Oxidants and Antioxidants in Metabolic Syndrome and Cancer

156 Pages·2014·34.76 MB·English

Oxidative Medicine and Cellular Longevity
Oxidants and Antioxidants in
Metabolic Syndrome and Cancer
Guest Editors: Si Jin, Yongzhong Wu, Shiwei Deng, Jinxiang Zhang,
and Xiao Qian Chen
Oxidants and Antioxidants in
Metabolic Syndrome and Cancer
Oxidative Medicine and Cellular Longevity
Oxidants and Antioxidants in
Metabolic Syndrome and Cancer
Guest Editors: Si Jin, Yongzhong Wu, Shiwei Deng,
Jinxiang Zhang, and Xiao Qian Chen
Copyright©2014HindawiPublishingCorporation.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
ZhaoZhongChong,USA RonKohen,Israel OrenTirosh,Israel
FelipeDal-Pizzol,Brazil Jean-ClaudeLavoie,Canada MadiaTrujillo,Uruguay
OzcanErel,Turkey ChristopherLillig,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 DonatellaPietraforte,Italy JingYi,China
DanielaGiustarini,Italy AurelPopa-Wagner,Germany GuillermoZalba,Spain
HunjooHa,RepublicofKorea Jose´L.Quiles,Spain
Contents
OxidantsandAntioxidantsinMetabolicSyndromeandCancer,SiJin,YongzhongWu,ShiweiDeng,
JinxiangZhang,andXiaoQianChen
Volume2014,ArticleID178962,3pages
LithiumChlorideSuppressesColorectalCancerCellSurvivalandProliferationthrough
ROS/GSK-3𝛽/NF-𝜅BSignalingPathway,HuiliLi,KunHuang,XinghuaLiu,JinlinLiu,XiaomingLu,
KaixiongTao,GuobinWang,andJiliangWang
Volume2014,ArticleID241864,8pages
PiperlongumineInhibitsMigrationofGlioblastomaCellsviaActivationofROS-Dependentp38and
JNKSignalingPathways,QianRongLiu,JuMeiLiu,YongChen,XiaoQiangXie,XinXinXiong,
XinYaoQiu,FengPan,DiLiu,ShangBinYu,andXiaoQianChen
Volume2014,ArticleID653732,12pages
PELP1SuppressionInhibitsColorectalCancerthroughc-SrcDownregulation,ZhifengNing,
YouzhiZhang,HanweiChen,JiliangWu,TieshanSong,QianWu,andFuxingLiu
Volume2014,ArticleID193523,9pages
Caenorhabditiselegans:AUsefulModelforStudyingMetabolicDisordersinWhichOxidativeStressIs
aContributingFactor,ElizabethMoreno-Arriola,Noem´ıCa´rdenas-Rodr´ıguez,ElviaCoballase-Urrutia,
Jose´Pedraza-Chaverri,LilianaCarmona-Aparicio,andDanielOrtega-Cuellar
Volume2014,ArticleID705253,9pages
MetabolicSyndrome:AnImportantRiskFactorforParkinson’sDisease,PeiZhangandBoTian
Volume2014,ArticleID729194,7pages
PiperlongumineInducesApoptosisandSynergizeswithCisplatinorPaclitaxelinHumanOvarian
CancerCells,Li-HuaGong,Xiu-XiuChen,HuanWang,Qi-WeiJiang,Shi-ShiPan,Jian-GeQiu,
Xiao-LongMei,You-QiuXue,Wu-MingQin,Fei-YunZheng,ZhiShi,andXiao-JianYan
Volume2014,ArticleID906804,10pages
InsulinRegulatesGlucoseConsumptionandLactateProductionthroughReactiveOxygenSpeciesand
PyruvateKinaseM2,QiLi,XueLiu,YuYin,Ji-TaiZheng,Cheng-FeiJiang,JingWang,HuaShen,
Chong-YongLi,MinWang,Ling-ZhiLiu,andBing-HuaJiang
Volume2014,ArticleID504953,10pages
LeucocyteTelomereShorteninginrelationtoNewlyDiagnosedType2DiabeticPatientswith
Depression,ZhelongLiu,JianhuaZhang,JiangtaoYan,YupingWang,andYongshengLi
Volume2014,ArticleID673959,8pages
Lentivirus-MediatedNox4shRNAInvasionandAngiogenesisandEnhancesRadiosensitivityinHuman
Glioblastoma,YongshengLi,NaHan,TiejunYin,LuluHuang,ShunfangLiu,DongboLiu,CuihongXie,
andMengxianZhang
Volume2014,ArticleID581732,9pages
SalidrosideStimulatesMitochondrialBiogenesisandProtectsagainstH O -InducedEndothelial
2 2
Dysfunction,ShashaXing,XiaoyanYang,WenjingLi,FangBian,DanWu,JiangyangChi,GaoXu,
YonghuiZhang,andSiJin
Volume2014,ArticleID904834,13pages
EffectofCentellaasiaticaonOxidativeStressandLipidMetabolisminHyperlipidemicAnimalModels,
YunZhao,PingShu,YouzhiZhang,LiminLin,HaihongZhou,ZhentianXu,DaqinSuo,AnzhiXie,
andXinJin
Volume2014,ArticleID154295,7pages
LeptinLevelandOxidativeStressContributetoObesity-InducedLowTestosteroneinMurine
TesticularTissue,JianZhao,LinglingZhai,ZhengLiu,ShuangWu,andLipingXu
Volume2014,ArticleID190945,14pages
EndogenousCeramideContributestotheTranscytosisofoxLDLacrossEndothelialCellsandPromotes
ItsSubendothelialRetentioninVascularWall,WenjingLi,XiaoyanYang,ShashaXing,FangBian,
WanjingYao,XiangliBai,TaoZheng,GuangjieWu,andSiJin
Volume2014,ArticleID823071,11pages
BL153PartiallyPreventsHigh-FatDietInducedLiverDamageProbablyviaInhibitionofLipid
Accumulation,Inflammation,andOxidativeStress,JianWang,ChiZhang,ZhiguoZhang,QiangChen,
XuemianLu,MinglongShao,LiangmiaoChen,HongYang,FangfangZhang,PengCheng,YiTan,
Ki-SooKim,KiHoKim,BochuWang,andYoungHeuiKim
Volume2014,ArticleID674690,10pages
ResveratrolOligomersforthePreventionandTreatmentofCancers,You-QiuXue,Jin-MingDi,YunLuo,
Ke-JunCheng,XingWei,andZhiShi
Volume2014,ArticleID765832,9pages
Hindawi Publishing Corporation
Oxidative Medicine and Cellular Longevity
Volume 2014, Article ID 178962, 3 pages
http://dx.doi.org/10.1155/2014/178962
Editorial
Oxidants and Antioxidants in Metabolic Syndrome and Cancer
SiJin,1YongzhongWu,2ShiweiDeng,3JinxiangZhang,4andXiaoQianChen5
1DepartmentofPharmacology,TongjiMedicalCollege,HuazhongUniversityofScienceandTechnology,Wuhan430030,China
2LaboratoryofMolecularPharmacology,OxidativeSignalingandMolecularTherapeuticsSection,CenterforCancerResearch,
NationalCancerInstitute,Bethesda,MD20892,USA
3DepartmentofPharmacology,UniversityMedicalCenteroftheJohannesGutenbergUniversityMainz,ObereZahlbacherStraße67,
55131Mainz,Germany
4DepartmentofSurgery,UnionHospital,TongjiMedicalCollege,HuazhongUniversityofScienceandTechnology,
Wuhan430022,China
5DepartmentofPathophysiology,TongjiMedicalCollege,HuazhongUniversityofScienceandTechnology,Wuhan430030,China
CorrespondenceshouldbeaddressedtoSiJin;[email protected]
Received25May2014;Accepted25May2014;Published24June2014
Copyright©2014SiJinetal.ThisisanopenaccessarticledistributedundertheCreativeCommonsAttributionLicense,which
permitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperlycited.
Metabolic syndrome, which includes hypertension, hyper- In this controversial context, we organized this special
lipidemia, obesity, insulin resistance or glucose intolerance, issue.
and fatty liver diseases, significantly contributes to the Although insulin is critically involved in metabolism
increased risk of cardio- or cerebral-vascular diseases and regulation and closely associates with both diabetes and
diabetes[1].Cancerrepresentsagroupofmalignantlyprolif- cancer, the precise molecular mechanism is not fully elu-
erativediseases.Recently,metabolicreprogrammingchanges cidated. In this special issue, Q. Li et al. conducted an
were extremely highlighted in cancer cells, putting forward interestingstudy,whichdemonstratesthatinsulinincreases
to a trend that cancer should also be treated as a type of pyruvatekinaseM2(PKM2)expressionthroughROSforthe
metabolic disease [2]. As a matter of fact, statins, the most regulation of glucose consumption and lactate production
prescribed low density lipoprotein (LDL) lowering agents, “Insulinregulatesglucoseconsumptionandlactateproduction
andmetformin,themostprescribedantidiabeticdrug,have through reactive oxygen species and pyruvate kinase M2”. J.
both been reported to associate with decreased cancer risk Zhaoetal.demonstratedthatpubertalobesitywasassociated
[3,4]. withincreasedoxidativestressintestistissueandhighlevels
Meanwhile, in the past decade, a growing body of of leptin, which maybe the cause of male hypogonadism
evidence has implicated that increased oxidative stress is a in obesity “Leptin level and oxidative stress contribute to
commonandkeyfeatureofmetabolicdiseases[5].Whereas obesity-induced low testosterone in murine testicular tissue.”
arecenthypothesispaperbyWatson,thefamousNobelPrize Oxidizedlowdensitylipoprotein(oxLDL)isthemajorlipid
winner, suggests that diabetes, dementias, cardiovascular found in atherosclerotic lesion and elevated plasma oxLDL
disease, and some cancers may be linked to a failure to is recognized to be a risk factor of atherosclerosis. W. Li
generatesufficientreactiveoxygenspecies(ROS)[6],which et al. in this special issue emphasized the critical role of
maybereflectsthesituationsinendstagesofthesecomplex oxLDLtranscytosisacrossendothelialcellsintheinitiationof
diseases. ROS play very important roles in carcinogenesis atherosclerosis,providingnovelinsightintothepathogenesis
and the maintenance of cancer cells. The ROS levels are of this complex metabolism disease “Endogenous ceramide
reportedtobeveryhighincancercells,whichdrivethehigh contributes to the transcytosis of oxLDL across endothelial
rate of proliferation in these malignant cells [7]. Whether cells and promotes its subendothelial retention in vascular
prooxidantsorantioxidantscouldbeusedtotreatcanceror wall.” For the therapy of metabolic syndrome-related dis-
notremainselusive. orders, J. Wang et al. reported in this special issue that
2 OxidativeMedicineandCellularLongevity
amagnolia extract, named BL153, could prevent obesity- plants with documented antioxidant activity “Resveratrol
induced liver damage via inhibition of lipid accumulation, oligomers for the prevention and treatment of cancers.” In
inflammation,oxidativestress“BL153partiallypreventshigh line with this review, Y. Li et al. reported that NADPH
fat diet induced liver damage probably via inhibition of lipid oxidase4(Nox4)-derivedreactiveoxygenspeciesmightplay
accumulation, inflammation, and oxidative stress.” Centella crucial roles in the invasion, angiogenesis and radioresis-
asiatica is a traditional Chinese medicine which has been tance in glioblastoma. Inhibition of Nox4 by lentivirus-
reported to have antioxidant effect in vitro. In this special mediated small hairpin interfering RNA (shRNA) could be
issue, Y. Zhao et al. further reported that Centella asiatica a strategy to overcome radioresistance and in turn improve
decreasedcholesterolandtriglycerideinmicemodel“Effect the therapeutic efficacy “Lentivirus-mediated Nox4 shRNA
ofCentellaasiaticaonoxidativestressandlipidmetabolismin invasion and angiogenesis and enhances radiosensitivity in
hyperlipidemicanimalmodels.”Salidroside(SAL)isanactive humanglioblastoma.”Thesestudiessuggestthatinaddition
componentofRhodiolaRoseawithdocumentedantioxidative to prooxidant therapy, antioxidants may also be the right
properties. S. Xing et al. in this issue further demonstrated optiontotreatcancersascancerinhibitingagents.
that SAL could protect endothelium against H2O2-induced In addition to above mentioned pathological or phar-
injury via promoting mitochondrial biogenesis and func- macologicalstudies,ElizabethMoreno-Arriolaetal.present
tion,thuspreventingtheover-activationofoxidativestress- an interesting review which suggests that Caenorhabditis
related downstream signaling pathways “Salidroside stim- elegans,whichmaybeoneofthemostfamousmodelorgan-
ulates mitochondrial biogenesis and protects against H O - isms,isalsoasuitablediseasemodelreflectingtheoxidative
2 2
Inducedendothelialdysfunction.” statusinmetabolicdisorders,providingnewapproachesfor
In cancer cells, the ROS is maintained at higher levels studyingmetabolicdiseases“Caenorhabditiselegans:auseful
thannormalcellsandmainlyexertsitsproliferativeactions. modelforstudyingmetabolicdisordersinwhichoxidativestress
When ROS levels are further increased by prooxidants so isacontributingfactor.”
as to exceed a border line level, the proapoptotic effects From these collected studies in this special issue, we
of ROS may exceed its proliferative effects and cytotoxic appeartocometotheconsensusthatupregulatedoxidative
effects display in cancer cells, whereas the ROS levels in stress indeed promotes the development of both metabolic
normal cells remain below the border line level which is syndrome and cancer. Antioxidants are suitable choices for
nontoxictonormalcells.Inconsistentwiththisview,several the prevention or treatment of metabolic syndrome-based
studies in this special issue reported chemicals could kill cardiovascular diseases or diabetic mellitus, which are also
cancercellsbyinducingROSaccumulationascancerkilling classifiedaschronicnonresolvinginflammatorydiseases[8].
agents.Piperlongumine(PL)isanaturalalkaloidfromPiper However,forthetreatmentofcancers,bothprooxidantsand
longumL.,possessinghighlyselectiveandeffectiveanticancer antioxidantsmightworkviadifferentmechanisms,provided
property. L.-H. Gong et al. reported in this special issue thatthedrugselectivityontargetedtissueisguaranteed.We
that PL notably induced cell apoptosis, G2/M phase arrest hope that the studies and discussions gathered in this issue
and intracellular ROS accumulation in a dose- and time- reflect the current trend in this area and could, to some
dependentmanner.PretreatmentwithantioxidantN–acety- extent, stimulate more in-depth studies in this somehow
L-cysteinecouldreversethePL-inducedROSaccumulation controversialfield.
andcellularapoptosis.Inaddition,low-doseofPL/cisplatin
or paclitaxel combination therapies had a synergistic anti-
Acknowledgments
growtheffectonhumanovariancancercells“Piperlongumine
inducesapoptosisandsynergizeswithcisplatinorpaclitaxelin We appreciate the great efforts of all authors and reviewers
human ovarian cancer cells.” Q. R. Liu et al. also reported participatinginthisissue.Withouttheirinvaluablecontribu-
that Piperlongumine effectively inhibited the migration of tion,thisspecialissuewouldnotbeasuccess.
humangliomacellsbutnotnormalastrocytesinthescratch-
woundculturemodel.PLincreasedROSproduction,reduced SiJin
glutathione, activated p38 and JNK pathway, increased I𝜅B YongzhongWu
and suppressed NF-𝜅B in LN229 cells after scratching ShiweiDeng
“Piperlongumine inhibits migration of glioblastoma cells via JinxiangZhang
activationofROS-dependentp38andJNKsignalingpathways”. XiaoQianChen
Similarly,H.Lietal.alsoreportedinthisissuethatLithium
chloride,theestablishedglycogensynthasekinase-3𝛽(GSK-
References
3𝛽) inhibitor, induced the apoptosis of colorectal cancer
cells by induction of ROS signaling “Lithium chloride sup- [1] I. Padmalayam and M. Suto, “Role of adiponectin in the
pressescolorectalcancercellsurvivalandproliferationthrough metabolicsyndrome:currentperspectivesonitsmodulationas
ROS/GSK-3𝛽/NF-𝜅Bsignalingpathway.” atreatmentstrategy,”CurrentPharmaceuticalDesign,vol.19,no.
Incontrasttoaboveobservationswhichdemonstratethat 32,pp.5755–5763,2013.
inductionofROSmaybeusedtotreatcancers,Y-Q.Xueet [2] C.V.Dang,“Linksbetweenmetabolismandcancer,”Genes&
al.,inthisspecialissuereviewsthepreventiveoranticancer Development,vol.26,no.9,pp.877–890,2012.
propertiesofresveratrololigomers.Resveratrolisanaturally [3] B.J.Quinn,H.Kitagawa,R.M.Memmott,J.J.Gills,andP.A.
derivedphytoalexinstilbeneisolatedfromgrapesandother Dennis,“Repositioningmetforminforcancerpreventionand
OxidativeMedicineandCellularLongevity 3
treatment,”TrendsinEndocrinology&Metabolism,vol.24,no.
9,pp.469–480,2013.
[4] S.F.Nielsen,B.G.Nordestgaard,andS.E.Bojesen,“Statinuse
andreducedcancer-relatedmortality,”TheNewEnglandJournal
ofMedicine,vol.367,no.19,pp.1792–1802,2012.
[5] C.K.RobertsandK.K.Sindhu,“Oxidativestressandmetabolic
syndrome,”LifeSciences,vol.84,no.21-22,pp.705–712,2009.
[6] J.D.Watson,“Type2diabetesasaredoxdisease,”TheLancet,
vol.383,no.9919,pp.841–843,2014.
[7] C. Gorrini, I. S. Harris, and T. W. Mark, “Modulation of
oxidativestressasananticancerstrategy,”NatureReviewsDrug
Discovery,vol.12,no.12,pp.931–947,2013.
[8] C.NathanandA.Ding,“Nonresolvinginflammation,”Cell,vol.
140,no.6,pp.871–882,2010.