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Evaluation of the protective effect of Ilex paraguariensis and Camellia sinensis extracts on the prevention of oxidative damage caused by ultraviolet radiation

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Evaluation of the protective effect of Ilex paraguariensis and Camellia sinensis extracts on the prevention of oxidative damage caused by ultraviolet radiation
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  env   i   r   o   nme   nta   lt   o   xico   logya   nd   ph   a   r   ma   co   lo   g   y   3   7(   2   014   )   195–201  Available   online   at   www.sciencedirect.com ScienceDirect   journalhomepage:www.elsevier.com/locate/etap Evaluation   ofthe   protectiveeffect    of    Ilex paraguariensis and   Camelliasinensis   extractson   the   prevention   ofoxidative   damage   caused byultraviolet    radiation MarlonBarg a ,   GislaineT.Rezin b ,   DanielaD.   Leffa c ,   FernandaBalbinot c ,Lara   M.Gomes a , d ,   MilenaCarvalho-Silva a , d ,FrancieliVuolo a , d ,FabriciaPetronilho b ,   FelipeDal-Pizzol a , d ,EmilioL.   Streck a , d ,Vanessa   M.Andrade c , ∗ a LaboratóriodeBioenergética,ProgramadePós-Graduac¸ãoemCiênciasdaSaúde,UniversidadedoExtremoSulCatarinense,Criciúma,SC,   Brazil b LaboratóriodeFisiopatologiaClínicaeExperimental,ProgramadePós-Graduac¸ão   emCiênciasdaSaúde,UniversidadedoSuldeSantaCatarina,Tubarão,SC,Brazil c LaboratóriodeBiologiaCelulare   Molecular,ProgramadePós-Graduac¸ão   emCiênciasdaSaúde,UniversidadedoExtremoSulCatarinense,Criciúma,SC,Brazil d InstitutoNacionaldeCiênciaeTecnologiaTranslacionalemMedicina,HospitaldeClínicasdePortoAlegre,PortoAlegre,RS,Brazil a   r   t   i   c   l   e   in   f   o  Articlehistory: Received26March2013Receivedin   revisedform3November2013Accepted28November2013Availableonline6December2013 Keywords: SkincancerGreenteaMateteaDNAdamageOxidativedamage a   bs   tr   a   ct We   evaluatedtheeffectsgreenandmateteasonoxidativeandDNAdamagesinrats   exposedto   ultravioletradiation.Wereutilized70   adultmaleWistarratsthatreceiveddailyoralortopic   greenor   mateteatreatmentduringexposedtoradiationbysevendays.After,animalswere   killedbydecapitation.Thiobarbituricacid-reactivespecieslevels,proteinoxidativedamagewereevaluatedinskinandDNAdamageinblood.Ourresultsshowthatthe   ratsexposedto   ultravioletradiationpresentedDNAdamageinbloodandincreasedproteincar-bonylationandlipidperoxidationinskin.Oralandtopictreatmentwithgreenteaandmateteapreventedlipidperoxidation,bothtreatmentswithmateteaalsopreventedDNAdam-age.   However,onlytopictreatmentwithgreenteaandmateteapreventedincreasesinproteincarbonylation.Ourfindingscontributetoelucidatethebeneficialeffectsof    greenteaandmatetea,hereindemonstratedby   theantioxidantandantigenotoxicpropertiespresentedbytheseteas.©2013ElsevierB.V.Allrightsreserved. ∗ Correspondingauthorat :Laboratóriode   BiologiaCelulareMolecular,Universidadedo   ExtremoSulCatarinense,UNESC,AvenidaUni-versitária,1105,88806-000Criciúma,SC,Brazil.Tel.:+5548   34312757.E-mailaddress:vmoraesdeandrade@yahoo.com.br(V.M.Andrade).1382-6689/$–   seefrontmatter©2013ElsevierB.V.Allrightsreserved.http://dx.doi.org/10.1016/j.etap.2013.11.028  196   e   nviro   nment   al   toxi   co   lo   g   y   andpha   r   maco   lo   gy   37(   2   014)   195–201 1.   Introduction Overtheyears,changesinlifestylesignificantlyincreasedhumanexposuretosolarradiation,leadingtoa   dramaticriseintheincidenceofskincancer(Gruijl,1999).Photo-induced cancersareduetoacomplexmultistagephenomenon,medi-atedbyalterationsinseveralcellularmechanisms(Sarasin,1999).Increasedultravioletradiationexposureis   consideredthemaincauseoftherisingprevalenceofskincancer(Vriesetal.,2005).   Inhumansandanimalmodels,bothultravioletAandBradiationscancausegenemutations(Agaretal.,2004;MelnikovaandAnanthaswamy,2005)andimmunitysuppres-sion(Hallidayetal.,2004;Ullrich,2005).Thesetwobiological eventsarerelatedtoskincancercausedbyultravioletradia-tion(GransteinandMatsui,2004). UltravioletA   andBradiationsareresponsibleforirreversiblegeneticalterations,whichultimatelyleadtoDNAmutations(Sarasin,1999).Theimplicationofultravio- letAradiationto   thisgenotoxicdamagehasbeenrecentlyproven,althoughitsaccuratebiologicaleffectsarestillunclear(BachelorandBowden,2004).ThereactiveoxygenspeciesproductionbybothultravioletAandBradiationsalsocontributestoinflammation,immuno-suppression,genemutationandcarcinogenesis(Halliday,2005;KvamandTyrrell,1997).Inaddition,studieshaveshownthatoxidativestressalsocancauseDNAdamage(Wanget   al.,1998;Wattet   al.,2007).DNAdamagecanincludechemicalandstructuralmodificationstopurineandpyrimidinebasesand2 ′ -deoxyribose,apartfromthe   formationofsingle-anddouble-strandbreaks.StrandbreakswithinDNAcanoccureitherdirectly,duetodamagefromreactiveoxygenspeciesexposure,or   indirectly,duetocleavageoftheDNAbackboneduringDNAbaseexcisionrepair(El-KhamisyandCaldecott,2006;Emerit,1994).Previousstudieshaveshownthatpolyphenolspresentingreentea( Camelliasinensis )canreduceultravioletradiations-inducedskincancerin   animalmodel(Mantenaetal.,2005). Greenteais   manufacturedfromthe   freshleavesoftheplant C.sinensis .   Theleavesofthisplantareimmersedinboilingwateraprocessthat,forthemostpart,preventsoxidationandpoly-merizationofthe   plant’spolyphenols.Itisthesecompoundsthatarethoughtto   bethemajorchemopreventivemediators(Yusufetal.,2007).Anotherteapresentingantioxidantpropertiesandprotec-tionagainstDNAoxidationismateteaoryerbamate( Ilex paraguariensis ).Mateteaextract,madefromdriedleavesof  I. paraguariensis ,   isa   tea-likebeverageconsumedin   SouthAmer-ica,mainlyinArgentina,Brazil,ParaguayandUruguay.Itspop-ularityiswidelyincreasingin   Europesinceitisacommerciallyavailableproductsoldasantirheumatic,diureticandcentralnervoussystemstimulant(Bracescoetal.,2003;Gugliucci,1996).Yerbamateis   richinseveralbioactivecompoundssuchascaffeine,phenolicacidsandsaponins,whichareabsorbedbythebodyandmay   actasantioxidantsorasfreeradicalscav-engers(Bastosetal.,2006;Filipetal.,2000;Gugliucci,1996;Ramirez-Maresetal.,2004;Schinellaet   al.,2000).Consideringthatultravioletradiationexposureinducesgenemutationsandleadstoan   increasedreactiveoxygenspeciesproduction,whichenhancesthisharmfuleffect,andthatgreenteaandmateteapossiblypresentantioxidantprop-ertiesandprotectionagainstDNAdamage,thepresentworkevaluatesthe   effectofgreenteaandmateteaonthiobarbituricacid-reactivespecieslevels.Oxidativedamageto   proteinsandDNAdamageinratsexposedtoultravioletradiationwerealsoassessed. 2.   Materials   and   methods 2.1.    Animals AdultmaleWistarrats(250–300g)   obtainedfromCentralAni-mal   HouseofUniversidadedoExtremoSulCatarinensewerehousedinsevengroupsoftenanimalstotaling70individ-ualswithfreeaccesstofoodandwater,andmaintainedona   12-hlight–darkcycle(lightsonat7:00a.m.)at22 ◦ C   ±   1 ◦ C.AllexperimentalprocedureswerecarriedoutinaccordancewiththeNationalInstitutesofHealthGuideforthe   CareandUseofLaboratoryAnimalsandtheBrazilianSocietyforNeu-roscienceandBehavior(SBNeC)recommendationsforanimalcare,withtheapprovaloflocalEthicsCommittee. 2.2.   Experimental    procedure Animalsweredividedintosevengroups,as   follows:(1)controlgroup,(2)oralsaline+ultravioletradiation,(3)basegel   +ultravioletradiation,(4)oralgreentea+ultravioletradi-ation,(5)greenteagel+ultravioletradiation,(6)oralmatetea+ultravioletradiation,(7)mateteagel+ultravioletradia-tion.Groups2,4,and6weretreatedforsevendaysorallywithsaline,greenteaandmatetea(respectively).Groups3,5,and7   weretreatedforsevendaystopicallywithbasegel,greenteagel   andmateteagel.Aftertreatment,animalswereexposedtoultravioletradiationfor1   h,onceaday.Ratswerekilled24hafterthe   lastexposuresessiontoultravioletradi-ation.BloodwascollectedtoevaluateDNAdamageandthewholeskin,wasremovedoftheanimaltoevaluateoxidativedamageparameters. 2.3.   Oral   administration   of    theextracts GreenandmateteadryextractswasobtainedfromEmbra-farma.ThesolutionswereprepareddailyinagreementwiththeBrazilianPharmacopeia.Adding15mL   ofboilingwaterto1.875gofgreenteaextractand20gofmateteaextractto   100mL   ofboilingwater.Aftera   15-minextractionperiod,thesolutionswerefilteredandadministeredtoanimals.Theanimalsreceived0.70g/kg    ofmateteaand0.45g/kggreenteasolutionsdailybygavage,30   min   beforeexposuretoultravioletradiation.Controlgroupsreceivedsaline(NaCl0.9%). 2.4.   Topic   administration   of    the   extracts Theaqueousextractswereobtainedas   describedaboveandwereincorporatedtobasegel(5%,w:w).Onegramofgelwasapplieddailyona   6cm ×   3   cmskinareapreviouslyshavenoneachrat’sback30min   beforeexposuretoultravioletradiation.Controlgroupsreceivedbasegelwithoutanyextract.  env   i   r   o   nm   enta   lt   o   xico   l   o   g   y   andph   ar   m   ac   o   l   o   g   y   37   (20   14)   195–201 197 Fig.1–Cometassay.EvaluationofDNAdamageusingethidiumbromide(400 ×  ).Thecellsare   assessedvisuallyandreceivedscoresfrom0(undamaged)to   4(maximallydamaged),accordingtothesizeandshapeofthetail. 2.5.   Exposure   to   radiation AnimalswereexposedtoultravioletAandBradiationsfor7days.UltravioletA   andBlampswereusedwithemissionspec-trumof280–320nmforUVB,and320–400nmforUVA.Therats’backwereatadistanceof60cmfromthefluoresanslamps.Ratswereirradiatedfor1hperday,allatthesametime.Intotal,70ratswereusedin   thepresentstudy.Allanimalswerekeptincagesthroughouttheexperiment(5   animalspercage,14cages). 2.6.   Comet   assay A   standardprotocolforCometassaypreparationandanalysiswas   adoptedfromTiceetal.(2000).Theslideswerepreparedbymixing5  Lofwholebloodwith95  L   oflow-melting-pointagarose(0.75%).Themixture(cells/agarose)wasaddedtoafullyfrostedmicroscopeslidecoatedwitha   layerof500  Lof normallymeltingagarose(1%).Aftersolidification,thecov-erslipwasgentlyremoved,andtheslideswereplacedinlysissolution(2.5MNaCl,100mM   EDTA,and10mMTris,pH10.0–10.5,withfreshlyadded1%TritonX-100and10%DMSO)for1day.Subsequently,theslideswereincubatedinfreshlypreparedalkalinebuffer(300mM   NaOHand1   mM   EDTA,pH13)for20min.TheDNAwas   electrophoresedfor15min   at25V(0.90V/cm)and300mA.   Afterelectrophoresis,theslideswereneutralizedwithTrisbuffer(0.4M;   pH7.5).Finally,theDNAwasstainedwithethidiumbromide.Imagesof100ran-domlyselectedcells(50cellsfromeachoftworeplicateslides)fromeachanimalwereblindlyanalyzedusinga   fluorescencemicroscopeequippedwithanexcitationfilterofBP546/12nmanda590nmbarrierfilter.Cellswerescoredfrom0(undam-aged)to4(maximallydamaged)accordingtothetailintensity(sizeandshape),resultingin   asingleDNAdamagescore(dam-ageindex)foreachsampleand,consequently,foreachgroup.Thus,adamageindex(DI)ofthegroupcouldrangefrom0(completelyundamaged100=cells × 0)   to400(maximumdamage=100cells × 4)(Collins,2004)   (Fig.1).Thepercentagedamagefrequency(DF)   wascalculatedforeachsampleonthebasisofthenumberofcellswithatail versus withnotail. 2.7.   Thiobarbituric   acid   reactive   species   (TBARS) Asanindexofoxidativedamage,weusedtheformationofTBARSduringanacid-heatingreaction,whichiswidelyadaptedasa   sensitivemethodformeasurementoflipidper-oxidation,aspreviouslydescribed(DraperandHadley,1990).Briefly,samplesweremixedwith1mL   oftrichloroaceticacid10%(TCA)and1mL   ofthiobarbituricacid0.67%(TBA),and Fig.2–Mean(  ± SD)valuesofdamageindexobservedinperipheralbloodofratstreatedwithgreenteaandmate   tea,oralandtopic,andsubmittedto   radiation.*Datasignificant inrelationto   controlat  P   <0.05(Kruskal–Wallis,Dunn). thenheatedina   boilingwaterbathfor15min.TBARSweredeterminedbyabsorbanceat535nm.   Resultsareexpressedas   malondialdehyde(MDA)equivalents(pmol/mgprotein). 2.8.   Measurement   of     protein   carbonyls Theoxidativedamageto   proteinswasassessedbythedeterminationofcarbonylgroupsbasedonthe   reactionwithdinitrophenylhydrazine(DNPH)aspreviouslydescribed(Levineetal.,1990).Briefly,proteinswereprecipitatedbytheadditionof20%   trichloroaceticacidandredissolvedin   DNPH,andtheabsorbancereadat370nm.   Resultsareexpressedasproteincarbonyls(pmol/mgprotein). 2.9.   Statistical   analysis FortheanalysesofDNAandoxidativedamageparameters,alldatawereexpressedasmean ±   standarddeviation(SD).Differencesamongexperimentalgroupsweredeterminedbyone-wayanalysisofvariance(ANOVA)whennormaldistri-butionwasobserved.MultiplecomparisonswereperformedbyDuncan’test.Whennonnormaldistributionwasobserved;comparisonsweremadeusingtheKruskal–WallistestwithDunn’stestas    posthoc. Inallexperiments, P <0.05was   consideredtoindicatesta-tisticalsignificance.Allanalyseswereperformedusingthe5.0BioEstatsoftware. 3.   Results Thepresentstudyshowedthatultravioletradiationexpo-surepresentedhigherlevelsofDNAdamageinperipheralbloodinbothparametersofthecometassay,damageindex(Fig.2)anddamagefrequency(Fig.3)( P <0.05;Kruskal–Wallis,Dunn).We   alsoshowedthatwasincreasedthiobarbituricacid-reactivespecieslevels(Fig.4),andproteincarbonylation(Fig.4) ( P <0.05;ANOVA–Duncan).Resultsforanimalstreatedwithboth   typesofherbsinthetwoadministrationroutesshowedthatonlymateteacansig-nificantlyreverseDNAdamagecausedbyUV   radiation,unlikegreentea,whichdoesnotpresenttheseprotectiveeffectsforthegenome,as   observedinthe   highlevelsofDNAdamagewhenorallyadministered,in   comparisontothecontrolgroup  198   e   nviro   nment   al   toxi   co   lo   g   y   andpha   r   maco   lo   gy   37(   2   014)   195–201 Fig.3–Mean(  ± SD)valuesofdamagefrequencyobservedinperipheralbloodofratstreatedwithgreenteaandmatetea,oralandtopic,andsubmittedtoradiation.*Datasignificantin   relationto   controlat  P   <0.05(Kruskal–Wallis,Dunn). ( P <0.05;Kruskal–Wallis,Dunn).However,bothparametersof thecometassay(Figs.2and3)   revealedthatthisherbledtoasimilardecreaseinDNAdamagein   animalstopicallytreatedwithmatetea.Furthermore,weobservedthatoralandtopictreatmentswithgreenteaor   mateteapreventedtheincreasedlipidper-oxidationinducedbyultravioletradiationexposure(Fig.4)( P <0.05;ANOVA–Duncan).However,proteincarbonylationwasonlypreventedbytopictreatmentwithgreenteagel   andmateteagel.Oraltreatmentwithgreenormateteasdid   notpreventtheincreasein   proteincarbonylationcausedbyultra-violetradiationexposure(Fig.5)( P <0.05;ANOVA–Duncan). 4.   Discussion Exposureto   solarultravioletradiationinducesinflammatoryresponses,oxidativestress,immunosuppression,DNAdam-ageandgenemutations,eventsrelatedto   skindiseases,includingskincancer(Katiyaretal.,2000,2007;Katiyar,2006).Multiplestudieshavedemonstratedarelationshipbetweenultravioletexposureandincreasedriskofdevelopingskincancer.Itwas   postulatedthatexposureofthe   skintosolarultravioletlightis   a   majorriskfactorforthedevelopmentof malignantmelanomaandnon-melanomaskincancer,and Fig.4–Mean(  ± SD)valuesofthiobarbituricacid   reactivesubstances(TBARS)in   skinofratstreatedwithgreenteaandmate   tea,oralandtopic,andsubmittedtoradiation.*Datasignificantinrelationtocontrolat    P <0.05(one-wayANOVA,Duncantest).Fig.5–Mean(  ± SD)valuesofproteincarbonylcontentinskinofratstreatedwithgreenteaandmate   tea,oralandtopic,andsubmittedtoradiation.*Datasignificantinrelationtocontrolat  P <0.05(one-wayANOVA,Duncantest). thatthiseffectis   mediatedbya   chainofevents,including DNAdamagebyultravioletlightandsubsequentformationofmutations(Runger,2003).Inthelifeofa   cell,DNAdamagerepresentsa   greatthreattogenomestability,leadingtolossor   amplificationofchromosomalactivity,whichmay   resultin   carcinogene-sisor   tissueaging(Nakanishietal.,2009).   Genomeintegrityiscontinuouslythreatenedbybothendogenous( e.g. reac-tiveoxygenspeciesproducedbynormalmetabolism,DNAreplication‘errors’)andexogenous(ultravioletlight,ionizing radiationsandchemicalcarcinogens)factors(Mocellinetal.,2009).InthepresentstudyweobservedtheoccurrenceofDNAdamagein   peripheralbloodandoxidativedamagein   the   skinofratsexposedtoradiation.Onthe   otherhand,weshowedthatgreenandmateteasadministeredthroughtwodifferentroutes(oralandtopicgel)havepreventedradiation-inducedlipidperoxidation.However,proteincarbonylationwas   pre-ventedonlybygreenandmateteasusedas   gel.   Also,onlytopicallyadministeredmateteapreventedtheharmfuleffectsofUVradiationtogeneticmaterial.ThestudyTürko ˘ gluet   al.(2010)showedthatnoUV-inducederythemawasobservedattheblackandgreenteagel   sitesinanyofthesubjects.UV-inducederythemawasconsistentlypresentin   variousgradesatcaffeinegel,carbomergel,andcontrolsites.Therefore,teaextractswerefoundtobepromis-ingcandidatesfortheirabilitytoprotectagainsttheharmfuleffectsofUVradiation,suchas   erythemaandprematureaging oftheskin.Studiesshowedthatconsumptionofgreenteapolyphe-nolsindrinkingwaterpreventsphotocarcinogenesisin   mice;however,themolecularmechanismsunderlyingthiseffecthavenotbeenfullyelucidated(Meeranetal.,2009).Studyof Xuetal.(2010)showedthatgreenteapolyphenolseffectivelysuppressedthedecreasein   viabilityoftheUVBstressedretinalpigmentepithelialcellsandtheUVBsuppressionofsurvivinggeneexpressionlevel.GreenteapolyphenolsalleviatedmitochondriadysfunctionandDNAfragmentationinducedbyUVB.Polyphenolsisolatedfromtheleavesofgreenteahavea   numberofbeneficialhealthyeffects,includinganti-carcinogenicactivity,whichhasbeendemonstratedin   various  env   i   r   o   nm   enta   lt   o   xico   l   o   g   y   andph   ar   m   ac   o   l   o   g   y   37   (20   14)   195–201 199 tumormodels(KatiyarandMukhtar,1996;Yangetal.,2002).Ithasbeenalsoshownthatoraladministrationof anaqueousextractofgreenteaorgreenteapolyphe-nols(amixtureofpolyphenols)in   drinkingwaterinhibitsultravioletradiation-inducedskincarcinogenesisinmiceintermsoftumorincidence,tumormultiplicityandtumorgrowth/size(Mantenaetal.,2005;Wanget   al.,1992).Inaddition,UVexposurecausesphysicalchangestotheskinduetoalterationsthatoccurin   the   connectivetissue via theformationoflipidperoxides,cellcontentsandenzymesandreactiveoxygenspecies(Benaigesetal.,   1998;Kauretal.,2006).Otherstudiesshowedthatgreenteaalsoexertsanti-oxidantactivity(Mantenaetal.,   2005;Okayasuetal.,2003).Flavonoidsandphenoliccompoundswereprovedtobepresentinmatetealeaves,andtheconsumptionofthesecom-poundshasbeenassociatedwiththepreventionofage-relatedchronicconditions,includingcancer(McKayandBlumberg,2002;Weisburger,2002).Variousphytochemicalconstituents,suchasflavonoids,havebeenisolatedfrommateplantsandrelatedspecies,andsomeofthesecompoundsmay   berespon-siblefortheobservedantioxidantactivity(Schinellaet   al.,2000).Furthermore,datafrom invitro and in   vivo studiessug-gestapotentialbeneficialeffectofteapolyphenolsagainstcanceratmoststagesofdevelopment(Hiroseet   al.,   2002;SuandArab,2002;Tapieroet   al.,   2002).Inthisscenery,studyof ChandraandDeMejia(2004)showedthattheconcentrationofpolyphenolsingreenteaismajorwhencomparedwithmatetea.Thus,the   concentra-tionofgreenandmateteausedinthepresentstudyresultinamountspolyphenolssimilarin   bothteas.Conversely,many   studiesincellculturemodelsaswellasinanimalsseemtoconvergetoshowan   antimutagenicandDNAprotectingeffectfor I.paraguariensis extractsanditsindividualcomponents,chlorogenicacid,rutinandquercetin(Bracescoetal.,   2003;Mirandaetal.,2008).Studyof Leonardetal.(2010)indicatedthatmatescavengedhydroxylradi-calsandsuperoxideradicals.Thisstudyindicatesthatmatepossessespotentantioxidanteffectsagainsthydroxylandsuperoxideradicalsinchemicalandcellculturesystems,aswellasDNA-protectiveproperties.Besides,studyof Mirandaetal.(2008)showedthatmateteaisnotgenotoxicin   liver,kidneyandbladdercells.Theregularingestionofmateteaincreasedtheresistanceof DNAtoH 2 O 2 -inducedDNAstrandbreaksandimprovedtheDNArepairafterH 2 O 2  challengeinlivercells.TheseresultssuggestthatmateteacouldprotectagainstDNAdamageandenhancetheDNArepairactivity.Protectionmay   beattributedto   theantioxidantactivityofthematebioactivecompoundscitedabove(Bracescoet   al.,2003;Mirandaetal.,2008).However,studyof Wnuk   et   al.(2009) invitro culturedhumanlymphocytesindicatesthatmateinfusionmaycausebothcytotoxicandgenotoxiceffects.Differencesconcentrationsofmatefrom1to   1000  g/mLwasevaluatedandfoundthat10  g/mLofmatesignificantlyincreasedthefrequencyof micronucleianddecreasedthe   nucleardivisionindexvalue.Atthehigherconcentrationsof100and1000  g/mL,matewasresponsibleforan   augmentationinthe   levelofapop-toticandnecroticcells.Moreover,nogenotoxiceffectofmate(175–1400  g/mL)onhumanlymphocyteswasreportedbyAlvesetal.(2008).Inconclusion,weshowedthattheexposureofratstoradia-tionledto   DNAandoxidativedamage,andthatgreenteaandmateteahavepreventedtheseeffects.Ourdataare   in   linewithpreviousworksthatdemonstratedtheanti-carcinogenicandantioxidantactivitiesofgreenteaandmatetea. Conflict    of    interest    statement  Theauthorsdeclarethattherearenoconflictsofinterest. Acknowledgment  ThisresearchwassupportedbygrantsfromUniversidadedoExtremoSulCatarinense–UNESC(Brazil). Appendix   A.   Supplementary   data Supplementarydataassociatedwiththisarticlecanbe   found,intheonlineversion,athttp://dx.doi.org/10.1016/j.etap.2013.11.028. r   ef   e   r   e   n   c   e   s Agar,N.S.,Halliday,G.M.,Barnetson,R.S.,Ananthaswamy,H.N.,Wheeler,M.,Jones,A.M.,2004.ThebasallayerinhumansquamoustumorsharborsmoreUVAthanUVBfingerprintmutations:aroleforUVAinhumanskincarcinogenesis.Proc.Natl.Acad.Sci.U.S.A.101,4954–4959.Alves,R.J.,Jotz,G.P.,doAmaral,V.S.,Montes,T.M.,Menezes,H.S.,de   Andrade,H.H.,2008.Theevaluationof    maté   ( Ilex paraguariensis )   genetictoxicityinhumanlymphocytesbythecytokinesis-blockinthemicronucleusassay.Toxicol.InVitro22,695–698.Bachelor,M.A.,Bowden,G.T.,2004.UVA-mediatedactivationof signalingpathwaysinvolvedinskintumorpromotionandprogression.Semin.CancerBiol.14,131–138.Bastos,D.H.,Ishimoto,E.Y.,Marques,M.O.M.,Ferri,A.F.,Torres,E.A.F.S.,2006.Essentialoilandantioxidantactivityofgreenmateandmatetea( Ilexparaguariensis )infusions.J.FoodCompos.Anal.19,538–543.Benaiges,A.,Marcet,P.,Armengol,R.,Betes,C.,Gironés,E.A.,1998.Studyoftherefirmingeffectof    a   plantcomplex.Int.J.Cosmet.Sci.20,223–233.Bracesco,N.,Dell,M.,Rocha,A.,Behtash,S.,Menini,T.,Gugliucci,A.,Nunes,E.,2003.Antioxidantactivityofabotanicalextractpreparationof  Ilexparaguariensis :preventionofDNAdouble-strandbreaksin Saccharomycescerevisiae andhumanlow-densitylipoproteinoxidation.J.Altern.ComplementMed.9,379–387.Chandra,S.,DeMejia,G.E.,2004.Polyphenoliccompounds,antioxidantcapacity,andquinonereductaseactivityofanaqueous   extractof   Ardisiacompressa incomparisonto   mate( Ilexparaguariensis )andgreen( Camelliasinensis )   teas.J.Agric.FoodChem.52,3583–3589.Collins,A.R.,2004.ThecometassayforDNAdamageandrepair:principles,applications,andlimitations.Mol.Biotechnol.26,249–326.Draper,H.H.,Hadley,M.,1990.Malondialdehydedeterminationasindexof    lipidperoxidation.MethodsEnzymol.186,421–431.
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