cites] Curr Opin Cell Biol. 2017 Oct;48:17-25 [28527754.001]
  • [Cites] Free Radic Biol Med. 2014 Dec;77:363-75 [25452142.001]
  • [Cites] Redox Biol. 2016 Dec;10 :148-156 [27744120.001]
  • [Cites] J Pineal Res. 2016 Oct;61(3):396-407 [27484637.001]
  • [Cites] Cell Mol Biol Lett. 2016 Sep 22;21:20 [28536622.001]
  • [Cites] Gastroenterology. 2017 Feb;152(3):616-630 [27864128.001]
  • [Cites] Cell. 2006 Jun 30;125(7):1253-67 [16814713.001]
  • [Cites] Genetics. 2016 Aug;203(4):1777-88 [27317679.001]
  • [Cites] Free Radic Biol Med. 2016 Dec;101:401-412 [27836781.001]
  • [Cites] Redox Biol. 2016 Aug;8:305-15 [26938939.001]
  • [Cites] Biochem Soc Trans. 2005 Dec;33(Pt 6):1260-4 [16246093.001]
  • [Cites] Elife. 2017 Mar 10;6:null [28282023.001]
  • [Cites] J Geriatr Cardiol. 2017 Jan;14 (1):57-66 [28270843.001]
  • [Cites] Sci Rep. 2015 Aug 07;5:12898 [26250571.001]
  • [Cites] J Pineal Res. 2016 May;60(4):383-93 [26882442.001]
  • [Cites] J Pineal Res. 2016 Mar;60(2):167-77 [26607298.001]
  • [Cites] EBioMedicine. 2017 Jul;21:94-103 [28679472.001]
  • [Cites] Redox Biol. 2017 Aug;12 :208-215 [28259101.001]
  • [Cites] Adv Exp Med Biol. 2013;986:103-19 [22879066.001]
  • [Cites] Redox Biol. 2016 Aug;8:24-7 [26722841.001]
  • [Cites] Postepy Hig Med Dosw (Online). 2017 May 5;71(0):339-351 [28513458.001]
  • [Cites] Cancer Res. 2016 Jul 1;76(13):3813-25 [27325643.001]
  • [Cites] Am J Clin Exp Urol. 2014 Apr 05;2(1):15-26 [25374905.001]
  • [Cites] Cell Adh Migr. 2013 Mar-Apr;7(2):199-213 [23302954.001]
  • [Cites] Curr Opin Cell Biol. 2014 Dec;31:74-83 [25259681.001]
  • [Cites] Redox Biol. 2016 Dec;10 :233-242 [27810738.001]
  • [Cites] Am J Med Sci. 2012 Dec;344(6):462-72 [22270398.001]
  • [Cites] Cancer. 2009 Oct 1;115(19):4576-85 [19551889.001]
  • [Cites] J Pineal Res. 2015 Sep;59(2):151-62 [25958928.001]
  • [Cites] Redox Biol. 2017 Oct;13:498-507 [28732308.001]
  • [Cites] J Pineal Res. 2016 Apr;60(3):313-26 [26797926.001]
  • [Cites] J Am Heart Assoc. 2017 Mar 13;6(3):null [28288978.001]
  • [Cites] J Pineal Res. 2016 Nov;61(4):479-492 [27600920.001]
  • [Cites] J Pineal Res. 2017 Aug;63(1):null [28398674.001]
  • [Cites] Hum Pathol. 2008 Nov;39(11):1582-9 [18703216.001]
  • [Cites] Ann Intern Med. 2014 Aug 19;161(4):261-9 [24934699.001]
  • [Cites] Cancer Cell. 2014 Feb 10;25(2):166-80 [24525233.001]
  • [Cites] Redox Biol. 2016 Aug;8:136-48 [26774751.001]
  • [Cites] Int J Mol Sci. 2016 Dec 22;18(1): [28025492.001]
  • [Cites] J Pineal Res. 2016 Apr;60(3):291-302 [26732476.001]
  • [Cites] Redox Biol. 2016 Oct;9:306-319 [27693992.001]
  • [Cites] Genes Dev. 2007 Nov 1;21(21):2747-61 [17974916.001]
  • [Cites] J Neurochem. 2013 Jun;125(6):885-96 [23550835.001]
  • (PMID = 28869833.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Bnip3 / CaMKII / Cofilin / F-actin / JNK / Lamellipodium / Migration / SERCA / Yap
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7. Heppner DE, Hristova M, Ida T, Mijuskovic A, Dustin CM, Bogdándi V, Fukuto JM, Dick TP, Nagy P, Li J, Akaike T, van der Vliet A: Cysteine perthiosulfenic acid (Cys-SSOH): A novel intermediate in thiol-based redox signaling? Redox Biol; 2018 Apr;14:379-385
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cysteine perthiosulfenic acid (Cys-SSOH): A novel intermediate in thiol-based redox signaling?
  • The reversible oxidation of protein cysteine residues (Cys-SH) is a key reaction in cellular redox signaling involving initial formation of sulfenic acids (Cys-SOH), which are commonly detected using selective dimedone-based probes.
  • Here, we report that significant portions of dimedone-tagged proteins are susceptible to cleavage by DTT reflecting the presence of perthiosulfenic acid species (Cys-SSOH) due to similar oxidation of hydropersulfides (Cys-SSH), since Cys-S-dimedone adducts are stable toward DTT.
  • Combined studies using molecular modeling, mass spectrometry, and cell-based experiments indicate that Cys-SSH are readily oxidized to Cys-SSOH, which forms stable adducts with dimedone-based probes.
  • We additionally confirm the presence of Cys-SSH within protein tyrosine kinases such as EGFR, and their apparent oxidation to Cys-SSOH in response NADPH oxidase activation, suggesting that such Cys-SSH oxidation may represent a novel, as yet uncharacterized, event in redox-based signaling.

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  • [Copyright] Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.
  • [Cites] Free Radic Biol Med. 2016 Dec;101:93-101 [27720842.001]
  • [Cites] Methods Enzymol. 2010;473:95-115 [20513473.001]
  • [Cites] J Chem Theory Comput. 2007 Nov;3(6):2011-33 [26636198.001]
  • [Cites] Nat Chem Biol. 2012 Aug;8(8):714-24 [22772154.001]
  • [Cites] Phys Rev Lett. 1996 Oct 28;77(18):3865-3868 [10062328.001]
  • [Cites] Amino Acids. 2011 Jun;41(1):113-21 [20191298.001]
  • [Cites] Cell Chem Biol. 2016 Jul 21;23 (7):837-48 [27427230.001]
  • [Cites] Biochemistry. 1999 Nov 23;38(47):15407-16 [10569923.001]
  • [Cites] J Cell Sci. 2012 Dec 15;125(Pt 24):6185-97 [23097045.001]
  • [Cites] J Biol Chem. 2015 Nov 6;290(45):26866-80 [26269587.001]
  • [Cites] Arch Biochem Biophys. 2017 Mar 1;617:26-37 [27693037.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2004;44:325-47 [14744249.001]
  • [Cites] Nat Commun. 2014 Sep 01;5:4776 [25175731.001]
  • [Cites] J Biol Chem. 2016 Oct 28;291(44):23282-23293 [27650496.001]
  • [Cites] Physiol Rev. 2012 Apr;92(2):791-896 [22535897.001]
  • [Cites] Anal Biochem. 2011 Jun 1;413(1):1-7 [21303647.001]
  • [Cites] FEBS J. 2013 Dec;280(23):6150-61 [24103186.001]
  • [Cites] Arch Biochem Biophys. 2017 Feb 15;616:40-46 [28126370.001]
  • [Cites] Chem Sci. 2016 Jan 1;7(1):400-415 [26819701.001]
  • [Cites] Biochem Pharmacol. 2013 Mar 1;85(5):689-703 [23103569.001]
  • [Cites] Antioxid Redox Signal. 2012 Apr 15;16(8):747-53 [22149235.001]
  • [Cites] ACS Chem Biol. 2009 Sep 18;4(9):783-99 [19645509.001]
  • [Cites] J Chem Theory Comput. 2007 Nov;3(6):2046-54 [26636200.001]
  • [Cites] Methods Enzymol. 2010;473:77-94 [20513472.001]
  • [Cites] JCI Insight. 2016 Nov 3;1(18):e88811 [27812543.001]
  • [Cites] J Am Chem Soc. 2017 Apr 19;139(15):5588-5595 [28355876.001]
  • [Cites] Redox Biol. 2014 Jan 15;2:436-46 [24624333.001]
  • [Cites] J Am Chem Soc. 2014 Jul 30;136(30):10573-6 [25010540.001]
  • [Cites] J Chem Phys. 2006 Nov 21;125(19):194101 [17129083.001]
  • [Cites] Nat Rev Mol Cell Biol. 2012 Jul 11;13(8):499-507 [22781905.001]
  • [Cites] Redox Biol. 2016 Aug;8:24-7 [26722841.001]
  • [Cites] Chem Rev. 2013 Jul 10;113(7):4633-79 [23514336.001]
  • [Cites] PLoS One. 2013;8(1):e54391 [23349873.001]
  • [Cites] Science. 2005 May 27;308(5726):1318-21 [15919995.001]
  • [Cites] Proc Natl Acad Sci U S A. 2014 Aug 5;111(31):11545-50 [25049418.001]
  • [Cites] J Allergy Clin Immunol. 2016 May;137(5):1545-1556.e11 [26597162.001]
  • [Cites] Sci Adv. 2016 Jan 22;2(1):e1500968 [26844296.001]
  • [Cites] Nat Chem Biol. 2011 Dec 11;8(1):57-64 [22158416.001]
  • [Cites] Biochim Biophys Acta. 2014 Feb;1840(2):847-75 [23748139.001]
  • [Cites] Proc Natl Acad Sci U S A. 2014 May 27;111(21):7606-11 [24733942.001]
  • [Cites] Thorax. 2017 Jul 19;:null [28724639.001]
  • [Cites] Bioconjug Chem. 2016 May 18;27(5):1411-8 [27123991.001]
  • [Cites] Free Radic Biol Med. 2016 Dec;101:20-31 [27677567.001]
  • [Cites] Free Radic Biol Med. 2014 Dec;77:82-94 [25229186.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):12022-7 [9751783.001]
  • [Cites] Nat Rev Mol Cell Biol. 2014 Jun;15(6):411-21 [24854789.001]
  • [Cites] Biochemistry. 2012 Dec 18;51(50):9954-65 [23186290.001]
  • (PMID = 29054072.001).
  • [ISSN] 2213-2317
  • [Journal-full-title] Redox biology
  • [ISO-abbreviation] Redox Biol
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / F32 HL129706; United States / NIEHS NIH HHS / ES / R01 ES021476; United States / NHLBI NIH HHS / HL / R01 HL085646
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Dimedone / Hydrogen peroxide / NADPH oxidase / Redox signaling / Sulfenic acid / Thiol oxidation
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8. Baca-Bocanegra B, Nogales-Bueno J, Hernández-Hierro JM, Heredia FJ: Evaluation of extractable polyphenols released to wine from cooperage byproduct by near infrared hyperspectral imaging. Food Chem; 2018 Apr 01;244:206-212
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of extractable polyphenols released to wine from cooperage byproduct by near infrared hyperspectral imaging.
  • Extractable total phenolic content of American non-toasted oak (Quercus alba L.) shavings has been determined using near infrared hyperspectral imaging.
  • A like-wine model solution was used for the simulated maceration procedure.
  • Calibrations were performed by partial least squares regression (MPLS) using a number of spectral pre-treatments.
  • The coefficient of determination of wood for extractable total phenolic content was 0.89, and the standard error of prediction was 6.3 mg g<sup>-1</sup>.
  • Thus, near infrared hyperspectral imaging arises as an attractive strategy for predicting extractable total phenolic content in the range of 0-65 mg g<sup>-1</sup>, of great relevance from the point of view of quality assurance regarding wood used in the wine sector.
  • Near infrared hyperspectral imaging arises as an attractive strategy for the feasibility of enhancing the value of cooperage byproduct through the fast determination of extractable bioactive molecules, such as polyphenols.

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  • (PMID = 29120772.001).
  • [ISSN] 0308-8146
  • [Journal-full-title] Food chemistry
  • [ISO-abbreviation] Food Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Keywords] NOTNLM ; Byproduct / Near infrared hyperspectral imaging / Oak / Phenolic compounds
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9. Reddy CK, Choi SM, Lee DJ, Lim ST: Complex formation between starch and stearic acid: Effect of enzymatic debranching for starch. Food Chem; 2018 Apr 01;244:136-142

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex formation between starch and stearic acid: Effect of enzymatic debranching for starch.
  • Effect of debranching for a high-amylose starch (∼70% amylose) on its V-complex formation with stearic acid was examined.
  • Gel-permeation chromatograms showed that amylopectin was degraded to smaller molecules as the debranching time increased from 6 to 24 h.
  • Increased formation of debranched starch/stearic acid complexes (recovery yield of stearic acid from 45.17 to 89.31% and starch from 39.92 to 55.43%) was observed with increased debranching time (from 6 to 24 h) and complexation time (from 6 to 24 h).
  • The X-ray diffraction patterns of the debranched starch/stearic acid complexes displayed a mixture of B-type and V-type patterns, with 2θ peaks at 7.6°, 13.1°, 17.2°, 20°, 21.6°, and 23.4°.
  • The melting temperature and enthalpy changes of the debranched starch/stearic acid complexes were gradually enhanced with increasing debranching time.
  • These results suggest that starch can be modified by debranching to produce a significant amount of debranched starch/stearic acid complexes.

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  • [Copyright] Copyright © 2017 Elsevier Ltd. All rights reserved.
  • (PMID = 29120761.001).
  • [ISSN] 0308-8146
  • [Journal-full-title] Food chemistry
  • [ISO-abbreviation] Food Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Keywords] NOTNLM ; High-amylose maize starch / Stearic acid / Thermal properties / V-complex / X-ray diffraction
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10. Pelvan E, Olgun EÖ, Karadağ A, Alasalvar C: Phenolic profiles and antioxidant activity of Turkish Tombul hazelnut samples (natural, roasted, and roasted hazelnut skin). Food Chem; 2018 Apr 01;244:102-108

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phenolic profiles and antioxidant activity of Turkish Tombul hazelnut samples (natural, roasted, and roasted hazelnut skin).
  • The phenolic profiles and antioxidant status of hazelnut samples [natural (raw) hazelnut, roasted hazelnut, and roasted hazelnut skin] were compared.
  • Free and bound (ester-linked and glycoside-linked) phenolic acids were examined using liquid chromatography-tandem mass spectrometry (LC-MS/MS).
  • Comprehensive identification of phenolics was carried out using Q-exactive hybrid quadrupole-orbitrap mass spectrometer (Q-OT-MS).
  • Samples were also assessed for their total phenolics and antioxidant activities using three different assays.
  • Ten free and bound phenolic acids were quantified in hazelnut samples.
  • Roasted hazelnut skin contained the highest content of total phenolic acids, followed by natural and roasted hazelnuts.
  • The majority of phenolic acids were present in the bound form.
  • Using a Q-OT-MS, 22 compounds were tentatively identified, 16 of which were identified for the first time in hazelnut samples.
  • The newly identified compounds consisted of flavonoids, phenolic acids and related compounds, hydrolysable tannins and related compounds, and other phenolics.
  • Three antioxidant assays demonstrated similar trends that roasted hazelnut skin rendered the highest activity.
  • The present work suggests that roasted hazelnut skin is a rich source of phenolics and can be considered as a value-added co-product for use as functional food ingredient and antioxidant.

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  • [Copyright] Copyright © 2017 Elsevier Ltd. All rights reserved.
  • (PMID = 29120757.001).
  • [ISSN] 0308-8146
  • [Journal-full-title] Food chemistry
  • [ISO-abbreviation] Food Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Keywords] NOTNLM ; Antioxidant activity / Natural hazelnut / Phenolic acids / Phenolics / Roasted hazelnut / Roasted hazelnut skin
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