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March,2014

Exhibit E: An Update on the Genetic Effects of Nonionizing Electromagnetic Fields by Prof. Henry Lai, PhD,

University of Washington, Emeritus

Introduction:

Thefollowingisanupdateofinformationandabstractsonresearchpaperspublishedsince2006/2007onthegeneticeffectsofnonionizingelectromagneticfields(EMF)intheradiofrequency(RF)andextremelylowfrequency(ELF)ranges.Twostaticmagneticfieldpapers(Jounietal.2012;Wangetal.,2009)arealsoincluded.Whereadditionalinformationisrelevant,someearlierpapers,orpapersnotspecificallyrelatedtogeneticeffects,arealsoincludedwithcitationscontainedwithinthediscussionbelow.Alistofabstracts,withsummarysentencesunderlinedforreaderconvenience,canbefoundattheendofthispaper.

Analysisoftheserecentpublicationsshowsthattherearemorepapersreportingeffectsthannoeffect.WithErepresentingabiologicaleffect,andNErepresentingnobiologicaleffects,therecentliteraturefindsRFRgeneticeffectsat:E=74publications(65%);NE=40publications(35%);andELFgeneticeffectsat:E=49(83%);NE=10(17%).Discussion:1. TheeffectsofbothRFandELFfieldsareverysimilar.Thisissurprisingbecausethe

energiescarriedbytheseEMFsarebillionsoffoldsdifferent.AnexplanationforsimilargeneticeffectshasbeenprovidedbyarecentpaperbyBlankandGoodman(BlankM,GoodmanR.DNAisafractalantennainelectromagneticfields.Int.J.Radiat.Biol.87(4):409415,2011)inwhichtheystatedthatthewidefrequencyrangeofinteractionwithEMFisthefunctionalcharacteristicofafractalantenna,andDNAappearstopossessthetwostructuralcharacteristicsoffractalantennas,electronicconductionandselfsymmetry.However,similaritiesineffectsbetweenELFandRFfieldshavealsobeenreportedinstudiesofotherphysiologicalprocesses,e.g.,neurochemicalandbehavioraleffects(Cf.Lai,H.,Carino,M.A.,Horita,A.andGuy,A.W.Opioidreceptorsubtypesthatmediateamicrowaveinduceddecreaseincentralcholinergicactivityintherat.Bioelectromagnetics13:237246,1992;Lai,H.andCarino,M.A.Intracerebroventricularinjectionsofmuanddeltaopiatereceptorantagonistsblock60Hzmagneticfieldinduceddecreasesincholinergicactivityinthefrontalcortexandhippocampusoftherat.Bioelectromagnetics19:433437,1998;Lai,H.,Carino,M.A.andUshijima,I.Acuteexposuretoa60Hzmagneticfieldaffectsrats'performanceinthewatermaze.Bioelectromagnetics19:117122,1998;Wang,B.M.andLai,H.Acuteexposuretopulsed2450MHzmicrowavesaffectswatermazelearningintherat.Bioelectromagnetics21:5256,2000.)Thus,thereisabasicinteractionmechanismofbiologicaltissueswithelectromagneticfieldsthatisindependentoffrequency.

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ManystudieshaveimplicatedtheinvolvementoffreeradicalprocessesinthegeneticeffectsofEMF:ELFEMF(Butdaketal.,2012;Jounietal.,2012;Luukkonenetal.,2014;Tiwarietal.,2014);RFR(Agarwaletal.,2009;Atasoyetal.,2012;Burlakaetal.,2013;Campisietal.,2010;DeIuliisetal.,2009;Esmekayaetal.,2011;Ferreiraetal.,2006;GajskiandGarajVrhovac,2009;GarajVrhovacetal.,2011;Guleretal.,2010,2012;KesariandBehari,2009;Kesarietal.,2010;Khaliletal.,2012;Kumaretal.,2010;Liuetal.,2013a,b;Luukkonanetal.,2009;Tomruketal.,2010;Tkalecetal.,2013;Wuetal.,2008;Xuetal.,2010;Yaoetal.,2003).IncreaseinfreeradicalactivityandchangesinenzymesinvolvedincellularoxidativeprocessesarethemostconsistenteffectsobservedincellsandanimalsafterEMFexposure.However,theyarereportsindicatingthatEMFcouldinducegeneticeffectswithouttheinvolvementoffreeradicals(ELFAlcarazetal.,2013;RFRFerreiraetal.,2006;FurtadoFilhoetal.,2013)andincreaseinfreeradicalafterEMFexposuredidnotleadtogeneticeffects(Frahmetal.,2006).ThereareatleastacoupleofhundredpublishedpapersontheeffectsofEMFexposureoncellularoxidativeprocesses.ManybiologicaleffectsofEMFcanbeexplainedbyintracellularchangesinoxidativestatus,includingthegeneticeffectsreportedinthisreview.

2. AnimportantobservationofthestudiesisthatEMFcaninteractwithotherentitiesand

synergisticallycausegeneticeffects.Theseentitiesinclude:ELFEMFcisplastin(Buldaketal.,2012;ElBialyetal.,2013),bleomycin(Choetal.,2007),gadolinium(Choetal.,2014);hydrogenperoxideandmethylmethanesulfonate(Koyamaetal.,2008),menadione(Luukkonanetal.,2011,2014;Markkanenetal.,2008),ionizingradiation(Mairsetal.,2007;Journietal.,2012Yoonetal.,2014);RFRchemicalmutagens(Baohongetal.,2005),clastogens(Kimetal.,2008),xrays(Mantietal.,2008),ultravioletray(Baohongetal.,2007),aphidicolin(Tiwarietal.,2008),picrotoxin(LpezMartnetal.,2009),doxorubicin(Zhijianetal.,2010),andincoherentelectromagneticnoise(Wuetal.,2008;Yaoetal.,2008).MostofthecompoundsthatinteractwithEMFaremutagens.Thisisimportantbecauseinreallifesituations,apersonisusuallyexposedtomanydifferentenvironmentalfactorssimultaneously.SynergismofthesefactorswithEMFshouldbeconsideredmoreseriously.

3. Severallongterm/repeatedexposurepapersareincludedinthisupdate:ELFEMF

(Borhanietal.,2011;Cuccurazzuetal.,2010;Erdaletal.,2007;FedrowitzandLoscher,2012;Mariuccietal.,2010;Panagopoulousetal.,2013;Udroiuetal.,2006),andRFR(Asasoyetal.,2012;AtliSerkerogluetal.,2013;Burlakaetal.,2013;Chavdoulaetal.,2010;Deshmukhetal.,2013;Ferreiraetal.,2006;GarajVrhovacetal.,2011;Guleretal.,2010,2012;KesariandBehari,2009;Kesarietal.,2010;Lakshmietal.,2010;PaulrajandBehari,2006;Tomruketal.,2010;Yanetal.,2008).ThesedataareimportantintheunderstandingofthebiologicaleffectsofEMFexposureinreallifesituation,sincehumanenvironmentalEMFexposureisbothchronicandintermittent.Withintheselongtermexposurestudies,thereareseveralthatinvestigatedtheeffectofEMFexposureondevelopinganimals(ELFEMF:Borhanietal.,2011;Cuccurazzuetal.,2010;

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Panagopoulousetal.,2013;Udroiuetal.,2006,RFR:Burlakaetal.,2013;Ferreiraetal.,2006;Guleretal.,2010,2012;Serkerogluetal.,2013;Tomruketal.,2010;Zalataetal.,Inpress).DataofeffectsofEMFexposureongrowthanddevelopmentofyounganimalsareurgentlyneeded.ThereareseveralstudiesindicatingthatRFRmayaffectreproduction,particularlywitheffectsonspermphysiologyandDNA(Agarwaletal.,2009;Atasoyetal.,2012;Avendanoetal.,2012;Chavdoulaetal.,2010;deIuliisetal.,2009;Liuetal.,2013b;Panagopoulousetal.,2007).SimilareffectsofELFEMFonspermhavealsobeenreported,e.g., HongR,ZhangY,LiuY,WengEQ.EffectsofextremelylowfrequencyelectromagneticfieldsonDNAoftesticularcellsandspermchromatinstructureinmice.ZhonghuaLaoDongWeiShengZhiYeBingZaZhi.23(6):414417,2005; IorioR,ScrimaglioR,RantucciE,DelleMonacheS,DiGaetanoA,FinettiN,FrancavillaF,SantucciR,TettamantiE,ColonnaR.Apreliminarystudyofoscillatingelectromagneticfieldeffectsonhumanspermatozoonmotility.Bioelectromagnetics.28(1):7275,2007; IorioR,DelleMonacheS,BennatoF,DiBartolomeoC,ScrimaglioR,CinqueB,ColonnaRC.InvolvementofmitochondrialactivityinmediatingELFEMFstimulatoryeffectonhumanspermmotility.Bioelectromagnetics.32(1):1527,2011.

4. Anotherareathatneedsmoreresearchisthebiologicaleffectsoflowintensity

exposure.ThisisparticularlytrueforELFEMF,sinceintensitiesofELFEMFintheenvironmentareinmicrotesla(T)levels.TherearemanystudiesonbiologicaleffectsoflowintensityRFR(seeTable1inLevitt,B.B.andLai,H.Biologicaleffectsfromexposuretoelectromagneticradiationemittedbycelltowerbasestationsandotherantennaarrays.Environ.Rev.18:369395,2010.)However,mostcellandanimalstudiesinELFEMFusedfieldsinthemillitesla(mT)level.ExceptionsarethestudyofSarimovetal.(2011)listedbelowinthereferencesectionandthestudyofdeBruynanddeJager(2010)(deBruynLanddeJagerL.Effectoflongtermexposuretoarandomlyvaried50Hzpowerfrequencymagneticfieldonthefertilityofthemouse.Electromag.Biol.Med.29(12):5261,2010).

5. TwootherimportantfindingsoftheserecentstudiesarethattheeffectsofEMFare

showntobewaveformspecificandcelltypespecific.Regardingwaveformspecificity,Campisietal.(2010)reportedincreasesinfreeradicalactivityandDNAfragmentationinbraincellsafteracuteexposuretoa50Hzamplitudemodulated900MHzRFR,whereasacontinuouswave9000MHzfieldproducednoeffect.Franzellittietal.(2010)showedincreasedDNAstrandbreaksintrophoblastsafterexposuretoa217Hzmodulated1.8GHzRFR,butacontinuouswavefieldofthesamecarrierfrequencywaswithouteffect.Tkalecetal(2013)reportedthatAMmodulated(1KHzsinusoidal)900MHzRFRismorepotentthannonmodulatedfieldincausingDNAdamageincoelomocytesofexposedearthworms.Luukkonenetal.(2009)reportedacontinuouswave872MHzRFRincreasedchemicallyinducedDNAstrandbreaksandfreeradicalsinhumanneuroblastomacells,whereasaGSMmodulated872MHzfieldhadnosignificanteffect.Zhangetal.(2008)foundthatgeneexpressioninratneuronsismoresensitivetointermittentthancontinuousexposuretoa1.8GHzRFR.LpezMartnetal.(2009)

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foundthatGSMandunmodulatedRFRcauseddifferenteffectsoncFosgeneexpressionintheratbrain.Regardingcelltypespecificity,NylundandLeszczynski(2006)andRemondinietal.(2006)reporteddifferentpatternsofgeneexpressionindifferenttypesofcellsafterexposuretoRFR.Zhaoetal.(2007)foundthanneuronsaremoresensitivetoa1.9GHzcellphoneradiationthanastrocytes.Schwarzetal.(2008)reportedDNAstrandbreaksandmicronucleusformationinhumanfibroblasts,butnotinlymphocytes,afterexposuretoa1950MHzUMTSfield.Furthermore,Xuetal(2013)foundDNAdamagesinsomecelltypesandnotinothersafterexposureto1800MHzRFR.Valbonesietat.(2014)reportedthatHSP70expressionandMAPKsignalingpathwaysinPC12cellswereaffectedbyGSM217HzsignalandnotbyCWorGSMtalksignals.InELFEMresearch,Giorgietal.(2011)foundthatDNAtranspositioninE.coliwasdecreasedafterexposuretoasinusoidalmagneticfieldandincreasedafterexposuretoapulsedmagneticfield.Kimetal.(2012)describedDNAstrandbreaksinhumanfibroblastsafterexposuretoELFmagneticfield.TheyfoundthatthepatternofchangesdependedontheeddycurrentandLorentzforceinthefield.Nahabetal.(2007)reportedthatasquarecontinuousELFmagneticfieldwasmoreeffectivethansinusoidalcontinuousorpulsedfieldininducingsisterchromatidexchangeinhumanlymphocytes.ThesefindingsunderscorethecomplicityofinteractionofEMFwithbiologicaltissuesandmaypartiallyexplainwhyeffectswereobservedinsomestudiesandnotothers.ItisessentialtounderstandwhyandhowcertainwavecharacteristicsofanEMFaremoreeffectivethanothercharacteristicsincausingbiologicaleffects,andwhycertaintypesofcellsaremoresusceptibletotheeffectofEMF?ThattherearedifferentbiologicaleffectselicitedbydifferentEMFwavecharacteristicsiscriticalprooffortheexistenceofnonthermaleffects.

6. Manybiological/healtheffectshavebeenreportedincellsandanimalsafterexposuretoEMFsinboththeELFandRFranges.(SixtyfivepercentoftheRFRpapersand82%oftheELFEMFpapersinthepublicationlistbelowreportedeffects.)ItishighlydishonestforascientisttosummarilydenytheexistenceofbiologicaleffectsofEMF.AbiologicaleffectofEMFcanbedetrimentaltohealth,butcanalsobeturnedintoabeneficialmeansforthetreatmentofhumandiseases.Denyinganyeffectshampersthedevelopmentofelectromagnetictreatmentsfordiseases.ExamplesofpossibleclinicalusesofEMFare:Alzheimersdisease(ArendashGW,SanchezRamosJ,MoriT,MamcarzM,LinX,RunfeldtM,WangL,ZhangG,SavaV,TanJ,CaoC.ElectromagneticfieldtreatmentprotectsagainstandreversescognitiveimpairmentinAlzheimer'sdiseasemice.JAlzheimersDis.19(1):191210,2010);Parkinsonsdisease(WangZ,ChePL,DuJ,HaB,YaremaKJ.StaticmagneticfieldexposurereproducescellulareffectsoftheParkinson'sdiseasedrugcandidateZM241385.PLoSOne.5(11):e13883,2010); boneregeneration(LeeHM,KwonUH,KimH,KimHJ,KimB,ParkJO,MoonES,MoonSH.Pulsedeltromagneticfieldstimulatescellularproliferationinhumanintervertebraldisccells.YonseiMed.J.51(6):954959,2010);cancertreatment(CostaFP,deOliveiraAC,MeirellesR,MachadoMC,ZanescoT,SurjanR,ChammasMC,deSouzaRochaM,MorganD,CantorA,ZimmermanJ,BrezovichI,KusterN,BarbaultA,PascheB.

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Treatmentofadvancedhepatocellularcarcinomawithverylowlevelsofamplitudemodulatedelectromagneticfields.Br.J.Cancer.105(5):640648,2011),andtissueregeneration(GaetaniR,LeddaM,BarileL,ChimentiI,DeCarloF,ForteE,IontaV,GiulianiL,D'EmiliaE,FratiG,MiraldiF,PozziD,MessinaE,GrimaldiS,GiacomelloA,LisiA.Differentiationofhumanadultcardiacstemcellsexposedtoextremelylowfrequencyelectromagneticfields.Cardiovasc.Res.82(3):411420,2009).

7. Itmustbepointedoutthat,consistentwithpreviousresearch,notverymuchofthecellularandanimalgeneticresearchdatadirectlyindicatethatEMF(bothRFandELFEMF)isacarcinogen.However,thedatashowthatEMFcanpossiblyaltergeneticfunctionsandthusitisadvisablethatoneshouldlimitonesexposuretoEMF.

Referencesandabstracts

Belowisakeytoabbreviationsusedthroughoutthefollowinglistofabstractsforrecentpaperspublishedsince2006andserveasmycommentstohelpthereaderquicklyidentifythesignificanceofeachwork.Thesummarysentencesbyeachauthorareunderlined.ThelistisdividedintoRFeffectspapers,andELFeffectspapers.

(Eeffectobserved;NEnoeffectobserved)(LElongtermexposure;GTgenotoxiceffect,e.g.,DNAdamage,micronucleusformation,chromosomealterations;GEgeneexpression;HUhumanstudy;OXoxidativeeffects,i.e.,involvementoffreeradicalsandoxidativeenzymes;IAinteractionwithotherfactorstocausegeneticeffects;DEeffectsondevelopinganimals;RPreproduction,e.g.,spermdamage;EHcomparedwithelectrohypersensitivesubjects;WSwaveformspecificeffect,e.g.,modulationandfrequency;CScelltypespecificeffect).

Anupdateontheresearchongeneticeffectsofradiofrequency/cellphoneradiation

(E)AgarwalA,DesaiNR,MakkerK,VargheseA,MouradiR,SabaneghE,SharmaR.Effectsofradiofrequencyelectromagneticwaves(RFEMW)fromcellularphonesonhumanejaculatedsemen:aninvitropilotstudy.FertilSteril9213181325,2009.(GT,RP,OX)

OBJECTIVE:Toevaluateeffectsofcellularphoneradiofrequencyelectromagneticwaves(RFEMW)duringtalkmodeonunprocessed(neat)ejaculatedhumansemen.DESIGN:Prospectivepilotstudy.SETTING:Centerforreproductivemedicinelaboratoryintertiaryhospitalsetting.SAMPLES:Neatsemensamplesfromnormalhealthydonors(n=23)andinfertilepatients(n=9).INTERVENTION(S):Afterliquefaction,neatsemensamplesweredividedintotwoaliquots.Onealiquot(experimental)fromeachpatientwasexposedtocellularphoneradiation(intalkmode)for1h,andthesecondaliquot(unexposed)servedasthecontrolsampleunderidenticalconditions.MAINOUTCOMEMEASURE(S):Evaluationofspermparameters(motility,viability),reactiveoxygenspecies(ROS),totalantioxidantcapacity(TAC)ofsemen,ROSTACscore,andspermDNAdamage.RESULT(S):SamplesexposedtoRFEMWshowedasignificantdecreasein

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spermmotilityandviability,increaseinROSlevel,anddecreaseinROSTACscore.LevelsofTACandDNAdamageshowednosignificantdifferencesfromtheunexposedgroup.CONCLUSION(S):Radiofrequencyelectromagneticwavesemittedfromcellphonesmayleadtooxidativestressinhumansemen.Wespeculatethatkeepingthecellphoneinatrouserpocketintalkmodemaynegativelyaffectspermatozoaandimpairmalefertility.

(E)AtasoyHI,GunalMY,AtasoyP,ElgunS,BugdayciG.ImmunohistopathologicdemonstrationofdeleteriouseffectsongrowingrattestesofradiofrequencywavesemittedfromconventionalWiFidevices.JPediatrUrol.2012Mar30.[Epubaheadofprint](GT,OX,LE,RP)

OBJECTIVE:ToinvestigateeffectsonrattestesofradiofrequencyradiationemittedfromindoorWiFiInternetaccessdevicesusing802.11.gwirelessstandards.METHODS:TenWistaralbinomaleratsweredividedintoexperimentalandcontrolgroups,withfiveratspergroup.Standardwirelessgatewayscommunicatingat2.437GHzwereusedasradiofrequencywavesources.Theexperimentalgroupwasexposedtoradiofrequencyenergyfor24hadayfor20weeks.Theratsweresacrificedattheendofthestudy.Intracardiacbloodwassampledforserum8hydroxy2'deoxyguanosinelevels.Testeswereremovedandexaminedhistologicallyandimmunohistochemically.Testistissueswereanalyzedformalondialdehydelevelsandprooxidantantioxidantenzymeactivities.RESULTS:Weobservedsignificantincreasesinserum8hydroxy2'deoxyguanosinelevelsand8hydroxyguanosinestaininginthetestesoftheexperimentalgroupindicatingDNAdamageduetoexposure(p

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treatmentandrecoverygroups.Thecytogenotoxicdamageinimmatureratswasstatisticallyhigherthanthematurerats.Therecoveryperioddidnotreducethedamagetothesameextentasthecorrespondingcontrolgroups.Conclusions:TheexposureofRFEMFleadstocytotoxicandgenotoxicdamageinimmatureandmaturerats.MoresensitivestudiesarerequiredtoelucidatethepossiblecarcinogenicriskofEMFexposureinhumans,especiallychildren.

(E)AvendaoC,MataA,SanchezSarmientoCA,DoncelGF.UseoflaptopcomputersconnectedtointernetthroughWiFidecreaseshumanspermmotilityandincreasesspermDNAfragmentation.FertilSteril97:3945,2012.(GT,RP)

OBJECTIVE:Toevaluatetheeffectsoflaptopcomputersconnectedtolocalareanetworkswirelessly(WiFi)onhumanspermatozoa.DESIGN:Prospectiveinvitrostudy.SETTING:Centerforreproductivemedicine.PATIENT(S):Semensamplesfrom29healthydonors.INTERVENTION(S):Motilespermwereselectedbyswimup.Eachspermsuspensionwasdividedintotwoaliquots.Onespermaliquot(experimental)fromeachpatientwasexposedtoaninternetconnectedlaptopbyWiFifor4hours,whereasthesecondaliquot(unexposed)wasusedascontrol,incubatedunderidenticalconditionswithoutbeingexposedtothelaptop.MAINOUTCOMEMEASURE(S):Evaluationofspermmotility,viability,andDNAfragmentation.RESULT(S):Donorspermsamples,mostlynormozoospermic,exposedexvivoduring4hourstoawirelessinternetconnectedlaptopshowedasignificantdecreaseinprogressivespermmotilityandanincreaseinspermDNAfragmentation.Levelsofdeadspermshowednosignificantdifferencesbetweenthetwogroups.CONCLUSION(S):Toourknowledge,thisisthefirststudytoevaluatethedirectimpactoflaptopuseonhumanspermatozoa.ExvivoexposureofhumanspermatozoatoawirelessinternetconnectedlaptopdecreasedmotilityandinducedDNAfragmentationbyanonthermaleffect.Wespeculatethatkeepingalaptopconnectedwirelesslytotheinternetonthelapnearthetestesmayresultindecreasedmalefertility.Furtherinvitroandinvivostudiesareneededtoprovethiscontention.

(E)BaohongWang,JiliangH,LifenJ,DeqiangL,WeiZ,JianlinL,HongpingD.Studyingthesynergisticdamageeffectsinducedby1.8GHzradiofrequencyfieldradiation(RFR)withfourchemicalmutagensonhumanlymphocyteDNAusingcometassayinvitro.MutatRes578:14957,2005.(GT,IA)

TheaimofthisinvestigationwastostudythesynergisticDNAdamageeffectsinhumanlymphocytesinducedby1.8GHzradiofrequencyfieldradiation(RFR,SARof3W/kg)withfourchemicalmutagens,i.e.mitomycinC(MMC,DNAcrosslinker),bleomycin(BLM,radiomimeticagent),methylmethanesulfonate(MMS,alkylatingagent),and4nitroquinoline1oxide(4NQO,UVmimeticagent).TheDNAdamageoflymphocytesexposedtoRFRand/orwithchemicalmutagenswasdetectedattwoincubationtime(0or21h)aftertreatmentwithcometassayinvitro.Threecombinativeexposurewayswereused.CellswereexposedtoRFRandchemicalmutagensfor2and3h,respectively.Taillength(TL)andtailmoment(TM)wereutilizedasDNAdamageindexes.TheresultsshowednodifferenceofDNAdamageindexesbetweenRFRgroupandcontrolgroupat0and21hincubationafterexposure(P>0.05).Thereweresignificant

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differenceofDNAdamageindexesbetweenMMCgroupandRFR+MMCcoexposuregroupat0and21hincubationaftertreatment(P

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analyzedblindtotreatmentcondition.Thechangesinchromatinconformationweremeasuredwiththemethodofanomalousviscositytimedependencies(AVTD).53BP1protein,whichhasbeenshowntocolocalizeinfociwithDNAdoublestrandbreaks(DSBs),wasanalyzedbyimmunostaininginsitu.Exposureatroomtemperaturetoeither915MHzor50Hzresultedinsignificantcondensationofchromatin,shownasAVTDchanges,whichwassimilartotheeffectofheatshockat41degreesC.Nosignificantdifferencesinresponsesbetweennormalandhypersensitivesubjectsweredetected.Neither915MHznor50Hzexposureinduced53BP1foci.Onthecontrary,adistinctdecreaseinbackgroundlevelof53BP1signalingwasobservedupontheseexposuresaswellasafterheatshocktreatments.ThisdecreasecorrelatedwiththeAVTDdataandmayindicatedecreaseinaccessibilityof53BP1toantibodiesbecauseofstressinducedchromatincondensation.ApoptosiswasdeterminedbymorphologicalchangesandbyapoptoticfragmentationofDNAasanalyzedbypulsedfieldgelelectrophoresis(PFGE).Noapoptosiswasinducedbyexposureto50Hzand915MHzmicrowaves.Inconclusion,50Hzmagneticfieldand915MHzmicrowavesunderspecifiedconditionsofexposureinducedcomparableresponsesinlymphocytesfromhealthyandhypersensitivedonorsthatweresimilarbutnotidenticaltostressresponseinducedbyheatshock.

(E)BelyaevIY,KochCB,TereniusO,RoxstromLindquistK,MalmgrenLO,HSommerW,SalfordLG,PerssonBR.Exposureofratbrainto915MHzGSMmicrowavesinduceschangesingeneexpressionbutnotdoublestrandedDNAbreaksoreffectsonchromatinconformation.Bioelectromagnetics27:295306,2006.(GE)

Weinvestigatedwhetherexposureofratbraintomicrowaves(MWs)ofglobalsystemformobilecommunication(GSM)inducesDNAbreaks,changesinchromatinconformationandingeneexpression.AnexposureinstallationwasusedbasedonatestmobilephoneemployingaGSMsignalat915MHz,allstandardmodulationsincluded,outputpowerlevelinpulses2W,specificabsorptionrate(SAR)0.4mW/g.RatswereexposedorshamexposedtoMWsduring2h.Afterexposure,cellsuspensionswerepreparedfrombrainsamples,aswellasfromspleenandthymus.Foranalysisofgeneexpressionpatterns,totalRNAwasextractedfromcerebellum.Changesinchromatinconformation,whichareindicativeofstressresponseandgenotoxiceffects,weremeasuredbythemethodofanomalousviscositytimedependencies(AVTD).DNAdoublestrandbreaks(DSBs)wereanalyzedbypulsedfieldgelelectrophoresis(PFGE).EffectsofMWexposurewereobservedonneitherconformationofchromatinnorDNADSBs.GeneexpressionprofileswereobtainedbyAffymetrixU34GeneChipsrepresenting8800ratgenesandanalyzedwiththeAffymetrixMicroarraySuite(MAS)5.0software.Incerebellumfromallexposedanimals,11geneswereupregulatedinarangeof1.342.74foldandonegenewasdownregulated0.48fold(P

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(E)BelyaevIY,MarkovE,HillertL,MalmgrenLO,PerssonBR.MicrowavesfromUMTS/GSMmobilephonesinducelonglastinginhibitionof53BP1/gammaH2AXDNArepairfociinhumanlymphocytes.Bioelectromagnetics30:12941,2009.(GT,EH)

Wehaverecentlydescribedfrequencydependenteffectsofmobilephonemicrowaves(MWs)ofglobalsystemformobilecommunication(GSM)onhumanlymphocytesfrompersonsreportinghypersensitivitytoelectromagneticfieldsandhealthypersons.ContrarytoGSM,universalglobaltelecommunicationssystem(UMTS)mobilephonesemitwidebandMWsignals.Hypothetically,UMTSMWsmayresultinhigherbiologicaleffectscomparedtoGSMsignalbecauseofeventual"effective"frequencieswithinthewideband.Here,wereportforthefirsttimethatUMTSMWsaffectchromatinandinhibitformationofDNAdoublestrandbreakscolocalizing53BP1/gammaH2AXDNArepairfociinhumanlymphocytesfromhypersensitiveandhealthypersonsandconfirmthateffectsofGSMMWsdependoncarrierfrequency.Remarkably,theeffectsofMWson53BP1/gammaH2AXfocipersistedupto72hfollowingexposureofcells,evenlongerthanthestressresponsefollowingheatshock.Thedataareinlinewiththehypothesisthatthetypeofsignal,UMTSMWs,mayhavehigherbiologicalefficiencyandpossiblylargerhealthriskeffectscomparedtoGSMradiationemissions.Nosignificantdifferencesineffectsbetweengroupsofhealthyandhypersensitivesubjectswereobserved,exceptfortheeffectsofUMTSMWsandGSM915MHzMWsontheformationoftheDNArepairfoci,whichweredifferentforhypersensitive(P0.05).ThenonparametricstatisticsusedheredidnotindicatespecificityofthedifferencesrevealedbetweentheeffectsofGSMandUMTSMWsoncellsfromhypersensitivesubjectsandmoredataareneededtostudythenatureofthesedifferences.

(NE)BourthoumieuS,JoubertV,MarinB,CollinA,LevequeP,TerroF,YardinC.CytogeneticstudiesinhumancellsexposedinvitrotoGSM900MHzradiofrequencyradiationusingRbandedkaryotyping.RadiatRes174:712718,2010.(GT)

Itisimportanttodeterminethepossibleeffectsofexposuretoradiofrequency(RF)radiationonthegeneticmaterialofcellssincedamagetotheDNAofsomaticcellsmaybelinkedtocancerdevelopmentorcelldeathanddamagetogermcellsmayleadtogeneticdamageinnextandsubsequentgenerations.TheobjectiveofthisstudywastoinvestigatewhetherexposuretoradiofrequencyradiationsimilartothatemittedbymobilephonesofsecondgenerationstandardGlobalSystemforMobileCommunication(GSM)inducesgenotoxiceffectsinculturedhumancells.ThecytogeneticeffectsofGSM900MHz(GSM900)RFradiationwereinvestigatedusingRbandedkaryotypingafterinvitroexposureofhumancells(amnioticcells)for24h.Theaveragespecificabsorptionrate(SAR)was0.25W/kg.Theexposureswerecarriedoutinwirepatchcells(WPCs)understrictlycontrolledconditionsoftemperature.Thegenotoxiceffectwasassessedimmediatelyor24hafterexposureusingfourdifferentsamples.Onehundredmetaphasecellswereanalyzedperassay.Positivecontrolswereprovidedbyusingbleomycin.WefoundnodirectcytogeneticeffectsofGSM900either0hor24hafterexposure.Tothebestofourknowledge,ourworkisthefirsttostudygenotoxicityusing

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completeRbandedkaryotyping,whichallowsvisualizingallthechromosomalrearrangements,eithernumericalorstructural.

(NE)BourthoumieuS,TerroF,LevequeP,CollinA,JoubertV,YardinC.AneuploidystudiesinhumancellsexposedinvitrotoGSM900MHzradiofrequencyradiationusingFISH.IntJRadiatBiol87:400408,2011.(GT)

PURPOSE:Sincepreviousresearchfoundanincreaseintherateofaneuploidiesinhumanlymphocytesexposedtoradiofrequencies,itseemsimportanttoperformfurtherstudies.TheobjectiveofthisstudywasthentoinvestigatewhethertheexposuretoRF(radiofrequency)radiationsimilartothatemittedbymobilephonesofasecondgenerationstandard,i.e.,GlobalSystemforMobilecommunication(GSM)mayinduceaneuploidyinculturedhumancells.MATERIALSANDMETHODS:ThepotentialinductionofgenomicinstabilitybyGSM900MHzradiofrequency(GSM900)wasinvestigatedafterinvitroexposureofhumanamnioticcellsfor24htoaveragespecificabsorptionrates(SAR)of0.25,1,2and4W/kginthetemperaturerangeof36.339.7C.Theexposureswerecarriedoutinawirepatchcell(WPC).Therateofaneuploidyofchromosomes11and17wasdeterminedbyinterphaseFISH(FluorescenceInSituHybridisation)immediatelyafterindependentexposureofthreedifferentdonorsfor24h.Atleast100interphasecellswereanalysedperassay.RESULTS:Nosignificantchangeintherateofaneuploidyofchromosomes11and17wasfoundfollowingexposuretoGSM900for24hataverageSARupto4W/kg.CONCLUSION:OurstudydidnotshowanyinvitroaneuploidogeniceffectofGSMusingFISHandisnotinagreementwiththeresultsofpreviousresearch.

(NE)BourthoumieuS,MagnaudeixA,TerroF,LevequeP,CollinA,YardinC.Studyofp53expressionandposttranscriptionalmodificationsafterGSM900radiofrequencyexposureofhumanamnioticcells.Bioelectromagnetics.2012Jul5.doi:10.1002/bem.21744.[Epubaheadofprint](GE)

Thepotentialeffectsofradiofrequency(RF)exposureonthegeneticmaterialofcellsareveryimportanttodeterminesincegenomeinstabilityofsomaticcellsmaybelinkedtocancerdevelopment.Inresponsetogeneticdamage,thep53proteinisactivatedandcaninducecellcyclearrestallowingmoretimeforDNArepairoreliminationofdamagedcellsthroughapoptosis.TheobjectiveofthisstudywastoinvestigatewhethertheexposuretoRFelectromagneticfields,similartothoseemittedbymobilephonesofthesecondgenerationstandard,GlobalSystemforMobileCommunications(GSM),mayinduceexpressionofthep53proteinanditsactivationbyposttranslationalmodificationsinculturedhumancells.Thepotentialinductionofp53expressionandactivationbyGSM900wasinvestigatedafterinvitroexposureofhumanamnioticcellsfor24htoaveragespecificabsorptionrates(SARs)of0.25,1,2,and4W/kginthetemperaturerangeof36.339.7C.Theexposureswerecarriedoutusingawirepatchcell(WPC)understrictlycontrolledconditionsoftemperature.Expressionandactivationofp53byphosphorylationatserine15and37werestudiedusingWesternblotassayimmediatelyafterthreeindependentexposuresofcellculturesprovidedfromthreedifferentdonors.Bleomycinexposedcellswereusedasapositivecontrol.Accordingtoourresults,no

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significantchangesintheexpressionandactivationofthep53proteinbyphosphorylationatserine15and37werefoundfollowingexposuretoGSM900for24hataverageSARsupto4W/kginhumanembryoniccells.

(E)BurlakaA,TsybulinO,SidorikE,LukinS,PolishukV,TsehmistrenkoS,YakymenkoI.Overproductionoffreeradicalspeciesinembryonalcellsexposedtolowintensityradiofrequencyradiation.ExpOncol.35(3):219225,2013.(GT,LE,DE,OX)Aim:Longtermexposureofhumanstolowintensityradiofrequencyelectromagneticradiation(RFEMR)leadstoastatisticallysignificantincreaseintumorincidence.Mechanismsofsuchtheeffectsareunclear,butfeaturesofoxidativestressinlivingcellsunderRFEMRexposurewerepreviouslyreported.Ourstudyaimstoassessaproductionofinitialfreeradicalspecies,whichleadtooxidativestressinthecell.MaterialsandMethods:EmbryosofJapanesequailswereexposedinovotoextremelylowintensityRFEMRofGSM900MHz(0.25W/cm2)during158360hdiscontinuously(48cON,12cOFF)beforeandintheinitialstagesofdevelopment.Thelevelsofsuperoxide(O2),nitrogenoxide(NO),thiobarbituricacidreactivesubstances(TBARS),8oxo2'deoxyguanosine(8oxodG)andantioxidantenzymes'activitieswereassessedincells/tissuesof38h,5and10dayRFEMRexposedandunexposedembryos.Results:Theexposureresultedinasignificantpersistentoverproductionofsuperoxideandnitrogenoxideinembryocellsduringallperiodofanalyses.Asaresult,significantlyincreasedlevelsofTBARSand8oxodGfollowedbysignificantlydecreasedlevelsofsuperoxidedismutaseandcatalaseactivitiesweredevelopedintheexposedembryocells.Conclusion:ExposureofdevelopingquailembryostoextremelylowintensityRFEMRofGSM900MHzduringatleastonehundredandfiftyeighthoursleadstoasignificantoverproductionoffreeradicals/reactiveoxygenspeciesandoxidativedamageofDNAinembryocells.Theseoxidativechangesmayleadtopathologiesuptooncogenictransformationofcells.

(E)ButtiglioneM,RocaL,MontemurnoE,VitielloF,CapozziV,CibelliG.Radiofrequencyradiation(900MHz)inducesEgr1geneexpressionandaffectscellcyclecontrolinhumanneuroblastomacells.JCellPhysiol.213(3):759767,2007.(GE)

Manyenvironmentalsignals,includingionizingradiationandUVrays,induceactivationofEgr1gene,thusaffectingcellgrowthandapoptosis.Thepaucityandthecontroversialknowledgeabouttheeffectofelectromagneticfields(EMF)exposureofnervecellspromptedustoinvestigatethebioeffectsofradiofrequency(RF)radiationonSHSY5Yneuroblastomacells.TheeffectofamodulatedRFfieldof900MHz,generatedbyawirepatchcell(WPC)antennaexposuresystemonEgr1geneexpression,wasstudiedasafunctionoftime.ShorttermexposuresinducedatransientincreaseinEgr1mRNAlevelparalleledwithactivationoftheMAPKsubtypesERK1/2andSAPK/JNK.TheeffectsofRFradiationsoncellgrowthrateandapoptosiswerealsostudied.ExposuretoRFradiationhadanantiproliferativeactivityinSH

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SY5Ycellswithasignificanteffectobservedat24h.RFradiationimpairedcellcycleprogression,reachingasignificantG2Marrest.Inaddition,theappearanceofthesubG1peak,ahallmarkofapoptosis,washighlightedaftera24hexposure,togetherwithasignificantdecreaseinmRNAlevelsofBcl2andsurvivingenes,bothinterferingwithsignalingbetweenG2Marrestandapoptosis.Ourresultsprovideevidencethatexposuretoa900MHzmodulatedRFradiationaffectbothEgr1geneexpressionandcellregulatoryfunctions,involvingapoptosisinhibitorslikeBcl2andsurvivin,thusprovidingimportantinsightsintoapotentiallybroadmechanismforcontrollinginvitrocellviability.

(E)CamST,SeyhanN.SinglestrandDNAbreaksinhumanhairrootcellsexposedtomobilephoneradiation.IntJRadiatBiol88(5):420424,2012(GT,HU)

Purpose:Toanalyzetheshorttermeffectsofradiofrequencyradiation(RFR)exposureongenomicdeoxyribonucleicacid(DNA)ofhumanhairrootcells.Subjectsandmethods:Hairsampleswerecollectedfrom8healthyhumansubjectsimmediatelybeforeandafterusinga900MHzGSM(GlobalSystemforMobileCommunications)mobilephonefor15and30minutes.SinglestrandDNAbreaksofhairrootcellsfromthesamplesweredeterminedusingthe'cometassay'.Results:Thedatashowedthattalkingonamobilephonefor15or30minutessignificantlyincreased(p

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importanceoftheamplitudemodulationintheinteractionbetweenEMFandneocorticalastrocytes.

(E)1

CervellatiF,ValacchiG,LunghiL,FabbriE,ValbonesiP,MarciR,BiondiC,VesceF.17estradiolcounteractstheeffectsofhighfrequencyelectromagneticfieldsontrophoblasticconnexinsandintegrins.OxidMedCellLongev.2013;2013:280850.doi:10.1155/2013/280850.(GE)

Weinvestigatedtheeffectofhighfrequencyelectromagneticfields(HFEMFs)and17estradiolonconnexins(Cxs),integrins(Ints),andestrogenreceptor(ER)expression,aswellasonultrastructureoftrophoblastderivedHTR8/SVneocells.HFEMF,17estradiol,andtheircombinationinducedanincreaseofCx40andCx43mRNAexpression.HFEMFdecreasedIntalpha1and1mRNAlevelsbutenhancedIntalpha5mRNAexpression.AlltheIntsmRNAexpressionswereincreasedby17estradiolandexposuretobothstimuli.ERmRNAwasreducedbyHFEMFbutaugmentedby17estradiolaloneorwithHFEMF.ERimmunofluorescenceshowedacytoplasmiclocalizationinshamandHFEMFexposedcellswhichbecamenuclearaftertreatmentwithhormoneorbothstimuli.Electronmicroscopyevidencedalossofcellularcontactinexposedcellswhichappearedcounteractedby17estradiol.Wedemonstratethat17estradiolmodulatesCxsandIntsaswellasERexpressioninducedbyHFEMF,suggestinganinfluenceofbothstimuliontrophoblastdifferentiationandmigration.

(NE)ChangSK,ChoiJS,GilHW,YangJO,LeeEY,JeonYS,LeeZW,LeeM,HongMY,HoSonT,HongSY.Genotoxicityevaluationofelectromagneticfieldsgeneratedby835MHzmobilephonefrequencyband.EurJCancerPrev14:175179,2005.(GT,IA)(Someinteractioneffectswithchemicalsarereportedinthispaper.)

Itisstillunclearwhethertheexposuretoelectromagneticfields(EMFs)generatedbymobilephoneradiationisdirectlylinkedtocancer.WeexaminedthebiologicaleffectsofanEMFat835MHz,themostwidelyusedcommunicationfrequencybandinKoreanCDMAmobilephonenetworks,onbacterialreversemutation(Amesassay)andDNAstability(invitroDNAdegradation).IntheAmesassay,testerstrainsaloneorcombinedwithpositivemutagenwereappliedinanartificialmobilephonefrequencyEMFgeneratorwithcontinuouswaveformataspecificabsorptionrate(SAR)of4W/kgfor48h.Inthepresenceofthe835MHzEMFradiation,incubationwithpositivemutagen4nitroquinoline1oxideandcumenehydroxidefurtherincreasedthemutationrateinEscherichiacoliWP2andTA102,respectively,whilethecontraryresultsinSalmonellatyphimuriumTA98andTA1535treatedwith4nitroquinoline1oxideandsodiumazide,respectively,wereshownasantimutagenic.However,thesemutagenicorcomutageniceffectsof835MHzradiationwerenotsignificantlyrepeatedinotherrelevantstrainswithsamemutationtype.IntheDNAdegradationtest,theexposureto835MHzEMFdidnotchangetherateofdegradationobservedusingplasmidpBluescriptSK(+)asanindicator.

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Thus,wesuggestthat835MHzEMFundertheconditionsofourstudyneitheraffectedthereversemutationfrequencynoracceleratedDNAdegradationinvitro.

(NE)ChauhanV,MariampillaiA,BellierPV,QutobSS,GajdaGB,LemayE,ThansandoteA,McNameeJP.Geneexpressionanalysisofahumanlymphoblastomacelllineexposedinvitrotoanintermittent1.9GHzpulsemodulatedradiofrequencyfield.RadiatRes.165(4):424429,2006.(GE)

Thisstudywasdesignedtodeterminewhetherradiofrequency(RF)fieldsofthetypeusedforwirelesscommunicationscouldelicitacellularstressresponse.Asgeneralindicatorsofacellularstressresponse,wemonitoredchangesinprotooncogeneandheatshockproteinexpression.Exponentiallygrowinghumanlymphoblastomacells(TK6)wereexposedto1.9GHzpulsemodulatedRFfieldsataveragespecificabsorptionrates(SARs)of1and10W/kg.PerturbationsintheexpressionlevelsoftheprotooncogenesFOS,JUNandMYCafterexposuretoshamandRFfieldswereassessedbyrealtimeRTPCR.Inaddition,thetranscriptlevelsofthecellularstressproteinsHSP27andinducibleHSP70werealsomonitored.WedemonstratedthattranscriptlevelsofthesegenesinRFfieldexposedcellsshowednosignificantdifferenceinrelationtotheshamtreatmentgroup.However,concurrentpositive(heatshock)controlsamplesdisplayedasignificantelevationintheexpressionofHSP27,HSP70,FOSandJUN.Conversely,thelevelsofMYCmRNAwerefoundtodeclineinthepositive(heatshock)control.Inconclusion,ourstudyfoundnoevidencethatthe1.9GHzRFfieldexposurecausedageneralstressresponseinTK6cellsunderourexperimentalconditions.

(NE)ChauhanV,MariampillaiA,GajdaGB,ThansandoteA,McNameeJP.Analysisofprotooncogeneandheatshockproteingeneexpressioninhumanderivedcelllinesexposedinvitrotoanintermittent1.9GHzpulsemodulatedradiofrequencyfield.IntJRadiatBiol.82(5):347354,2006.(GE)

Purpose:Severalstudieshavereportedthatradiofrequency(RF)fields,asemittedbymobilephones,maycausechangesingeneexpressioninculturedhumancelllines.Thecurrentstudywasundertakentoevaluatethispossibilityintwohumanderivedimmunecelllines.Materialsandmethods:HL60andMonoMac6(MM6)cellswereindividuallyexposedtointermittent(5minon,10minoff)1.9GHzpulsemodulatedRFfieldsataaveragespecificabsorptionrate(SAR)of1and10W/kgat37+/0.5degreesCfor6h.Concurrentnegativeandpositive(heatshockfor1hat43degreesC)controlswereconductedwitheachexperiment.ImmediatelyfollowingRFfieldexposure(T=6h)and18hpostexposure(T=24h),cellpelletswerecollectedfromeachoftheculturedishesandanalyzedfortranscriptlevelsofprotooncogenes(cjun,cmycandcfos)andthestressrelatedgenes(heatshockproteins(HSP)HSP27andHSP70B)byquantitativereversetranscriptasepolymerasechainreaction(RTPCR).Results:NosignificanteffectswereobservedinmRNAexpressionofHSP27,HSP70,cjun,cmycorcfosbetweentheshamandRFexposedgroups,ineitherofthetwocelllines.However,thepositive

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(heatshock)controlgroupdisplayedasignificantelevationintheexpressionofHSP27,HSP70,cfosandcjuninbothcelllinesatT=6and24h,relativetotheshamandnegativecontrolgroups.Conclusion:Thisstudyfoundnoevidencethatexposureofcellstononthermalizinglevelsof1.9GHzpulsemodulatedRFfieldscancauseanydetectablechangeinstressrelatedgeneexpression.

(NE)ChauhanV,QutobSS,LuiS,MariampillaiA,BellierPV,YaukCL,DouglasGR,WilliamsA,McNameeJP.Analysisofgeneexpressionintwohumanderivedcelllinesexposedinvitrotoa1.9GHzpulsemodulatedradiofrequencyfield.Proteomics.7(21):38963905,2007.(GE)

Thereisconsiderablecontroversysurroundingthebiologicaleffectsofradiofrequency(RF)fields,asemittedbymobilephones.Previousworkfromourlaboratoryhasshownnoeffectrelatedtotheexposureof1.9GHzpulsemodulatedRFfieldsontheexpressionof22,000genesinahumanglioblastomaderivedcellline(U87MG)at6hfollowinga4hRFfieldexposureperiod.Asafollowuptothisstudy,wehavenowexaminedtheeffectofRFfieldexposureonthepossibleexpressionoflateonsetgenesinU87MGcellsaftera24hRFexposureperiod.Inaddition,ahumanmonocytederivedcellline(MonoMac6,MM6)wasexposedtointermittent(5minON,10minOFF)RFfieldsfor6handthengeneexpressionwasassessedimmediatelyafterexposureandat18hpostexposure.Bothcelllineswereexposedto1.9GHzpulsemodulatedRFfieldsfor6or24hatspecificabsorptionrates(SARs)of0.110.0W/kg.Insupportofourpreviousresults,wefoundnoevidencethatnonthermalRFfieldexposurecouldaltergeneexpressionineitherculturedU87MGorMM6cells,relativetononirradiatedcontrolgroups.However,exposureofbothcelllinestoheatshockconditions(43degreesCfor1h)causedanalterationintheexpressionofanumberofwellcharacterizedheatshockproteins.

(E)ChavdoulaED,PanagopoulosDJ,MargaritisLH.ComparisonofbiologicaleffectsbetweencontinuousandintermittentexposuretoGSM900MHzmobilephoneradiation:detectionofapoptoticcelldeathfeatures.MutatRes700:5161,2010.(RP,LE,GT)

Inthepresentstudyweuseda6mindailyexposureofdipteranflies,Drosophilamelanogaster,toGSM900MHz(GlobalSystemforMobileTelecommunications)mobilephoneelectromagneticradiation(EMR),tocomparetheeffectsbetweenthecontinuousandfourdifferentintermittentexposuresof6mintotalduration,andalsototestwhetherintermittentexposureprovidesanycumulativeeffectsontheinsect'sreproductivecapacityaswellasontheinductionofapoptoticcelldeath.Accordingtoourpreviousexperiments,a6mincontinuousexposureperdayforfivedaystoGSM900MHzandDCS1800MHz(DigitalCellularSystem)mobilephoneradiation,broughtaboutalargedecreaseintheinsect'sreproductivecapacity,asdefinedbythenumberofFpupae.ThisdecreasewasfoundtobenonthermalandcorrelatedwithanincreasedpercentageofinducedfragmentedDNAintheeggchambers'cellsatearlyandmidoogenesis.Inthepresentexperimentsweshowthatintermittentexposurealsodecreasesthereproductivecapacityandalterstheactincytoskeletonnetworkoftheeggchambers,anotherknownaspectofcelldeaththatwasnotinvestigatedinpreviousexperiments,andthattheeffectisalsoduetoDNAfragmentation.Intermittentexposureswith

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10minintervalsbetweenexposuresessionsprovedtobealmostequallyeffectiveascontinuousexposureofthesametotalduration,whereaslongerintervalsbetweentheexposuresseemedtoallowtheorganismthetimerequiredtorecoverandpartlyovercometheabovementionedeffectsoftheGSMexposure.

(E)ChenG,LuD,ChiangH,LeszczynskiD,XuZ.UsingmodelorganismSaccharomycescerevisiaetoevaluatetheeffectsofELFMFandRFEMFexposureonglobalgeneexpression.Bioelectromagnetics.33(7):550560,2012.(GE)

Thepotentialhealthhazardofexposuretoelectromagneticfields(EMF)continuestocausepublicconcern.However,thepossibilityofbiologicalandhealtheffectsofexposuretoEMFremainscontroversialandtheirbiophysicalmechanismsareunknown.Inthepresentstudy,weusedSaccharomycescerevisiaetoidentifygenesrespondingtoextremelylowfrequencymagneticfields(ELFMF)andtoradiofrequencyEMF(RFEMF)exposures.Theyeastcellswereexposedfor6htoeither0.4mT50HzELFMFor1800MHzRFEMFataspecificabsorptionrateof4.7W/kg.Geneexpressionwasanalyzedbymicroarrayscreeningandconfirmedusingrealtimereversetranscriptionpolymerasechainreaction(RTPCR).WewereunabletoconfirmmicroarraydetectedchangesinthreeoftheELFMFresponsivecandidategenesusingRTPCR(P>0.05).Ontheotherhand,outofthe40potentialRFEMFresponsivegenes,onlytheexpressionsofstructuralmaintenanceofchromosomes3(SMC3)andaquaporin2(AQY2(m))wereconfirmed,whilethreeothergenes,thatis,halotoleranceprotein9(HAL9),yetanotherkinase1(YAK1)andonefunctionunknowngene(openreadingframe:YJL171C),showedoppositechangesinexpressioncomparedtothemicroarraydata(P

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humanspermatozoainvitro.PRINCIPALFINDINGS:Purifiedhumanspermatozoawereexposedtoradiofrequencyelectromagneticradiation(RFEMR)tunedto1.8GHzandcoveringarangeofspecificabsorptionrates(SAR)from0.4W/kgto27.5W/kg.InstepwithincreasingSAR,motilityandvitalityweresignificantlyreducedafterRFEMRexposure,whilethemitochondrialgenerationofreactiveoxygenspeciesandDNAfragmentationweresignificantlyelevated(P

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BACKGROUND:Nonionizingradiofrequencyradiationhasbeenincreasinglyusedinindustry,commerce,medicineandespeciallyinmobilephonetechnologyandhasbecomeamatterofseriousconcerninpresenttime.OBJECTIVE:Thepresentstudywasdesignedtoinvestigatethepossibledeoxyribonucleicacid(DNA)damagingeffectsoflowlevelmicrowaveradiationinbrainofFischerrats.MATERIALSANDMETHODS:ExperimentswereperformedonmaleFischerratsexposedtomicrowaveradiationfor30daysatthreedifferentfrequencies:900,1800and2450MHz.Animalsweredividedinto4groups:GroupI(Shamexposed):Animalsnotexposedtomicrowaveradiationbutkeptundersameconditionsasthatofothergroups,GroupII:Animalsexposedtomicrowaveradiationatfrequency900MHzatspecificabsorptionrate(SAR)5.95310(4)W/kg,GroupIII:Animalsexposedto1800MHzatSAR5.83510(4)W/kgandGroupIV:Animalsexposedto2450MHzatSAR6.67210(4)W/kg.AttheendoftheexposureperiodanimalsweresacrificedimmediatelyandDNAdamageinbraintissuewasassessedusingalkalinecometassay.RESULTS:Inthepresentstudy,wedemonstratedDNAdamagingeffectsoflowlevelmicrowaveradiationinbrain.CONCLUSION:WeconcludedthatlowSARmicrowaveradiationexposureatthesefrequenciesmayinduceDNAstrandbreaksinbraintissue.

(E)EngelmannJC,DeekenR,MllerT,NimtzG,RoelfsemaMR,HedrichR.IsgeneactivityinplantcellsaffectedbyUMTSirradiation?Awholegenomeapproach.AdvApplBioinformChem.1:7183,2008.(GE)

Mobilephonetechnologymakesuseofradiofrequency(RF)electromagneticfieldstransmittedthroughadensenetworkofbasestationsinEurope.PossibleharmfuleffectsofRFfieldsonhumansandanimalsarediscussed,buttheireffectonplantshasreceivedlittleattention.InsearchforphysiologicalprocessesofplantcellssensitivetoRFfields,cellsuspensionculturesofArabidopsisthalianawereexposedfor24htoaRFfieldprotocolrepresentingtypicalmicrowaveexpositioninanurbanenvironment.mRNAofexposedculturesandcontrolswasusedtohybridizeAffymetrixATH1wholegenomemicroarrays.Differentialexpressionanalysisrevealedsignificantchangesintranscriptionof10genes,buttheydidnotexceedafoldchangeof2.5.Besidesthat3ofthemaredarkinducible,theirfunctionsdonotpointtoanyknownresponsesofplantstoenvironmentalstimuli.Thechangesintranscriptionofthesegeneswerecomparedwithpublishedmicroarraydatasetsandrevealedaweaksimilarityofthemicrowavetolighttreatmentexperiments.Consideringthelargechangesdescribedinpublishedexperiments,itisquestionableifthesmallalterationscausedbya24hcontinuousmicrowaveexposurewouldhaveanyimpactonthegrowthandreproductionofwholeplants.

(E)EsmekayaMA,AytekinE,OzgurE,GlerG,ErgunMA,OmeroluS,SeyhanN.Mutagenicandmorphologicimpactsof1.8GHzradiofrequencyradiationonhumanperipheralbloodlymphocytes(hPBLs)andpossibleprotectiveroleofpretreatmentwithGinkgobiloba(EGb761).SciTotalEnviron.410411:5964,2011.(GT,OX)

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Themutagenicandmorphologiceffectsof1.8GHzGlobalSystemforMobileCommunications(GSM)modulatedRF(radiofrequency)radiationaloneandincombinationwithGinkgobiloba(EGb761)pretreatmentinhumanperipheralbloodlymphocytes(hPBLs)wereinvestigatedinthisstudyusingSisterChromatidExchange(SCE)andelectronmicroscopy.Cellviabilitywasassessedwith3(4,5dimethylthiazol2yl)2,5diphenyltetrazoliumbromide(MTT)reductionassay.ThelymphocytecultureswereexposedtoGSMmodulatedRFradiationat1.8GHzfor6,8,24and48hwithandwithoutEGb761.WeobservedmorphologicalchangesinpulsemodulatedRFradiatedlymphocytes.Longerexposureperiodsledtodestructionoforganelleandnucleusstructures.ChromatinchangeandthelossofmitochondrialcristaoccurredincellsexposedtoRFfor8hand24handweremorepronouncedincellsexposedfor48h.Cytoplasmiclysisanddestructionofmembraneintegrityofcellsandnucleiwerealsoseenin48hRFexposedcells.Therewasasignificantincrease(p

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maycausebiologicaleffects,suchasDNAdamageandchangesonoxidativemetabolism.Aninvivomammaliancytogenetictest,themicronucleus(MN)assay,wasusedtoinvestigatetheoccurrenceofchromosomaldamageinerythrocytesfromratoffspringexposedtoanonthermalUHFEMFfromacellularphoneduringtheirembryogenesis;theirradiatedgroupshowedasignificantincreaseinMNoccurrence.InordertoinvestigateifUHFEMFcouldalsoalteroxidativeparametersintheperipheralbloodandintheliveranimportanthematopoietictissueinratembryosandnewbornswealsomeasuredtheactivityofantioxidantenzymes,quantifiedtotalsulfhydrylcontent,proteincarbonylgroups,thiobarbituricacidreactivespeciesandtotalnonenzymaticantioxidantdefense.Nosignificantdifferenceswerefoundinanyoxidativeparameterofoffspringbloodandliver.Theaveragenumberofpupsineachlitterhasalsonotbeensignificantlyaltered.Ourresultssuggestthat,underourexperimentalconditions,UHFEMFisabletoinduceagenotoxicresponseinhematopoietictissueduringtheembryogenesisthroughanunknownmechanism.

(NE)FinnieJW,CaiZ,BlumbergsPC,ManavisJ,KuchelTR.Expressionoftheimmediateearlygene,cfos,infetalbrainafterwholeofgestationexposureofpregnantmicetoglobalsystemformobilecommunicationmicrowaves.Pathology.38(4):333335,2006.(GE,DE)

AIMS:Tostudyimmediateearlygene,cfos,expressionasamarkerofneuralstressafterwholeofgestationexposureofthefetalmousebraintomobiletelephonetyperadiofrequencyfields.METHODS:Usingapurposedesignedexposuresystemat900MHz,pregnantmiceweregivenasingle,farfield,wholebodyexposureataspecificabsorptionrateof4W/kgfor60min/dayfromday1today19ofgestation.Pregnantcontrolmicewereshamexposedorfreelymobileinacagewithoutfurtherrestraint.Immediatelypriortoparturitionongestationalday19,fetalheadswerecollected,fixedin4%paraformaldehydeandparaffinembedded.Anystressresponseinthebrainwasdetectedbycfosimmunohistochemistryinthecerebralcortex,basalganglia,thalamus,hippocampus,midbrain,cerebellumandmedulla.RESULTS:cfosexpressionwasoflimited,butconsistent,neuroanatomicaldistributionandtherewasnodifferenceinimmunoreactivitybetweenexposedandcontrolbrains.CONCLUSION:Inthisanimalmodel,nostressresponsewasdetectedinthefetalbrainusingcfosimmunohistochemistryafterwholeofgestationexposuretomobiletelephony.

(E)FranzellittiS,ValbonesiP,CiancagliniN,BiondiC,ContinA,BersaniF,FabbriE.TransientDNAdamageinducedbyhighfrequencyelectromagneticfields(GSM1.8GHz)inthehumantrophoblastHTR8/SVneocelllineevaluatedwiththealkalinecometassay.MutatRes683(12):3542,2010.(GT,WS)

Oneofthemostcontroversialissueregardinghighfrequencyelectromagneticfields(HFEMF)istheirputativecapacitytoaffectDNAintegrity.ThisisofparticularconcernduetotheincreasinguseofHFEMFincommunicationtechnologies,includingmobilephones.Althoughepidemiologicalstudiesreportnodetrimentaleffectsonhumanhealth,thepossibledisturbancegeneratedbyHFEMFoncellphysiologyremainscontroversial.Inaddition,thequestionremainsastowhethercellsareabletocompensatetheirpotentialeffects.Wehavepreviouslyreportedthata1hexposuretoamplitudemodulated1.8GHzsinusoidalwaves

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(GSM217Hz,SAR=2W/kg)largelyusedinmobiletelephonydidnotcauseincreasedlevelsofprimaryDNAdamageinhumantrophoblastHTR8/SVneocells.Nevertheless,furtherinvestigationsontrophoblastcellresponsesafterexposuretoGSMsignalsofdifferenttypesanddurationswereconsideredofinterest.Inthepresentwork,HTR8/SVneocellswereexposedfor4,16or24hto1.8GHzcontinuouswave(CW)anddifferentGSMsignals,namelyGSM217HzandGSMTalk(intermittentexposure:5minfieldon,10minfieldoff).ThealkalinecometassaywasusedtoevaluateprimaryDNAdamagesand/orstrandbreaksduetouncompletedrepairprocessesinHFEMFexposedsamples.TheamplitudemodulatedsignalsGSM217HzandGSMTalkinducedasignificantincreaseincometparametersintrophoblastcellsafter16and24hofexposure,whiletheunmodulatedCWwasineffective.However,alterationswererapidlyrecoveredandtheDNAintegrityofHFEMFexposedcellswassimilartothatofshamexposedcellswithin2hofrecoveryintheabsenceirradiation.OurdatasuggestthatHFEMFwithacarrierfrequencyandmodulationschemetypicaloftheGSMsignalmayaffecttheDNAintegrity.

(E) Furtado-Filho OV, Borba JB, Dallegrave A, Pizzolato TM, Henriques JA, Moreira JC, Saffi J. Effect of 950 MHz UHF electromagnetic radiation on biomarkers of oxidative damage, metabolism of UFA and antioxidants in the livers of young rats of different ages. Int J Radiat Biol. 2013 Jul 25. [Epub ahead of print] (LE, GT, OX)

Purpose: To assess the effect of 950 MHz ultra-high-frequency electromagnetic radiation (UHF EMR) on biomarkers of oxidative damage, as well as to verify the concentration of unsaturated fatty acids (UFA) and the expression of the catalase in the livers of rats of different ages. Materials and methods: Twelve rats were equally divided into two groups as controls (CR) and exposed (ER), for each age (0, 6, 15 and 30 days). Radiation exposure lasted half an hour per day for up to 51 days (21 days of gestation and 6, 15 or 30 days of life outside the womb). The specific absorption rate (SAR) ranged from 1.3-1.0 W/kg. The damage to lipids, proteins and DNA was verified by thiobarbituric acid reactive substances (TBARS), protein carbonyls and comets, respectively. UFA were determined by gas chromatography with a flame ionization detector. The expression of catalase was by Western blotting. Results: The neonates had low levels of TBARS and concentrations of UFA after exposure. There was no age difference in the accumulation of protein carbonyls for any age. The DNA damage of ER 15 or 30 days was different. The exposed neonates exhibited lower expression of catalase. Conclusions: 950 MHz UHF EMR does not cause oxidative stress (OS), and it is not genotoxic to the livers of neonates or those of 6 and 15 day old rats, but it changes the concentrations of polyunsaturated fatty acid (PUFA) in neonates. For rats of 30 days, no OS, but it is genotoxic to the livers of ER to total body irradiation.

(E)GajskiG,GarajVrhovacV.Radioprotectiveeffectsofhoneybeevenom(Apismellifera)against915MHzmicrowaveradiationinducedDNAdamageinwistarratlymphocytes:invitrostudy.IntJToxicol28:8898,2009.(GT,OX)

TheaimofthisstudyistoinvestigatetheradioprotectiveeffectofbeevenomagainstDNAdamageinducedby915MHzmicrowaveradiation(specificabsorptionrateof0.6W/kg)in

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Wistarrats.WholebloodlymphocytesofWistarratsaretreatedwith1microg/mLbeevenom4hourspriortoandimmediatelybeforeirradiation.StandardandformamidopyrimidineDNAglycosylase(Fpg)modifiedcometassaysareusedtoassessbasalandoxidativeDNAdamageproducedbyreactiveoxygenspecies.BeevenomshowsadecreaseinDNAdamagecomparedwithirradiatedsamples.ParametersofFpgmodifiedcometassayarestatisticallydifferentfromcontrols,makingthisassaymoresensitiveandsuggestingthatoxidativestressisapossiblemechanismofDNAdamageinduction.BeevenomisdemonstratedtohavearadioprotectiveeffectagainstbasalandoxidativeDNAdamage.Furthermore,beevenomisnotgenotoxicanddoesnotproduceoxidativedamageinthelowconcentrationsusedinthisstudy.

(E)GandhiG,Anita,Geneticdamageinmobilephoneusers:somepreliminaryfindings.IndJHumGenet11:99104,2005.(GT,HU)

BACKGROUND:Theimpactofmicrowave(MW)/radiofrequencyradiation(RFR)onimportantbiologicalparametersisprobablymorethanasimplythermalone.Exposuretoradiofrequency(RF)signalsgeneratedbytheuseofcellulartelephoneshaveincreaseddramaticallyandreportedtoaffectphysiological,neurological,cognitiveandbehaviouralchangesandtoinduce,initiateandpromotecarcinogenesis.GenotoxicityofRFRhasalsobeenreportedinvarioustestsystemsafterinvitroand/orinvivoexposurebutnoneinmobilephoneusers.AIMS:Inthepresentstudy,DNAandchromosomaldamageinvestigationswerecarriedoutontheperipheralbloodlymphocytesofindividualsusingmobilephones,beingexposedtoMWfrequencyrangingfrom800to2000MHz.METHODS:DNAdamagewasassessedusingthesinglecellgelelectrophoresisassayandaneugenicandclastogenicdamagebytheinvivocapillarybloodmicronucleustest(MNT)inatotalof24mobilephoneusers.RESULTS:Meancomettaillength(26.760.054mm;39.75%ofcellsdamaged)inmobilephoneuserswashighlysignificantfromthatinthecontrolgroup.TheinvivocapillarybloodMNTalsorevealedhighlysignificant(0.25)frequencyofmicronucleated(MNd)cells.CONCLUSIONS:Theseresultshighlightacorrelationbetweenmobilephoneuse(exposuretoRFR)andgeneticdamageandrequireinterimpublichealthactionsinthewakeofwidespreaduseofmobiletelephony.

(E)GandhiG,SinghP.Cytogeneticdamageinmobilephoneusers:preliminarydata.IntJHumGenet5:259265,2005.(GT,HU)

Mobiletelephones,sometimescalledcellular(cell)phonesorhandies,arenowanintegralpartofmodernlife.Themobilephonehandsetsarelowpoweredradiofrequencytransmitters,emittingmaximumpowersintherangeof0.2to0.6watts.Scientificconcenrnshaveincreasedsufficientlyoverthepossiblehazardtohealthfromusingcellphones.Thereportedadversehealtheffectsincludephysiological,behaviouralandcognitivechangesaswellastumourformationandgeneticdamage.Howeverfindingsarecontroversialandnoconsensusexists.Genotoxicityhasbeenobservedeitherinlowerorganismsorinvitrostudies.Theaimofthepresentstudyhencewastodetectanycytogenerticdamageinmobilephoneusersbyanalysingshorttermperipherallymphocyteculturesforchromosomalaberrationsandthebuccalmucosalcellsformicronuclei(aneugenicityandclastogenicity).Theresultsrevealedincreased

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numberofmicronucleatedbuccalcellsandcytologicalabnormalitiesinculturedlymphocytesindicatingthegenotoxicresponsefrommobilephoneuse.

(E)GarajVrhovacV,GajskiG,PaaninS,SaroliA,DomijanAM,FlajsD,PeraicaM.Assessmentofcytogeneticdamageandoxidativestressinpersonneloccupationallyexposedtothepulsedmicrowaveradiationofmarineradarequipment.IntJHygEnvironHealth.4(1):5965,2011.(GT,HU,OX)

Duetoincreasedusageofmicrowaveradiation,thereareconcernsofitsadverseeffectintoday'ssociety.Keepingthisinview,studywasaimedatworkersoccupationallyexposedtopulsedmicrowaveradiation,originatingfrommarineradars.Electromagneticfieldstrengthwasmeasuredatassignedmarineradarfrequencies(3GHz,5.5GHzand9.4GHz)andcorrespondingspecificabsorptionratevaluesweredetermined.Parametersofthecometassayandmicronucleustestwerestudiedbothintheexposedworkersandincorrespondingunexposedsubjects.Differencesbetweenmeantailintensity(0.67vs.1.22)andmoment(0.08vs.0.16)ascometassayparametersandmicronucleustestparameters(micronuclei,nucleoplasmicbridgesandnuclearbuds)werestatisticallysignificantbetweenthetwoexaminedgroups,suggestingthatcytogeneticalterationsoccurredaftermicrowaveexposure.Concentrationsofglutathioneandmalondialdehydeweremeasuredspectrophotometricallyandusinghighperformanceliquidchromatography.Theglutathioneconcentrationinexposedgroupwassignificantlylowerthanincontrols(1.24vs.0.53)whereastheconcentrationofmalondialdehydewassignificantlyhigher(1.74vs.3.17),indicatingoxidativestress.ResultssuggeststhatpulsedmicrowavesfromworkingenvironmentcanbethecauseofgeneticandcellalterationsandthatoxidativestresscanbeoneofthepossiblemechanismsofDNAandcelldamage.

(E)GulerG,TomrukA,OzgurE,SeyhanN.TheeffectofradiofrequencyradiationonDNAandlipiddamageinnonpregnantandpregnantrabbitsandtheirnewborns.GenPhysiolBiophys29:5966,2010.(GT,OX,LE,DE)

Theconcernsofpeopleonpossibleadversehealtheffectsofradiofrequencyradiation(RFR)generatedfrommobilephonesaswellastheirsupportingtransmitters(basestations)haveincreasedmarkedly.RFReffectonoversensitivepeople,suchaspregnantwomenandtheirdevelopingfetuses,andolderpeopleisanothersourceofconcernthatshouldbeconsidered.Inthisstudy,oxidativeDNAdamageandlipidperoxidationlevelsinthebraintissueofpregnantandnonpregnantNewZealandWhiterabbitsandtheirnewbornsexposedtoRFRwereinvestigated.Thirteenmontholdrabbitswerestudiedinfourgroupsasnonpregnantcontrol,nonpregnantRFRexposed,pregnantcontrolandpregnantRFRexposed.TheywereexposedtoRFR(1800MHzGSM;14V/masreferencelevel)for15min/dayduring7days.Malondialdehyde(MDA)and8hydroxy2'deoxyguanosine(8OHdG)levelswereanalyzed.MDAand8OHdGlevelsofnonpregnantandpregnantRFRexposedanimalssignificantlyincreasedwithrespecttocontrols(p0.05,MannWhitney).Thereexistveryfewexperimentalstudiesonthe

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effectsofRFRduringpregnancy.ItwouldbebeneficialtoincreasethenumberofthesestudiesinordertoestablishinternationalstandardsfortheprotectionofpregnantwomenfromRFR.

(E)GlerG,TomrukA,OzgurE,SahinD,SepiciA,AltanN,SeyhanN.TheeffectofradiofrequencyradiationonDNAandlipiddamageinfemaleandmaleinfantrabbits.IntJRadiatBiol.88(4):367373,2012.(LE,GT,OX,DE)

PURPOSE:Weaimedtodesignaprolongedradiofrequency(RF)radiationexposureandinvestigateinananimalmodel,possiblebioeffectsofRFradiationontheongoingdevelopmentalstagesofchildrenfromconceptiontochildhood.MATERIALSANDMETHODS:Atotalof72NewZealandfemaleandmalewhiterabbitsagedonemonthwereused.FemaleswereexposedtoRFradiationfor15min/dayduring7days,whereasmaleswereexposedtothesamelevelofradiationfor15min/dayduring14days.Thirtysixfemaleand36maleinfantrabbitswererandomlydividedintofourgroups:GroupI[Intrauterine(IU)exposure();Extrauterine(EU)exposure()]:Shamexposurewhichmeansrabbitswereexposedto1800MHzGlobalSystemforMobileTelecommunication(GSM)likeRFsignalsneitherintheIUnorintheEUperiods.GroupII[IUexposure();EUexposure(+)]:Infantrabbitswereexposedto1800MHzGSMlikeRFsignalswhentheyreachedonemonthofage.GroupIII[IUexposure(+);EUexposure()]:Infantrabbitswereexposedto1800MHzGSMlikeRFsignalsintheIUperiod(between15thand22nddaysofthegestationalperiod).GroupIV[IUexposure(+);EUexposure(+)]:Infantrabbitswereexposedto1800MHzGSMlikeRFsignalsbothintheIUperiod(between15thand22nddaysofthegestationalperiod)andintheEUperiodwhentheyreachedonemonthofage.BiochemicalanalysisforlipidperoxidationandDNAdamagewerecarriedoutintheliversofallrabbits.RESULTS:LipidperoxidationlevelsinthelivertissuesoffemaleandmaleinfantrabbitsincreasedunderRFradiationexposure.Liver8hydroxy2'deoxyguanosine(8OHdG)levelsoffemalerabbitsexposedtoRFradiationwerealsofoundtoincreasewhencomparedwiththelevelsofnonexposedinfants.However,therewerenochangesinliver8OHdGlevelsofmalerabbitsunderRFexposure.CONCLUSION:Consequently,itcanbeconcludedthatGSMlikeRFradiationmayinducebiochemicalchangesbyincreasingfreeradicalattackstostructuralbiomoleculesintherabbitasanexperimentalanimalmodel.

(NE)GurbuzN,SiravB,YuvaciHU,TurhanN,CoskunZK,SeyhanN.Isthereanypossiblegenotoxiceffectinexfoliatedbladdercellsofratundertheexposureof1800MHzGSMlikemodulatedradiofrequencyradiation(RFR)?ElectromagnBiolMed.29(3):98104,2010.(LE,GT)

Peopleareexposedtomanycarcinogenicandmutagenicchemicalsintheireverydaylives.Theseincludeantineoplasticdrugs,Polycyclicaromatichydrocarbons(PAH)s,aromaticamines,nitrosamines,metals,andelectromagneticradiation.Basedonthestateofknowledgeacquiredduringthelast50yearsofresearchonpossiblebiologicaleffectsofelectromagneticfields(EMF),themajorityofthescientificcommunityisconvincedthatexposuretoEMFbelowtheexistingsecuritylimitsdoesnotcausearisktothehealthofthegeneralpublic.However,this

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positionisquestionedbyothers,whoareoftheopinionthattheavailableresearchdataarecontradictoryorinconsistentand,therefore,unreliable.Inthisstudy,weaimedtoinvestigateifthereisanyeffectof1800MHzGSMmodulatedradiofrequencyradiation(RFR)onthenumberofmicronucleusinexfoliatedbladdercellsofratwhichwillbeinformativeaboutthegenotoxicdamage.Exposureperiodwas20min/day,5days/weekduringamonth.SixfemaleWistarratswereusedfortwogroups:GroupI(n=6):controls;GroupII(n=6):1.8GHzexposedanimals.1800MHzRFRdidnotshowedasignificantMNfrequenciesinratbladdercellswhencomparedwiththecontrolgroup(p>0.05).1800MHzRFRexposedanimalsdidnotproduceanygenotoxiceffectwhencomparedwiththecontrolgroup(p>0.05).Kineticstudiesareimportantforanybiomarker,especiallythoseinwhichtissuedifferentiationandmaturationprocesseswillheavilyinfluencethetimebetweeninductionofdamageandcollectionofdamagedcellsformicronucleusanalysis.

(NE)GurbuzN,SiravB,ColbayM,YetkinI,SeyhanN.Nogenotoxiceffectinexfoliatedbladdercellsofratundertheexposureof1800and2100MHzradiofrequencyradiation.ElectromagnBiolMed.2013Nov27.[Epubaheadofprint](GT,LE)

AbstractInthisstudy,weaimedtoinvestigatetheeffectsof1800and2100MHzRadioFrequency(RF)radiationonthenumberofmicronucleus(MN)inexfoliatedbladdercellsofratwhichshowsthegenotoxicdamage.Exposureperiodwas30min/day,6days/weekforamonthandtwomonthsexposureperiods.Thirtymalewistaralbinoratswereusedforfivegroups:GroupI(n=6):1800MHzRFexposedanimalsforonemonth,GroupII(n=6):2100MHzRFexposedanimalsforonemonth,GroupIII(n=6):2100MHzRFexposedfortwomonths,GroupIV(n=6):controlgroupforonemonth,GroupV(n=6):controlgroupfortwomonths.Ratsofthecontrolgroupswerehousedintheirhomecagesduringtheentireexperimentalperiodwithoutsubjectingtoanyexperimentalmanipulation.1800and2100MHzRFexposuresdidnotresultinanysignificantMNfrequenciesinratbladdercellswithrespecttothecontrolgroups(p>0.05).Therewasnostatisticallysignificantdifferencebetween2100MHzRFexposedgroups,either.Furtherstudiesareneededtodemonstrateifthereisanygenotoxiceffect,micronucleusformationinothertissuesofrats.

(NE)HansteenIL,LgeideL,ClausenKO,HauganV,SvendsenM,EriksenJG,SkiakerR,HaugerE,VistnesAI,KureEH.Cytogeneticeffectsof18.0and16.5GHzmicrowaveradiationonhumanlymphocytesinvitro.AnticancerRes29:28852892,2009.(GT,IA,WS)

BACKGROUND:Therearefewcellstudiesonthedirectgenotoxiceffectsofmicrowaveradiation.Inthisstudy,cytogeneticeffectsofmicrowaveradiationaloneorincombinationwithmitomycinC(MMC)wereinvestigated.MATERIALSANDMETHODS:Lymphocytesfromtwosmokingandfournonsmokingdonorswereexposedfor53hoursinvitroto1.0W/mcontinuouswaveradiationat18.0GHzor10W/mpulsedwaveat16.5GHz,aloneorincombinationwithMMC.DNAsynthesisandrepairwereinhibitedinvitroinsomecultures.RESULTS:NosynergisticeffectwasobservedincellsexposedtocombinationsofmicrowaveradiationandinvitroexposuretoMMC,ortocellspreexposedinvivototobaccosmoke.For

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the16.5GHzpulsedexposure,anonsignificanttrendconsistingofanincreaseinaberrationfrequencieswithmicrowaveradiationwasshownfortheDNAsynthesisandrepairinhibitedculturesbothwithandwithoutMMC.CONCLUSION:Neither18.0GHzcontinuouswavenor16.5GHzpulsedwaveexposuretohumanlymphocytesinvitroinducedstatisticallysignificantincreasesinchromosomalaberrationfrequencies.16.5GHzpulsedwaveexposurerequiresfurtherdocumentationbeforeatruenegativeconclusioncanbedrawn.

(NE)HansteenIL,ClausenKO,HauganV,SvendsenM,SvendsenMV,EriksenJG,SkiakerR,HaugerE,LgeideL,VistnesAI,KureEH.Cytogeneticeffectsofexposureto2.3GHzradiofrequencyradiationonhumanlymphocytesinvitro.AnticancerRes29:43234330,2009.(GT,IA)

BACKGROUND:Nopreviousinvitrostudieshavetestedradiofrequencyradiationforatleastonefullcellcycleinculture.TheaimwastotestifexposureusedinmobilephonesandwirelessnetworktechnologieswouldinduceDNAdamageinculturedhumanlymphocyteswithandwithoutaknownclastogen.MATERIALSANDMETHODS:Lymphocytesfromsixdonorswereexposedto2.3GHz,10W/mcontinuouswaves,or2.3GHz,10W/mpulsedwaves(200Hzpulsefrequency,50%dutycycle).MitomycinCwasaddedtohalfofthecultures.DNAsynthesisandrepairwereinhibitedinoneexperiment.RESULTS:Nostatisticallysignificantdifferenceswereobservedbetweencontrolandexposedcultures.AweaktrendformorechromosomaldamagewiththeinteractionofpulsedfieldswithmitomycinCcomparedtoaconstantfieldwasobserved.CONCLUSION:Exposureduringthewholecellcycleininhibitedculturesdidnotresultedinsignificantdifferencesinchromosomalaberrationsascomparedtocontrols.

(E)HekmatA,SabouryAA,MoosaviMovahediAA.Thetoxiceffectsofmobilephoneradiofrequency(940MHz)onthestructureofcalfthymusDNA.EcotoxicolEnvironSaf.2012Nov16.pii:S01476513(12)003685.doi:10.1016/j.ecoenv.2012.10.016.[Epubaheadofprint](GT)

Currently,thebiologicaleffectsofnonionizingelectromagneticfields(EMFs)includingradiofrequency(RF)radiationhavebeenthesubjectofnumerousexperimentalandtheoreticalstudies.TheaimofthisstudyistoevaluatethepossiblebiologicaleffectsofmobilephoneRF(940MHz,15V/mandSAR=40mW/kg)onthestructureofcalfthymusDNA(ctDNA)immediatelyafterexposureand2hafter45minexposureviadiverserangeofspectroscopicinstruments.TheUVvisandcirculardichroism(CD)experimentsdepictthatmobilephoneEMFscanremarkablycausedisturbanceonctDNAstructure.Inaddition,theDNAsamples,immediatelyafterexposureand2hafter45minexposure,arerelativelythermallyunstablecomparedtotheDNAsolution,whichwasplacedinasmallshieldedbox(unexposedctDNA).Furthermore,theexposedDNAsamples(theDNAsamplesthatwereexposedto940MHzEMF)havemorefluorescenceemissionwhencomparedwiththeunexposedDNA,whichmayhaveoccurredattributabletoexpansionoftheexposedDNAstructure.Theresultsofdynamiclightscattering(DLS)andzetapotentialexperimentsdemonstratethatRFEMFsleadtoincrementinthesurfacechargeandsizeofDNA.ThestructureofDNAimmediatelyafterexposureisnotsignificantlydifferentfromtheDNAsample2hafter45minexposure.Inotherwords,theEMF

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inducedconformationalchangesareirreversible.Collectively,ourresultsrevealthat940MHzcanalterthestructureofDNA.ThedisplacementofelectronsinDNAbyEMFsmayleadtoconformationalchangesofDNAandDNAdisaggregation.ResultsfromthisstudycouldhaveanimportantimplicationonthehealtheffectsofRFEMFsexposure.Inaddition,thisfindingcouldprofferanovelstrategyforthedevelopmentofnextgenerationofmobilephone.

(NE)HintzscheH,StopperH.Micronucleusfrequencyinbuccalmucosacellsofmobilephoneusers.ToxicolLett.193(1):124130,2010.(GT,HU)

Mobilephonesarebeingusedextensivelythroughouttheworld,withmorethanfourbillionaccountsexistingin2009.Thistechnologyapplieselectromagneticradiationinthemicrowaverange.Healtheffectsofthisradiationhavebeensubjectofdebateforalongtime,bothwithinthescientificcommunityandwithinthegeneralpublic.Thisstudyinvestigatedtheeffectofmobilephoneuseongenomicinstabilityofthehumanoralcavity'smucosacells.131Individualsdonatedbuccalmucosacellsextractedbyslightlyscrapingtheoralcavitywithacottonswab.Everyparticipantfilledoutaquestionnaireaboutmobilephoneuseincludingdurationofweeklyuse,overallperiodofexposureandheadsetusage.13Individualsdidnotusemobilephonesatall,85reportedusingthemobilephoneforthreehoursperweekorless,and33reporteduseofmorethanthreehoursperweek.Additionally,informationonage,gender,bodyweight,smokingstatus,medicationandnutritionwasretrieved.ForstainingofthecellsaprocedureusingalphatubulinantibodyandchromomycinA(3)wasapplied.Micronucleiandothermarkerswereevaluatedin1000cellsperindividualatthemicroscope.Asecondscorercountedanother1000cells,resultingin2000analyzedcellsperindividual.Mobilephoneusedidnotleadtoasignificantlyincreasedfrequencyofmicronuclei.

(NE)HintzscheH,JastrowC,KleineOstmannT,SchraderT,StopperH.900MHzradiationdoesnotinducemicronucleusformationindifferentcelltypes.Mutagenesis.27(4):477483,2012.(GT)

Theexposureofthepopulationtononionisingelectromagneticradiationisstillincreasing,mainlyduetomobilecommunication.Whetherlowintensityelectromagneticfieldscancauseothereffectsapartfromheatinghasbeenasubjectofdebate.Oneoftheeffects,whichwereproposedtobecausedbymobilephoneradiation,istheoccurrenceofmitoticdisturbances.Theaimofthisstudywastoinvestigatepossibleconsequencesofthesemitoticdisturbancesasmanifestgenomicdamage,i.e.micronucleusinduction.Cellswereirradiatedatafrequencyof900MHz,whichislocatedinoneofthemainfrequencybandsappliedformobilecommunication.Twocelltypeswereused,HaCaTcellsashumancellsandA(L)cells(humanhamsterhybridcells),inwhichmitoticdisturbanceshadbeenreportedtooccur.Afterdifferentpostexposureincubationperiods,cellswerefixedandmicronucleusfrequencieswereevaluated.Bothcelltypesdidnotshowanygenomicdamageafterexposure.Toadapttheprotocolforthemicronucleustestintothedirectionoftheprotocolformitoticdisturbances,thepostexposureincubationperiodwasreducedandexposuretimewasextendedtoonecellcyclelength.Thisdidnotresultinanyincreaseofthegenomicdamage.Inconclusion,

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micronucleusinductionwasnotobservedasaconsequenceofexposuretononionisingradiation,eventhoughthisagentwasreportedtocausemitoticdisturbancesundersimilarexperimentalconditions.

(NE)HiroseH,SakumaN,KajiN,SuharaT,SekijimaM,NojimaT,MiyakoshiJ.Phosphorylationandgeneexpressionofp53arenotaffectedinhumancellsexposedto2.1425GHzbandCWorWCDMAmodulatedradiationallocatedtomobileradiobasestations.Bioelectromagnetics27:494504,2006.(GT)

Alargescaleinvitrostudyfocusingonlowlevelradiofrequency(RF)fieldsfrommobileradiobasestationsemployingtheInternationalMobileTelecommunication2000(IMT2000)cellularsystemwasconductedtotestthehypothesisthatmodulatedRFfieldsinduceapoptosisorothercellularstressresponsethatactivatep53orthep53signalingpathway.First,weevaluatedtheresponseofhumancellstomicrowaveexposureataspecificabsorptionrate(SAR)of80mW/kg,whichcorrespondstothelimitoftheaveragewholebodySARforgeneralpublicexposuredefinedasabasicrestrictionbytheInternationalCommissiononNonIonizingRadiationProtection(ICNIRP)guidelines.Second,weinvestigatedwhethercontinuouswave(CW)andwidebandcodedivisionmultipleaccess(WCDMA)modulatedsignalRFfieldsat2.1425GHzinducedapoptosisoranysignsofstress.HumanglioblastomaA172cellswereexposedtoWCDMAradiationatSARsof80,250,and800mW/kg,andCWradiationat80mW/kgfor24or48h.HumanIMR90fibroblastsfromfetallungswereexposedtobothWCDMAandCWradiationataSARof80mW/kgfor28h.UndertheRFfieldexposureconditionsdescribedabove,nosignificantdifferencesinthepercentageofapoptoticcellswereobservedbetweenthetestgroupsexposedtoRFsignalsandtheshamexposednegativecontrols,asevaluatedbytheAnnexinVaffinityassay.Nosignificantdifferencesinexpressionlevelsofphosphorylatedp53atserine15ortotalp53wereobservedbetweenthetestgroupsandthenegativecontrolsbythebeadbasedmultiplexassay.Moreover,microarrayhybridizationandrealtimeRTPCRanalysisshowednonoticeabledifferencesingeneexpressionofthesubsequentdownstreamtargetsofp53signalinginvolvedinapoptosisbetweenthetestgroupsandthenegativecontrols.OurresultsconfirmthatexposuretolowlevelRFsignalsupto800mW/kgdoesnotinducep53dependentapoptosis,DNAdamage,orotherstressresponseinhumancells.

(NE)HiroseH,SakumaN,KajiN,NakayamaK,InoueK,SekijimaM,NojimaT,MiyakoshiJ.MobilephonebasestationemittedradiationdoesnotinducephosphorylationofHsp27.Bioelectromagnetics28:99108,2007.(GE)

Aninvitrostudyfocusingontheeffectsoflowlevelradiofrequency(RF)fieldsfrommobileradiobasestationsemployingtheInternationalMobileTelecommunication2000(IMT2000)cellularsystemwasconductedtotestthehypothesisthatmodulatedRFfieldsacttoinducephosphorylationandoverexpressionofheatshockproteinhsp27.First,weevaluatedtheresponsesofhumancellstomicrowaveexposureataspecificabsorptionrate(SAR)of80mW/kg,whichcorrespondstothelimitoftheaveragewholebodySARforgeneralpublicexposuredefinedasabasicrestrictionintheInternationalCommissiononNonIonizing

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RadiationProtection(ICNIRP)guidelines.Second,weinvestigatedwhethercontinuouswave(CW)andWidebandCodeDivisionMultipleAccess(WCDMA)modulatedsignalRFfieldsat2.1425GHzinducedactivationorgeneexpressionofhsp27andotherheatshockproteins(hsps).HumanglioblastomaA172cellswereexposedtoWCDMAradiationatSARsof80and800mW/kgfor248h,andCWradiationat80mW/kgfor24h.HumanIMR90fibroblastsfromfetallungswereexposedtoWCDMAat80and800mW/kgfor2or28h,andCWat80mW/kgfor28h.UndertheRFfieldexposureconditionsdescribedabove,nosignificantdifferencesintheexpressionlevelsofphosphorylatedhsp27atserine82(hsp27[pS82])wereobservedbetweenthetestgroupsexposedtoWCDMAorCWsignalandtheshamexposednegativecontrols,asevaluatedimmediatelyaftertheexposureperiodsbybeadbasedmultiplexassays.Moreover,nonoticeabledifferencesinthegeneexpressionofhspswereobservedbetweenthetestgroupsandthenegativecontrolsbyDNAChipanalysis.OurresultsconfirmthatexposuretolowlevelRFfieldupto800mW/kgdoesnotinducephosphorylationofhsp27orexpressionofhspgenefamily.

(NE)HuangTQ,LeeMS,OhE,ZhangBT,SeoJS,ParkWY.MolecularresponsesofJurkatTcellsto1763MHzradiofrequencyradiation.IntJRadiatBiol84:734741,2008.(GT,GE)

PURPOSE:Thebiologicaleffectsofexposuretomobilephoneemittedradiofrequency(RF)radiationarethesubjectofintensestudy,yetthehypothesisthatRFexposureisapotentialhealthhazardremainscontroversial.Inthispaper,wemonitoredcellularandmolecularchangesinJurkathumanTlymphomacellsafterirradiatingwith1763MHzRFradiationtounderstandtheeffectonRFradiationinimmunecells.MATERIALSANDMETHODS:JurkatTcellswereexposedtoRFradiationtoassesstheeffectsoncellproliferation,cellcycleprogression,DNAdamageandgeneexpression.Jurkatcellswereexposedto1763MHzRFradiationat10W/kgspecificabsorptionrate(SAR)andcomparedtoshamexposedcells.RESULTS:RFexposuredidnotproducesignificantchangesincellnumbers,cellcycledistributions,orlevelsofDNAdamage.Ingenomewideanalysisofgeneexpressions,therewerenogeneschangedmorethantwofolduponRFradiationwhiletengeneschangeto1.3approximately1.8fold.Amongtengenes,twocytokinereceptorgenessuchaschemokine(CXCmotif)receptor3(CXCR3)andinterleukin1receptor,typeII(IL1R2)weredownregulateduponRFradiation,buttheywerenotdirectlyrelatedtocellproliferationorDNAdamageresponses.CONCLUSION:Theseresultsindicatethatthealterationsincellproliferation,cellcycleprogression,DNAintegrityorglobalgeneexpressionwasnotdetectedupon1763MHzRFradiationunder10W/kgSARfor24htoJurkatTcells.

(NE)HuangTQ,LeeMS,OhEH,KalinecF,ZhangBT,SeoJS,ParkWY.Characterizationofbiologicaleffectof1763MHzradiofrequencyexposureonauditoryhaircells.IntJRadiatBiol84:909915,2008.(GT,GE)

Purpose:Radiofrequency(RF)exposureatthefrequencyofmobilephoneshasbeenreportednottoinducecellulardamageininvitroandinvivomodels.WechoseHEIOC1immortalizedmouseauditoryhaircellstocharacterizethecellularresponseto1763MHzRFexposure,becauseauditorycellscouldbeexposedtomobilephonefrequencies.Materialsandmethods:

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Cellswereexposedto1763MHzRFata20W/kgspecificabsorptionrate(SAR)inacodedivisionmultipleaccess(CDMA)exposurechamberfor24and48htocheckforchangesincellcycle,DNAdamage,stressresponse,andgeneexpression.Results:NeitherofcellcyclechangesnorDNAdamagewasdetectedinRFexposedcells.Theexpressionofheatshockproteins(HSP)andthephosphorylationofmitogenactivatedproteinkinases(MAPK)didnotchange,either.Wetriedtoidentifyanyalterationingeneexpressionusingmicroarrays.UsingtheAppliedBiosystems1700fullgenomeexpressionmousemicroarray,wefoundthatonly29genes(0.09%oftotalgenesexamined)werechangedbymorethan1.5foldonRFexposure.Conclusion:Fromtheseresults,wecouldnotfindanyevidenceoftheinductionofcellularresponses,includingcellcycledistribution,DNAdamage,stressresponseandgeneexpression,after1763MHzRFexposureatanSARof20W/kginHEIOC1auditoryhaircells.

(E)JiangB,NieJ,ZhouZ,ZhangJ,TongJ,CaoY.Adaptiveresponseinmiceexposedto900MHzradiofrequencyfields:primaryDNAdamage.PLoSOne.7(2):e32040,2012.(LE,GT,IA)

Thephenomenonofadaptiveresponse(AR)inanimalandhumancellsexposedtoionizingradiationiswelldocumentedinscientificliterature.WehaveexaminedwhethersuchARcouldbeinducedinmiceexposedtononionizingradiofrequencyfields(RF)usedforwirelesscommunications.Micewerepreexposedto900MHzRFat120W/cm(2)powerdensityfor4hours/dayfor1,3,5,7and14daysandthensubjectedtoanacutedoseof3Gyradiation.TheprimaryDNAdamageintheformofalkalilabilebasedamageandsinglestrandbreaksintheDNAofperipheralbloodleukocyteswasdeterminedusingthealkalinecometassay.TheresultsindicatedthattheextentofdamageinmicewhichwerepreexposedtoRFfor1dayandthensubjectedtoradiationwassimilarandnotsignificantlydifferentfromthoseexposedtoradiationalone.However,micewhichwerepreexposedtoRFfor3,5,7and14daysshowedprogressivelydecreaseddamageandwassignificantlydifferentfromthoseexposedtoradiationalone.Thus,thedataindicatedthatRFpreexposureiscapableofinducingARandsuggestedthatthepreexposureformorethan4hoursfor1dayisnecessarytoelicitsuchAR.

(NE)JuutilainenJ,HeikkinenP,SoikkeliH,MkiPaakkanenJ.Micronucleusfrequencyinerythrocytesofmiceafterlongtermexposuretoradiofrequencyradiation.IntJRadiatBiol.83(4):213220,2007.(LE,GT)

PURPOSE:Theaimofthestudywastoinvestigategenotoxicityoflongtermexposuretoradiofrequency(RF)electromagneticfieldsbymeasuringmicronucleiinerythrocytes.ThebloodsampleswerecollectedintwoanimalstudiesevaluatingpossiblecocarcinogeniceffectsofRFfields.METHODS:InstudyA,femaleCBA/Smicewereexposedfor78weeks(1.5h/d,5d/week)toeitheracontinuous902.5MHzsignalsimilartothatemittedbyanalogNMT(NordicMobileTelephone)phonesatawholebodyspecificabsorptionrate(SAR)of1.5W/kg,ortoapulsed902.4MHzsignalsimilartothatofdigitalGSM(GlobalSystemforMobileCommunications)phonesat0.35W/kg.Athirdgroupwasshamexposed,andafourthgroupservedascagecontrols.Allbutthecagecontrolanimalswereexposedto4Gyofxraysduringthreefirstweeksoftheexperiment.InstudyB,femaletransgenicmice(lineK2)andtheir

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nontransgeniclittermateswereexposedfor52weeks(1.5h/d,5d/week).Twodigitalmobilephonesignals,GSMandDAMPS(DigitalAdvancedMobilePhoneSystem),wereusedat0.5W/kg.Allbutthecagecontrolanimalswereexposed3timesperweektoanultravioletradiationdoseof1.2MED(minimumerythemadose).RESULTSANDCONCLUSIONS:TheresultsdidnotshowanyeffectsofRFfieldsonmicronucleusfrequencyinpolychromaticornormochromaticerythrocytes.Theresultswereconsistentintwomousestrains(andinatransgenicvariantofthesecondstrain),after52or78weeksofexposure,atthreeSARlevelsrelevanttohumanexposurefrommobilephones,andforthreedifferentmobilesignals.

(E)KaracaE,DurmazB,AltugH,YildizT,GuducuC,IrgiM,KoksalMG,OzkinayF,GunduzC,CoguluO.Thegenotoxiceffectofradiofrequencywavesonmousebrain.JNeurooncol106:5358,2012.(GT,GE)

Erratum:JNeurooncol2012May;107:665.

Concernsaboutthehealtheffectsofradiofrequency(RF)waveshavebeenraisedbecauseofthegradualincreaseinusageofcellphones,andtherearescientificquestionsanddebatesaboutthesafetyofthoseinstrumentsindailylife.TheaimofthisstudyistoevaluatethegenotoxiceffectsofRFwavesinanexperimentalbraincellculturemodel.Braincellculturesofthemicewereexposedto10.715GHzwithspecificabsorbtionrate(SAR)0.725W/kGsignalsfor6hin3daysat25Ctocheckforthechangesinthemicronucleus(MNi)assayandintheexpressionof11proapoptoticandantiapoptoticgenes.ItwasfoundthatMNirateincreased11foldandSTAT3expressiondecreased7foldinthecellcultureswhichwereexposedtoRF.CellphoneswhichspreadRFmaydamageDNAandchangegeneexpressioninbraincells.

(E)KesariKK,BehariJ.FiftygigahertzMicrowaveexposureeffectofradiationsonratbrain.ApplBiochemBiotechnol158:126139,2009.(GT,OX,LE)

Theobjectofthisstudyistoinvestigatetheeffectsof50GHzmicrowaveradiationonthebrainofWistarrats.MaleratsoftheWistarstrainwereusedinthestudy.Animalsof60dayageweredividedintotwogroupsgroup1,shamexposed,andgroup2,experimental(microwaveexposed).Theratswerehousedinatemperaturecontrolledroom(25degreesC)withconstanthumidity(4050%)andreceivedfoodandwateradlibitum.Duringexposure,ratswereplacedinPlexiglascageswithdrilledventilationholesandkeptinananechoicchamber.Theanimalswereexposedfor2hadayfor45dayscontinuouslyatapowerlevelof0.86muW/cmwithnominalspecificabsorptionrate8.0x10(4)w/kg.Aftertheexposureperiod,theratswerekilledandhomogenized,andproteinkinaseC(PKC),DNAdoublestrandbreak,andantioxidantenzymeactivity[superoxidesdismutase(SOD),catalase,andglutathioneperoxidase(GPx)]wereestimatedinthewholebrain.ResultshowsthatthechronicexposuretotheseradiationscausesDNAdoublestrandbreak(headandtaillength,intensityandtailmigration)andasignificantdecreaseinGPxandSODactivity(p=

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0.05).Alldataareexpressedasmean+/standarddeviation.Weconcludethattheseradiationscanhaveasignificanteffectonthewholebrain.

(E)KesariKK,BehariJ,KumarS.Mutagenicresponseof2.45GHzradiationexposureonratbrain.IntJRadiatBiol86:334343,2010.(GT,OX,LE)

Purpose:Toinvestigatetheeffectof2.45GHzmicrowaveradiationonratbrainofmalewistarstrain.Materialandmethods:Maleratsofwistarstrain(35daysoldwith130+/10gbodyweight)wereselectedforthisstudy.Animalsweredividedintotwogroups:Shamexposedandexperimental.Animalswereexposedfor2hadayfor35daysto2.45GHzfrequencyat0.34mW/cmpowerdensity.Thewholebodyspecificabsorptionrate(SAR)wasestimatedtobe0.11W/Kg.ExposuretookplaceinaventilatedPlexiglascageandkeptinanechoicchamberinafarfieldconfigurationfromthehornantenna.Afterthecompletionofexposureperiod,ratsweresacrificedandthewholebraintissuewasdissectedandusedforstudyofdoublestrandDNA(Deoxyribonucleicacid)breaksbymicrogelelectrophoresisandthestatisticalanalysiswascarriedoutusingcometassay(IV2versionsoftware).Thereafter,antioxidantenzymesandhistonekinaseestimationwasalsoperformed.Results:Asignificantincreasewasobservedincomethead(P

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(E)KimJY,HongSY,LeeYM,YuSA,KohWS,HongJR,SonT,ChangSK,LeeM.Invitroassessmentofclastogenicityofmobilephoneradiation(835MHz)usingthealkalinecometassayandchromosomalaberrationtest.EnvironToxicol23:319327,2008.(GT,IA)

Recentlywedemonstratedthat835MHzradiofrequencyradiationelectromagneticfields(RFEMF)neitheraffectedthereversemutationfrequencynoracceleratedDNAdegradationinvitro.Here,twokindsofcytogeneticendpointswerefurtherinvestigatedonmammaliancellsexposedto835MHzRFEMF(themostwidelyusedcommunicationfrequencybandinKoreanCDMAmobilephonenetworks)aloneandincombinationwithmodelclastogens:invitroalkalinecometassayandinvitrochromosomeaberration(CA)test.Nodirectcytogeneticeffectof835MHzRFEMFwasfoundintheinvitroCAtest.ThecombinedexposureofthecellstoRFEMFinthepresenceofethylmethanesulfonate(EMS)revealedaweakandinsignificantcytogeneticeffectwhencomparedtocellsexposedtoEMSaloneinCAtest.Also,thecometassayresultstoevaluatetheabilityofRFEMFalonetodamageDNAwerenearlynegative,althoughshowingasmallincreaseintailmoment.However,theappliedRFEMFhadpotentiationeffectincometassaywhenadministeredincombinationwithmodelclastogens(cyclophosphamideor4nitroquinoline1oxide).Thus,ourresultsimplythatwecannotconfidentlyexcludeanypossibilityofanincreasedriskofgeneticdamage,withimportantimplicationsforthepossiblehealtheffectsofexposureto835MHzelectromagneticfields.

(E)KumarS,KesariKK,BehariJ.EvaluationofgenotoxiceffectsinmaleWistarratsfollowingmicrowaveexposure.IndianJExpBiol48:586592,2010.(GT,OX)

Wistarrats(70daysold)wereexposedfor2hadayfor45dayscontinuouslyat10GHz[powerdensity0.214mW/cm2,specificabsorptionrate(SAR)0.014W/kg]and50GHz(powerdensity0.86microW/cm2,SAR8.0x10(4)W/kg).Micronuclei(MN),reactiveoxygenspecies(ROS),andantioxidantenzymesactivitywereestimatedinthebloodcellsandserum.TheseradiationsinducemicronucleiformationandsignificantincreaseinROSproduction.Significantchangesinthelevelofserumglutathioneperoxidase,superoxidedismutaseandcatalasewereobservedinexposedgroupascomparedwithcontrolgroup.Itisconcludedthatmicrowaveexposurecanbeaffectiveatgeneticlevel.Thismaybeanindicationoftumorpromotion,whichcomesthroughtheoverproductionofreactiveoxygenspecies.

(E)LakshmiNK,TiwariR,BhargavaSC,AhujaYR.InvestigationsonDNAdamageandfrequencyofmicronucleiinoccupationalexposuretoelectromagneticfields(EMFs)emittedfromvideodisplayterminals(VDTs).GenMolBiol33,154158,2010.(GT,HU,LE)

Thepotentialeffectofelectromagneticfields(EMFs)emittedfromvideodisplayterminals(VDTs)toelicitbiologicalresponseisamajorconcernforthepublic.ThesoftwareprofessionalsaresubjectedtocumulativeEMFsintheiroccupationalenvironments.ThisstudywasundertakentoevaluateDNAdamageandincidencesofmicronucleiinsuchprofessionals.Tothebestofourknowledge,thepresentstudyisthefirstattempttocarryoutcytogeneticinvestigationsonassessingbioeffectsinpersonalcomputerusers.Thestudysubjects(n=138)includedsoftwareprofessionalsusingVDTsformorethan2yearswithage,gender,

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socioeconomicstatusmatchedcontrols(n=151).DNAdamageandfrequencyofmicronucleiwereevaluatedusingalkalinecometassayandcytochalasinblockedmicronucleusassayrespectively.OverallDNAdamageandincidenceofmicronucleishowednosignificantdifferencesbetweentheexposedandcontrolsubjects.Withexposurecharacteristics,suchastotalduration(years)andfrequencyofuse(minutes/day)subgroupswereassessedforsuchparameters.AlthoughcumulativefrequencyofuseshowednosignificantchangesintheDNAintegrityoftheclassifiedsubgroups,thelongtermusers(>10years)showedhigherinductionofDNAdamageandincreasedfrequencyofmicronucleiandmicronucleatedcells.

(E)LiuC,DuanW,XuS,ChenC,HeM,ZhangL,YuZ,ZhouZ.Exposureto1800MHzradiofrequencyelectromagneticradiationinducesoxidativeDNAbasedamageinamousespermatocytederivedcellline.ToxicolLett218(1):29,2013a.(GT,OX,RP)

Whetherexposuretoradiofrequencyelectromagneticradiation(RFEMR)emittedfrommobilephonescaninduceDNAdamageinmalegermcellsremainsunclear.Inthisstudy,weconducteda24hintermittentexposure(5minonand10minoff)ofamousespermatocytederivedGC2celllineto1800MHzGlobalSystemforMobileCommunication(GSM)signalsinGSMTalkmodeatspecificabsorptionrates(SAR)of1W/kg,2W/kgor4W/kg.Subsequently,throughtheuseofformamidopyrimidineDNAglycosylase(FPG)inamodifiedcometassay,wedeterminedthattheextentofDNAmigrationwassignificantlyincreasedataSARof4W/kg.FlowcytometryanalysisdemonstratedthatlevelsoftheDNAadduct8oxoguanine(8oxoG)werealsoincreasedataSARof4W/kg.Theseincreaseswereconcomitantwithsimilarincreasesinthegenerationofreactiveoxygenspecies(ROS);thesephenomenaweremitigatedbycotreatmentwiththeantioxidanttocopherol.However,nodetectableDNAstrandbreakagewasobservedbythealkalinecometassay.Takingtogether,thesefindingsmayimplythenovelpossibilitythatRFEMRwithinsufficientenergyforthedirectinductionofDNAstrandbreaksmayproducegenotoxicitythroughoxidativeDNAbasedamageinmalegermcells.

(E)LiuC,GaoP,XuSC,WangY,ChenCH,HeMD,YuZP,ZhangL,ZhouZ.MobilephoneradiationinducesmodedependentDNAdamageinamousespermatocytederivedcellline:aprotectiveroleofmelatonin.IntJRadiatBiol.2013bAug19.[Epubaheadofprint](GT,OX,RP)

Purpose:Toevaluatewhetherexposuretomobilephoneradiation(MPR)caninduceDNAdamageinmalegermcells.Materialsandmethods:AmousespermatocytederivedGC2celllinewasexposedtoacommercialmobilephonehandsetonceevery20minutesinstandby,listen,dialedordialingmodesfor24h.DNAdamagewasdeterminedusinganalkalinecometassay.Results:ThelevelsofDNAdamageweresignificantlyincreasedfollowingexposuretoMPRinthelisten,dialedanddialingmodes.Moreover,thereweresignificantlyhigherincreasesinthedialedanddialingmodesthaninthelistenmode.Interestingly,theseresultswereconsistentwiththeradiationintensitiesofthesemodes.However,theDNAdamageeffectsof

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MPRinthedialingmodewereefficientlyattenuatedbymelatoninpretreatment.Conclusions:TheseresultsregardingmodedependentDNAdamagehaveimportantimplicationsforthesafetyofinappropriatemobilephoneusebymalesofreproductiveageandalsosuggestasimplepreventivemeasure,keepingourbodyfrommobilephonesasfarawayaspossible,notonlyduringconversationsbutduring"dialed"and"dialing"operationmodesaswell.Sincethe"dialed"modeisactuallypartofthestandbymode,mobilephonesshouldbekeptatasafedistancefromourbodyevenduringstandbyoperation.Furthermore,theprotectiveroleofmelatoninsuggeststhatitmaybeapromisingpharmacologicalcandidateforpreventingmobilephoneuserelatedreproductiveimpairments.

(E)LixiaS,YaoK,KaijunW,DeqiangL,HuajunH,XiangweiG,BaohongW,WeiZ,JianlingL,WeiW.Effectsof1.8GHzradiofrequencyfieldonDNAdamageandexpressionofheatshockprotein70inhumanlensepithelialcells.MutatRes602(12):13542,2006.(GT,GE)

ToinvestigatetheDNAdamage,expressionofheatshockprotein70(Hsp70)andcellproliferationofhumanlensepithelialcells(hLEC)afterexposuretothe1.8GHzradiofrequencyfield(RF)ofaglobalsystemformobilecommunications(GSM).AnXc1800RFexposuresystemwasusedtoemployaGSMsignalat1.8GHz(217Hzamplitudemodulated)withtheoutputpowerinthespecificabsorptionrate(SAR)of1,2and3W/kg.After2hexposuretoRF,theDNAdamageofhLECwasaccessedbycometassayatfivedifferentincubationtimes:0,30,60,120and240min,respectively.WesternblotandRTPCRwereusedtodeterminetheexpressionofHsp70inhLECsafterRFexposure.Theproliferationrateofcellswasevaluatedbybromodeoxyuridineincorporationondays0,1and4afterexposure.TheresultsshowthatthedifferenceofDNAbreaksbetweentheexposedandshamexposed(control)groupsinducedby1and2W/kgirradiationwerenotsignificantatanyincubationtimepoint(P>0.05).TheDNAdamagecausedby3W/kgirradiationwassignificantlyincreasedatthetimesof0and30minafterexposure(P0.05).DetectablemRNAaswellasproteinexpressionofHsp70wasfoundinallgroups.ExposureatSARsof2and3W/kgfor2hexhibitedsignificantlyincreasedHsp70proteinexpression(P0.05).Nodifferenceofthecellproliferationratebetweentheshamexposedandexposedcellswasfoundatanyexposuredosetested(P>0.05).TheresultsindicatethatexposuretononthermaldosagesofRFforwirelesscommunicationscaninducenoorrepairableDNAdamageandtheincreasedHsp70proteinexpressioninhLECsoccurredwithoutchangeinthecellproliferationrate.ThenonthermalstressresponseofHsp70proteinincreasetoRFexposuremightbeinvolvedinprotectinghLECfromDNAdamageandmaintainingthecellularcapacityforproliferation.

(E)LpezMartnE,BregainsJ,RelovaQuinteiroJL,CadarsoSurezC,JorgeBarreiroFJ,AresPenaFJ.TheactionofpulsemodulatedGSMradiationincreasesregionalchangesinbrainactivityandcFosexpressionincorticalandsubcorticalareasinaratmodelofpicrotoxininducedseizureproneness.JNeurosciRes.87(6):14841499,2009.(AS,GE,WS,IA)

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TheactionofthepulsemodulatedGSMradiofrequencyofmobilephoneshasbeensuggestedasaphysicalphenomenonthatmighthavebiologicaleffectsonthemammaliancentralnervoussystem.Inthepresentstudy,GSMexposedpicrotoxinpretreatedratsshoweddifferencesinclinicalandEEGsigns,andincFosexpressioninthebrain,withrespecttopicrotoxintreatedratsexposedtoanequivalentdoseofunmodulatedradiation.Neitherradiationtreatmentcausedtissueheating,sothermaleffectscanberuledout.ThemostmarkedeffectsofGSMradiationoncFosexpressioninpicrotoxintreatedratswereobservedinlimbicstructures,olfactorycortexareasandsubcorticalareas,thedentategyrus,andthecentrallate