Oxidative Medicine and Cellular Longevity Antioxidants in Longevity and Medicine Guest Editors: Nilanjana Maulik, David Mcfadden, Hajime Otani, Mahesh Thirunavukkarasu, and Narasimham L. Parinandi Antioxidants in Longevity and Medicine Oxidative Medicine and Cellular Longevity Antioxidants in Longevity and Medicine Guest Editors: Nilanjana Maulik, David Mcfadden, Hajime Otani, Mahesh Thirunavukkarasu, and Narasimham L. Parinandi Copyright©2013HindawiPublishingCorporation.Allrightsreserved. Thisisaspecialissuepublishedin“OxidativeMedicineandCellularLongevity.”Allarticlesareopenaccessarticlesdistributedunderthe CreativeCommonsAttributionLicense,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedthe originalworkisproperlycited. Editorial Board MohammadAbdollahi,Iran GilesE.Hardingham,UK PranelaRameshwar,USA AntonioAyala,Spain MichaelR.Hoane,USA SidharthaD.Ray,USA PeterBackx,Canada VladimirJakovljevic,Serbia FranciscoJavierRomero,Spain ConsueloBorras,Spain RaoufA.Khalil,USA GabrieleSaretzki,UK ElisaCabiscol,Spain NeelamKhaper,Canada HonglianShi,USA VittorioCalabrese,Italy MikeKingsley,UK CinziaSignorini,Italy Shao-yuChen,USA EugeneA.Kiyatkin,USA RichardSiow,UK ZhaoZ.Chong,USA RonKohen,Israel OrenTirosh,Israel FelipeDal-Pizzol,Brazil Jean-ClaudeLavoie,Canada MadiaTrujillo,Uruguay OzcanErel,Turkey ChristopherH.Lillig,Germany JeannetteVasquez-Vivar,USA ErsinFadillioglu,Turkey KennethMaiese,USA VictorM.Victor,Spain QingpingFeng,Canada BrunoMeloni,Australia MichalWozniak,Poland SwaranJ.S.Flora,India LuisaMinghetti,Italy Sho-ichiYamagishi,Japan JanuszGebicki,Australia RyuichiMorishita,Japan Liang-JunYan,USA HusamGhanim,USA D.Pietraforte,Italy JingYi,China DanielaGiustarini,Italy AurelPopa-Wagner,Germany GuillermoZalba,Spain HunjooHa,RepublicofKorea Jose´L.Quiles,Spain Contents AntioxidantsinLongevityandMedicine,NilanjanaMaulik,DavidMcfadden,HajimeOtani, MaheshThirunavukkarasu,andNarasimhamL.Parinandi Volume2013,ArticleID820679,3pages Erratumto“Site-SpecificAntioxidativeTherapyforPreventionofAtherosclerosisandCardiovascular Disease”,HajimeOtani Volume2013,ArticleID936436,1page BrazilianGreenPropolisSuppressestheHypoxia-InducedNeuroinflammatoryResponsesbyInhibiting NF-𝜅BActivationinMicroglia,ZhouWu,AiqinZhu,FumikoTakayama,RyoOkada,YicongLiu, YukaHarada,ShizhengWu,andHiroshiNakanishi Volume2013,ArticleID906726,10pages GrapePolyphenolsIncreasetheActivityofHDLEnzymesinOldandObeseRats,AndriyL.Zagayko, GannaB.Kravchenko,OksanaA.Krasilnikova,andYuriO.Ogai Volume2013,ArticleID593761,7pages ResveratrolPreventsDendriticCellMaturationinResponsetoAdvancedGlycationEndProducts, BrigittaButtari,ElisabettaProfumo,FrancescoFacchiano,ElifInciOzturk,LucaSegoni,LucianoSaso, andRacheleRigano` Volume2013,ArticleID574029,12pages EffectofTaiChiversusWalkingonOxidativeStressinMexicanOlderAdults,JuanaRosado-Pe´rez, Roc´ıoOrtiz,EdelmiroSantiago-Osorio,andV´ıctorManuelMendoza-Nu´n˜ez Volume2013,ArticleID298590,8pages Age-RelatedHearingLossinMn-SODHeterozygousKnockoutMice,MakotoKinoshita, TakashiSakamoto,AkinoriKashio,TakahikoShimizu,andTatsuyaYamasoba Volume2013,ArticleID325702,12pages ChrononutritionagainstOxidativeStressinAging,M.Garrido,M.P.Terro´n,andA.B.Rodr´ıguez Volume2013,ArticleID729804,9pages EfficacyofFishOilonSerumofTNF𝛼,IL-1𝛽,andIL-6OxidativeStressMarkersinMultipleSclerosis TreatedwithInterferonBeta-1b,V.Ramirez-Ramirez,M.A.Macias-Islas,G.G.Ortiz,F.Pacheco-Moises, E.D.Torres-Sanchez,T.E.Sorto-Gomez,J.A.Cruz-Ramos,G.Orozco-Avin˜a,andA.J.CelisdelaRosa Volume2013,ArticleID709493,8pages NaturalAntioxidantActivityofCommonlyConsumedPlantFoodsinIndia:EffectofDomestic Processing,D.Sreeramulu,C.V.K.Reddy,AnithaChauhan,N.Balakrishna,andM.Raghunath Volume2013,ArticleID369479,12pages Polyphenols:MultipotentTherapeuticAgentsinNeurodegenerativeDiseases,KhushwantS.Bhullarand H.P.VasanthaRupasinghe Volume2013,ArticleID891748,18pages ResveratrolSuppressesPAI-1GeneExpressioninaHumanInVitroModelofInflamedAdiposeTissue, IvanaZagotta,ElitsaY.Dimova,Jan-BerndFuncke,MartinWabitsch,ThomasKietzmann, andPamelaFischer-Posovszky Volume2013,ArticleID793525,13pages SivelestatAttenuatesMyocardialReperfusionInjuryduringBriefLowFlowPostischemicInfusion, SverreE.Aune,SteveT.Yeh,PeriannanKuppusamy,M.LakshmiKuppusamy,MahmoodKhan, andMarkG.Angelos Volume2013,ArticleID279847,9pages RedOrange:ExperimentalModelsandEpidemiologicalEvidenceofItsBenefitsonHumanHealth, GiuseppeGrosso,FabioGalvano,AntonioMistretta,StefanoMarventano,FrancescaNolfo, GiorgioCalabrese,SilvioBuscemi,FilippoDrago,UmbertoVeronesi,andAlessandroScuderi Volume2013,ArticleID157240,11pages Site-SpecificAntioxidativeTherapyforPreventionofAtherosclerosisandCardiovascularDisease, HajimeOtani Volume2013,ArticleID796891,14pages AReviewofPterostilbeneAntioxidantActivityandDiseaseModification,DeniseMcCormackand DavidMcFadden Volume2013,ArticleID575482,15pages TherapeuticEffectofMG132ontheAorticOxidativeDamageandInflammatoryResponseinOVE26 Type1DiabeticMice,XiaoMiao,WenpengCui,WeixiaSun,YingXin,BoWang,YiTan,LuCai, LiningMiao,YaowenFu,GuanfangSu,andYuehuiWang Volume2013,ArticleID879516,12pages Gamma-TocotrienolModulatedGeneExpressioninSenescentHumanDiploidFibroblastsasRevealed byMicroarrayAnalysis,SuzanaMakpol,AzalinaZainuddin,KienHuiChua,YasminAnumMohdYusof, andWanZurinahWanNgah Volume2013,ArticleID454328,11pages EffectsofCaloricRestrictiononCardiacOxidativeStressandMitochondrialBioenergetics:Potential RoleofCardiacSirtuins,KenShinmura Volume2013,ArticleID528935,11pages NordihydroguaiareticAcidAttenuatestheOxidativeStress-InducedDecreaseofCD33Expressionin HumanMonocytes,SilviaGuzma´n-Beltra´n,Jose´Pedraza-Chaverri,SusanaGonzalez-Reyes, FernandoHerna´ndez-Sa´nchez,UlisesE.Juarez-Figueroa,YolandaGonzalez,KarenBobadilla, andMarthaTorres Volume2013,ArticleID375893,14pages HindawiPublishingCorporation OxidativeMedicineandCellularLongevity Volume2013,ArticleID820679,3pages http://dx.doi.org/10.1155/2013/820679 Editorial Antioxidants in Longevity and Medicine NilanjanaMaulik,1DavidMcFadden,1HajimeOtani,2MaheshThirunavukkarasu,1 andNarasimhamL.Parinandi3 1DepartmentofSurgery,UniversityofConnecticutHealthCenter,Farmington,CT-06030,USA 2DepartmentofInternalMedicine,KansaiMedicalUniversity,MoriguchiCity570-8507,Japan 3DivisionofPulmonary,Allergy,CriticalCare,andSleepMedicine,DorothyM.DavisHeart&LungResearchInstitute, TheOhioStateUniversityCollegeofMedicine,Columbus,OH43210,USA CorrespondenceshouldbeaddressedtoNilanjanaMaulik;[email protected] Received9September2013;Accepted9September2013 Copyright©2013NilanjanaMauliketal. This is an open access article distributed under the Creative Commons Attribution License,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperly cited. Oxidative stress has emerged as a critical player in the BhullarandH.P.V.Rupasinghehavereviewedtheeffectof pathogenesisandpathophysiologyofmanydiseasesinexper- polyphenols on age-related neurological disorders and dis- imental animal models and humans. The oxidative stress cussedtheroleofpolyphenolsinmultiplesignalingpathways, theory of aging emphasizes that a progressive and irre- includingPI3K/Akt,Nrf2/HO1PPAR,STAT,NF-𝜅B,HIF,and versible escalation of oxidative damage caused by reactive MAPK. All of the pathways can alleviate oxidative damage oxygenspecies(ROSs)exertssevereinfluenceonthecritical and inflammation. This review article offers insights into aspects of the biology of aging and contributes to impaired the complex interactions of polyphenols with intracellular physiologicalfunctions,increasedincidenceofdiseases,and signaling pathways in neuronal cells and provides novel shortening of life span. The focus of this special issue is to approachtoneurologicaldisorders. identifyavenuesthataffectboththelifespanandage-related Resveratrol is a calorie restriction (CR) mimetic agent. diseases in humans. In order to accomplish this, experts CRreversesmanyoftheobesity-relatedincreasesininflam- in the field have contributed original research articles and matory cytokines. I. Zagotta et al. have reported that PAI- reviews focusing on the current state of understanding of 1 gene expression is increased in adipose tissue in obese the molecular pathology of oxidative stress underlying the subjects, and this is critically involved in chronic inflam- biologyofagingandage-relateddiseasesanddevelopmentof mation of blood vessels that leads to atherosclerosis and strategiestoalleviateortreattheseconditions. cardiovasculardisease.PAI-1geneisfoundtobeupregulated S. Gazman-Beltran et al. demonstrate that a natural due to inflammatory conditions associated with obesity. antioxidant, nordihydroguaiaretic acid (NDGA) attenuates Resveratrol treatment has been shown to suppress the PAI- theoxidativestress-induceddecreaseofCD33expressionin 1 gene in human inflamed adipose tissue. Interestingly, the human monocytes, which is decreased in diabetic patients effectofresveratrolonPAI-1isnotmediatedbymodulationof underoxidativestress.TheantioxidantmechanismofNDGA PI3K/Akt,SIRT1,AMPK,andNrf2orreactiveoxygenspecies appears to be multifactorial and includes the increased (ROS) but proceeds through the inhibition of the NF-𝜅B availability of glutathione and activation of nuclear factor pathway.Thissuggeststhatresveratrolinhibitsthegeneration E2-related factor-2 (Nrf2), which is known to orchestrate of inflammatory cytokines in the adipose tissue via a novel antioxidativeandcytoprotectiveresponsestooxidativestress. anti-inflammatorypathway. NDGA appears to be an effective antioxidant to prevent Advancedglycationendproducts(AGEs)playacrucial chronicinflammationinducedbymonocytes. role in senescence. B. Buttari et al., have demonstrated that Recently,studiesconductedwithdietarypolyphenolson resveratrolmaybeeffectiveintreatingautoimmunediseases neurological disorders have shown promising results. K. S. thatareintimatelyrelatedtotheactivationofdendriticcells 2 OxidativeMedicineandCellularLongevity (DCs)withtheAGEs.B.Buttarietal.havealsoshownthat mitochondriarepresentsapowerfulstrategytopreventcel- resveratrol pretreatment of human monocyte-derived DCs lularsenescence.ThereviewarticleauthoredbyK.Shinmura prevents the activation of DCs in response to the AGE- highlightstheimportanceofpreventingmitochondrialgen- albumin.ThemechanismisbyinhibitingtheDCmaturation erationofROS.Age-relatedmitochondrialdysfunctionisdue andproinflammatorycytokineexpressionassociatedwiththe tooxidativestress-mediatedaccumulationofsomationmuta- inhibition of NF-𝜅B activation. Because the specific recep- tion in mitochondrial DNA. A growing body of evidence tor for AGE (RAGE) is down-regulated in the resveratrol- suggests that caloric restriction (CR) mediates attenuation pretreated DCs, resveratrol inhibits oxidative stress and of mitochondrial oxidative damage via decreasing the pro- inflammatory response at the level of RAGE upstream of ductionofmitochondrialROSratherthanbyenhancingthe PI3K/Akt,MAPK,orNF-𝜅B.Thisfindingisinterestingsince antioxidantdefense.K.Shinmurasuggeststhatsirtuinmight the NF-𝜅B pathway is modulated by resveratrol in other beinvolvedintheCR-inducedattenuationofmitochondrial biological systems. This unique pharmacological action of oxidative damage. This review article concludes that CR- resveratrolonDCsthatareactivatedbyAGEsisasubjectfor mimeticagents,suchasresveratrolandsirtuinactivators,are furtherinvestigation. promisingagentstoimprovethemitochondrialfunctionand ROSderivedfromthemitochondriaactivatestheredox- prolonglifespan,althoughtheirexactmechanism(s)ofaction sensitive transcriptional factor, nuclear respiration factor-2 shouldbecarefullyexamined. (NRF2). NRF2-induced mitochondrial biogenesis improves Myocardial reperfusion injury is mediated at least in the function of electoral transfer chain (ETC) and prevents part by oxidative stress. Yet, there have been no antioxi- ROS generation in mitochondria. Thus, the agents that can dants that unequivocally confer benefit in the postischemic activateNRF2areattractiveinamelioratingoxidativestress- heartintheclinicalsetting,althoughnumerousagentshave induced pathology. X. Miao et al. have demonstrated that been shown to exert cardioprotective effects on animal an NRF2 activator MG132 has prevented the aortic injury models of ischemia/reperfusion injury. Angelos et al. have in type-1 diabetic mice, suggesting that activation of NRF2 demonstratedthattheneutrophilesteraseinhibitorsivelestat representsapromisingapproachforhyperglycemia-induced reducestheinfarctsizeandimprovescardiacfunctioninan vascularcomplications. isolatedratheartthatlacksneutrophils.Thecardioprotective Aging is related to circadian rhythm disruption. The effect of sivelestat appears to be mediated by nitric oxide, concept of chrononutrition raised by M. Garrido et al. has whichhasconsistentlybeenimplicatedinthecardioprotec- prompted development of a strategy that takes timing of tionagainstmyocardialischemia/reperfusioninjury.Future tryptophan-enrichedfoodintakeintoaccountwhendeliver- clinical trials using sivelestat are warranted to test whether ingantioxidativemedicine.Chrononutritionstudiessuggest thisclinicallyavailabledrugisindeedeffectiveinameliorat- thatalongwiththecontentoffood,thetimeofingestionis ingmyocardialreperfusioninjuryinhumans. essentialforthenaturalfunctioningofthecircadiansystem, G. Grosso et al. have advocated in favor of the health which stimulates melatonin secretion at night. Melatonin benefits of red orange on the basis of research on experi- producescircadianrhythmandactsasapotentantioxidant mental models and epidemiological evidence. The authors and ROS scavenger. It also inhibits ROS generation by argue that the beneficial effects of the red orange fruit may preventingtheelectronleakagefrommitochondria,thereby be exerted through the synergistic actions of the natural stimulating the antioxidative defense system. Thus, it is productspresentinthefruit.Thesenaturalproductspossess anticipated that administration of melatonin either directly antioxidant actions, which may protect against oxidative orindirectlyfromfoodenhancesone’santioxidantstatus. damage, and the total beneficial actions of all the natural A review article described by H. Otani opens a new products(antioxidants)presentintheredorangefruitcould avenueforantioxidativemedicine.AlthoughROSisinvolved bemoreeffectivethananindividualantioxidant. inmanypathologicalphenomenainhumanswithadvanced The lack of mitochondrial superoxide dismutase (Mn- age,antioxidativemedicineisnotalwayssuccessfulinallevi- SOD) leading to the loss of hearing during aging has been atinghuman disease. Thelimitationofgeneralantioxidants clearlydemonstratedbyM.Kinoshitaetal.Withtheuseof inpreventingoxidativestress-induceddiseasesisattributed Mn-SOD heterozygous knockout mice as the experimental toROSplayingapivotalroleingeneratingredoxsignaling. modelofmitochondria-derivedoxidativestress,theauthors Thisisnecessaryformaintaininghomeostasisandgenerating haveshownthatlossofMn-SODbyhalfappearstoelevate adaptiveresponsetolethaloxidativedamage.Thus,antioxi- theoxidativestressinthecochleatoacertaindegree,butthat dants must be more site specific to eliminate only harmful may not be adequate to speed up the age-induced damage ROS and leave beneficial ROS. Recent new drugs used for of the cochlea. Nevertheless, the role of Mn-SOD in the treatinglifestyle-relateddiseasessuchashypertension,hyper- mitochondria that scavenges the superoxide radical in the lipidemia,andhyperuricemiapossessapleiotropiceffectthat oxidativestressthatleadstolossofhearingduringaginghas isdesignatedasthesite-specificantioxidantagainstendothe- beenattemptedinthisstudy. lialNADPHoxidaseandxanthineoxidase.Antioxidantsthat Z. Makpol et al. have studied the gene expression- specifically reduce mitochondrial ROS generation will also modulating actions of gamma-tocotrienol in the senescent be putative drugs to ameliorate age-associated disease and human diploid fibroblasts by utilizing the microarray anal- prolonglifespan. ysis.Thisstudyhasemphasizedonthelipid-solubleantiox- Mitochondrial generation of ROS is intimately related idant (gamma-tocotrienol) actions on the modulation of to aging. Eliminating the harmful production of ROS from genesassociatedwiththecellularagingandoxidativestress. OxidativeMedicineandCellularLongevity 3 Thisstudyhasdemonstratedthatgamma-tocotrienolappears These papers represent an exciting and insightful snap- to block cellular aging of human fibroblasts through the shotofcurrentantioxidantresearch.State-of-the-art,exciting modulation of gene expression in the cells. In addition, the challenges, which still present many new challenges, are roleoflipidperoxidationincellularagingandassociatedgene highlightedinthisspecialissue,whichmayinspireandhelp expressionisapparentfromthisstudy. advance antioxidant research. We would like to thank all D. McCormack and D. McFadden have discussed in authors,reviewers,andtheeditorsforproducingthisspecial depth the antioxidant and disease-modifying actions of issue. pterostilbene. The antioxidant actions of pterostilbene have Antioxidative medicine has become a practical tool to been connected with cancer protection, treatment of neu- treatage-associateddiseaseandtoprolongthelifespansince rological diseases, suppression/treatment of inflammation, oxidative stress is critically involved in human aging. The attenuation of vascular diseases, and improvement of dia- purposeofthetopicscoveredinthisspecialissueistoprovide betes. The authors have provided an excellent account on additionalopportunitiestoalltheinvestigatorsinthefieldin the clinical use of pterostilbene in prevention/treatment of ordertoidentifyavenuesthatimpactboththelifespanand severaldisordersanddiseases. age-relateddiseasesinhumans.Therefore,thecontributions A.B.Rodriguezetal.showedthatfishoilscontainingthe madebytheexpertsinthisissueasoriginalresearcharticles omega-3polyunsaturatedfattyacids(n3-PUFA)arecapable andreviewswillhopefullystimulatethecontinuingeffortsof of attenuating the levels of inflammatory cytokines and the investigators to understand and establish the molecular oxidative stress markers in the serum of multiple sclerosis pathologyofoxidativestressunderlyingthebiologyofaging patients. From this study, the authors have concluded that and age-related diseases and development of strategies to thefishoilsupplementationtothemultiplesclerosispatients alleviateortreattheseconditions. effectively lowers the levels of inflammatory cytokines and NilanjanaMaulik nitricoxide(oxidant),thusleadingtotheprotectionagainst DavidMcFadden multiplesclerosis. HajimeOtani J. Rosado-Perez et al. have shown that physical exercise MaheshThirunavukkarasu like Tai Chi offers beneficial effects in lowering oxidative NarasimahamL.Parinandi stress in humans. In their study on Mexican adults, the authors have revealed that the subjects who have practiced Tai Chi have exhibited lower extent of lipid peroxidation and elevated superoxide dismutase activity as compared to the control individuals. From this study, the authors have concluded that Tai Chi is more effective in elevating the antioxidantstatusinhumansascomparedtowalking. S.Dandeetal.havediscussedonthenaturalantioxidant actions of the commonly consumed foods of plant origin in India. In this review, the authors have emphasized on thedomesticprocessingofplantfoodsthatcouldaffectthe quality of the plant foods that are consumed. The authors discussedtheimportanceofpolyphenolspresentintheplant foodsthatcouldactasnaturalantioxidants.Theauthorshave stated that the domestic processing of plant foods may not alterthecontentofpolyphenolsandantioxidantactivitiesin theplantfoods. In a study on the hypoxia-induced neuroinflammation, Z. Wu et al. have shown that the Brazilian green propolis inhibits the NF-𝜅B activation in the microglia. The authors have demonstrated that the mitochondrial ROS formation is crucial for the activation of NF-𝜅B activation in the microglia.Therefore,itappearsthatpropoliscouldhavealso acted as an antioxidant in attenuating the hypoxia-induced neuroinflammationinthemicroglia. A.L.Zagaykoetal.haveshownthatthegrapepolyphe- nolsincreasetheactivityofhigh-densitylipoprotein(HDL) enzymes in old and obese rats. The authors have revealed that the activity of paraoxonase, lecithin: cholesterol acyl- transferase (LCAT) in plasma have been lowered and the cholesterol ester transfer protein (CETP) activity has been elevated in old rats. This study emphasizes the actions of grapepolyphenolsontheelevationofHDLenzymesduring aging.
Description: