紅葡萄酒中英文對(duì)照外文翻譯文獻(xiàn)

中英文對(duì)照外文翻譯文獻(xiàn)(文檔含英文原文和中文翻譯)英文文獻(xiàn):RedwineconsumptionincreasesantioxidantstatusanddecreasesoxidativestressinthecirculationofbothyoungandoldhumansBackground:Redwinecontainsanaturallyrichsourceofantioxidants,whichmayprotectthebodyfromoxidativestress,adeterminantofage-relateddisease.Thecurrentstudysetouttodeterminetheinvivoeffectsofmoderateredwineconsumptiononantioxidantstatusandoxidativestressinthecirculation.Methods:20young(18–30yrs)and20older(≥50yrs)volunteerswererecruited.Eachagegroupwasrandomlydividedintotreatmentsubjectswhoconsumed400mL/dayofredwinefortwoweeks,orcontrolsubjectswhoabstainedfromalcoholfortwoweeks,afterwhichtheycrossedoverintotheothergroup.Bloodsampleswerecollectedbeforeandafterredwineconsumptionandwereusedforanalysisofwholebloodglutathione(GSH),plasmamalondialdehyde(MDA)andserumtotalantioxidantstatus.Results:Resultsfromthisstudyshowconsumptionofredwineinducedsignificantincreasesinplasmatotalantioxidantstatus(P<0.03),andsignificantdecreasesinplasmaMDA(P<0.001)andGSH(P<0.004)inyoungandoldsubjects.Theresultsshowthattheconsumptionof400mL/dayofredwinefortwoweeks,significantlyincreasesantioxidantstatusanddecreasesoxidativestressinthecirculation.Conclusion:Itmaybeimpliedfromthisdatathatredwineprovidesgeneraloxidativeprotectionandtolipidsystemsincirculationviatheincreaseinantioxidantstatus.BackgroundEffortstodefinetheroleofnutritioninhealthhavecapturedresearcher'sinterestinantioxidantsandtheircapacitytoprotectthebodyfromdamageinducedbyoxidativestress.Extensiveresearchhasdemonstratedtheprotectivepropertiesofantioxidants,whichscavengereactiveoxygenspecies(ROS)andtheirprecursors,aswellasup-regulateenzymesinvolvedintherepairofcellulardamage.Redwinecontainsarichsourceofalargenumberofantioxidants,namelythephenolicacidsandpolyphenols,whichprovideitwithitsprotectiveredoxpotential.Epidemiologicalstudieshaveshownthatdespitethehighintakeofsaturatedfattyacidswithinthedietsofsomepopulations,areducedmortalityratefromcardiovasculardiseaseisattributedtothehighconsumptionofredwine,independentofitsalcoholcontent,the‘FrenchParadox’.Studiesalsoindicatethatsub-populationsalreadyatahighriskofcoronaryheartdisease(CHD)(i.e.elderly)maypotentiallyexperienceagreaterbeneficialeffectfrommoderatewineconsumption[5].Moderateconsumptionofredwinehasalsobeenshowntoretardorslowtheplasmaclearanceofhighdensitylipoproteins(HDL),anegativeriskfactorforthedevelopmentofcardiovasculardisease(CVD).Indoingso,apositivecorrelationbetweenHDLparticlesandmoderateredwineintakebecomesevident.Furthermore,theincubationoflowdensitylipoproteinsLDL)invaryingconcentrationsofredandwhitewineshoweda50%declineinoxidationatconcentrationsof0.04and0.7mg/ethanol/mLrespectively,uptoaconcentrationof1.0mg/mL.TheseresultsindicatethatredwineinhibitscellmediatedLDLoxidationmoreefficientlythenwhitewineandatmuchlowerconcentrations.Toinvestigatefurther,therelationshipbetweenredwineconsumptionandoxidativedamageinhumanshasbeenstudiedbyGreenrodandFenech,inaseriesofinvitroandexvivostudydesigns.Theydemonstratedastrong(>70%)reductioninH2O2inducedgeneticdamageafter1hourpostconsumptionof300mLofredwine.ThesefindingsarealsosupportedbyasimilarstudybySzetoandBenzie,showingthatDNAdamagewassignificantlyreducedinaH2O2challenge,withtreatmentofcaffeicacid,apolyphenolfoundinredwine.Oxidativedamagetoarangeofbiomoleculesisofparticularinteresttoresearchers.Thetripeptideglutathione(GSH)functionsasanantioxidant,whichscavengesfreeradicalspeciesincirculation.GSHisoxidizedastheenzymeglutathioneperoxidasecatalyzesthedegradationofH2O2.IncreasingevidencedemonstratesGSHplaysanintegralroleintheprotectionagainstoxidativestressinthecirculationduetoitsabilitytofacilitatetherecyclingofoxidizedα-tocopherolandascorbicacid,twoimportantantioxidantsinthecirculationandiswidelyusedasabiomarkerofcirculatingantioxidantlevels.WithinplasmafattyacidresiduesofphospholipidsandLDL,areextremelysusceptibletooxidativedamagebyfreeradicalintermediatesresultinginoxidizedfattyacidsandperoxidationbyproducts,suchasconjugateddiennes(CD)andmalondialdehyde(MDA)derivatives.MDAappearstobeoneofthemosttoxicandmutagenicaldehydesgeneratedbylipidperoxidationofpolyunsaturatedfattyacidsofcellmembranes.Itisalsoapopularmeasurementusedtoquantifytheeffectsofradicaldamagetocellularlipids.AlargebodyofevidencewhichindicatesthatfreeradicalproductioncandirectlyorindirectlyplayamajorroleincellularprocessesimplicatedinatherosclerosisandCVD,.Thereforetheaimofthisstudywerefirstlytounderstandhowmoderateredwineconsumption(400ml/day)fortwoweekseffectedcirculatinglipids,antioxidantlevelandtotalantioxidantcapacityinthecirculationandsecondlyassessthedifferencesinbioefficacyofredwineinyoungandolderpopulations.MethodsRecruitmentofvolunteersThisstudyprotocolwasapprovedbytheHumanResearchEthicsCommitteeofVictoriaUniversity(HRETH.SET15/05).Fortyvolunteerswereselectedbasedupontheirresponsestoageneralhealthquestionnaireandaftergivingwritteninformedconsent.Thosewhoweretakinganyanti-coagulantoranti-inflammatorymedicationsorhadahistoryofcardiovascularorliverdiseasewereexcluded.Twoagegroupswereselected,thesewere20volunteersagedbetween18–30yearsold(younggroup)and20volunteersagedolderthen50yearsold(oldergroup).Volunteerswererandomlyassignedtobeginintheredwineorcontrolgroupwithintheirrespectiveagegroup(Figure1).InterventiondesignPriortodrinkingtheredwineorcontrolperiodvolunteerswereaskedtoabstainfromconsuminganyalcohol,grapesorgrapeproductsforoneweek.Afterthisoneweekleadinsubjectshadthree10mLtubesoffastingbloodcollectedviavenipuncturetodeterminebaselinemeasuresofMDA,GSH,andtotalantioxidantcapacityandBMI(kg/m2)calculated,afterwhichtheybegantheredwineorcontrolperiod.Duringtheredwineperiodparticipantsconsumed400mLofredwineeachday(CabernetSauvignon)overaperiodoftwoconsecutiveweeksandabstainedfromotheralcohol,grapesorgrapeproducts.Aplacebosuchasalcoholfreewinewasnotusedduetodifficultiesinmatchingtheflavourandmouthfeeloftheredwineused.Insteadacrossoverdesignwasusedwherebyaftercompletingeithertheredwineorcontrolperiodvolunteersweregivenatwoweekwashoutperiodbeforecrossingoverintotheothergroup.Duringthecontrolperiodvolunteersabstainedfromconsuminganysourceofalcohol,grapesorgrapeproductsfortwoweeks.Three10mLtubesoffastingbloodwereagaincollectedafterthetreatmentorcontrolphase(seeFigure1).Participantswerealsoencouragedtomaintaintheirusualdietandexercisehabitsthroughouttheentirestudyphasewhichwasmonitoredbyparticipantskeepingafoodandactivitydiarybeforeandduringthestudy.Therewerenospecificinstructionsgiventoavoidfoodscontaininglargeamountsofphenoliccompounds,otherthanabstainfromconsuminganyalcohol,grapesorgrapeproductsaspreviouslydescribed.WinesupplementationTheredwineusedthroughoutthisstudywasaCabernetSauvignon,suppliedasacaskwinetopreventtheoxidationofthewine.Thisstylewaschosensinceitisknowntobepalatabletomostpeopleandtothevolunteersinthestudy.Participantsconsumedthewineatanytimeduringtheday,however,itwassuggestedthattheydosoatatimewhentheywouldnormallyconsumealcohol(e.g.withaneveningmeal).Importantly,duringtheperiodofsupplementationparticipantswereaskedtorefrainfromconsuminganyothersourcesofalcohol,grapesorgrapeproducts.WinecompositionTheconcentrationsoftotalanthocyanins,degreeofanthocyaninionisation,totalphenoliccompounds,redwinecolour(densityandhue)andtwoindicesprovidingameasureofpolymerisationofmonomericforms(Chemicalageindex#1and#2)weredeterminedbyspectrophotometricmethods.DeterminationoftheconcentrationoffreeandboundsulphurdioxideinthewinewasmadeusingthemethodofRankineandPocock.Alcoholcontentwasprovidedbythewineproducer.ThecompositionofthewineusedinthisstudywasanalysedcanbeseeninTable1.Allcomponentsofthewineusedinthisstudy,exceptforredwinecolour–hueandfreesulfurdioxide,wereslightlyhigherthantheredwineusedinastudybyGreenrodetal.AnalysesofglutathioneGlutathionewasmeasuredasitisanimportantantioxidantinthecirculationusingacommerciallyavailablecolorimetrickit(NorthwestLifeSciences)basedonthemethodofTeitzefollowingthemanufacturesinstructions.BloodwascollectedviavenipunctureusingEDTAcoatedtubesandstoredat4°C.Wholebloodsampleswerethendeproteinatedmixingaliquotswith100ulofcold5%metaphosphoricacidfollowedbycentrifugationat1500×gfor5min,thesupernatantwasthenremovedandstoredat-20°Cawaitingfurtheranalysis.AllsampleswerethenassayedforreducedGSHasabatch.Thisinvolvedmixing50μLofcalibratorsorsampleswith50μLDTNBreagentand50μLglutathionereductasereagentinthewellsofmicroplate.Thisreactionmixwasthenincubatedatambienttemperaturefor3minafterwhich50ulNADPHreagentwasaddedtoallwellsandabsorbancevaluesreadat405nmwithdatacollectedat15secintervalsfor3min.Absorbancevalueswerethenplottedasafunctionoftimeforeachcalibratorandsample.Acalibrationcurvewasthenconstructedbyplottingthe△A405/minforeachcalibratorasafunctionoftheGSHconcentrationandtheequationforthecalibrationcurvewasthenusedtocalculatetheconcentrationofGSHinallsamples.AnalysesofmalondialdehydePlasmamalondialdehydewasasamarkeroflipidperoxidationusingacommerciallyavailablecolorimetrickit(NorthwestLifeSciences)followingthemanufacturesinstructions.BloodwascollectedviavenipunctureusingEDTAcoatedtubes,storedat4°Candplasmaseparatedwithin2hrsbycentrifugationat3000×gfor10minutesatroomtemperature.Plasmasampleswerethenstoredat-20°Cawaitingfurtheranalysis.AllsampleswerethenassayedforMDAasabatch.Thisinvolvedmixing250ulcalibratororsamplewith10uLofButylatedhydroxytoluenereagent,250ulPhosphoricacidreagentand250ul2-Thiobarbituricacidreagent.Thisreactionmixwasthenincubatedat60°Cfor60minfollowedbycentrifugationat10000×gfor3min.Absorbanceofcalibratorsandsampleswasthenreadat532nminaspectrophotometer(Biorad).AbsorbancevaluesforcalibratorswerethenusedtoconstructacalibrationcurveandtheequationforcalibrationcurvewasthenusedtocalculatetheconcentrationofMDAinallsamples.AnalysesoftotalantioxidantstatusSerumtotalantioxidantstatus(TAS)wasdeterminedforaquantitativeassessmentofinvivoantioxidantstatususingacommerciallyavailablekit(Randox)basedonthetroloxequivalentantioxidantcapacitymethodofMillerfollowingthemanufacturesinstructions.Bloodwascollectedviavenipunctureusingserumseparatortubes,storedat4°Candserumseparatedwithin2hrs.Serumsampleswerethenstoredat-20°Cawaitingfurtheranalysis.AllsampleswerethenassayedforTASasabatch.Thisinvolvedmixing20μLcalibrator(6-hydroxy-2,5,7,8-etramethylchroman-2-carboxylicacid1.79mmol/L)orsamplewith1mlofchromogen(metmyoglobin6.1μmol/L,ABTS610μmol/L)andincubatingat37°Cfor3min.Initialabsorbancewasthenreadat600nminaspectrophotometer(Biorad).Afterwhich200μLofsubstrate(hydrogenperoxide250μmol/L)wasaddedtocalibratorandsampleandincubatedat37°Cfor3min.Finalabsorbancewasthenreadat600nm.ThechangeinabsorbancevalueforsamplesrelativetothechangeinabsorbanceofthecalibratorwasthentocalculatetheTASinallsamples.Thetotalantioxidantstatusoftheredwine(CabernetSauvignon)usedinthisstudywasalsomeasuredusingthesameassay.AnalysesofserumglucoseandplasmalipidsSerumglucosewasdeterminedusingacommercialglucoseoxidasereagentandstandard(ThermoElectronCorporation).Thisinvolvedmixing3μLofcalibratororsamplewith450μLofglucoseoxidasereagentandincubatingat37°Cfor5min.Absorbanceofcalibratorsandsampleswasthenreadat500nminaspectrophotometer(Biorad).Theabsorbancevalueofsamplesrelativetotheabsorbanceofthecalibratorwasthentocalculatetheglucoselevelinallsamples.Plasmatriglyceridesweredeterminedusingcommerciallyavailablecolorimetrickit(ThermoElectronCorporation).Thisinvolvedmixing6μLofcalibratororsamplewith600μLoftriglyceridereagentandincubatingat37°Cfor3min.Absorbanceofcalibratorsandsampleswasthenreadat500nminaspectrophotometer(Biorad).Theabsorbancevalueofsamplesrelativetotheabsorbanceofthecalibratorwasthentocalculatethetriglyceridelevelinallsamples.Totalcholesterolwasdeterminedusingcommerciallyavailablecolorimetrickit(ThermoElectronCorporation).Thisinvolvedmixing6μLofcalibratororsamplewith600μL ofcholesterolreagentandincubatingat37°Cfor3min.Absorbanceofcalibratorsandsampleswasthenreadat500nminaspectrophotometer(Biorad).Theabsorbancevalueofsamplesrelativetotheabsorbanceofthecalibratorwasthentocalculatethecholesterollevelinallsamples.HDLcholesterolwasdeterminedusingcommerciallyavailablecolorimetrickit(ThermoElectronCorporation).Thisinvolvedmixing4μLofcalibratororsamplewith300μLofHDLreagent1andincubatingat37°Cfor5min.Afterwhich100μLofHDLreagent2wasaddedtocalibratorandsampleandincubatedat37°Cfor3min.Absorbanceofcalibratorsandsampleswasthenreadat600nminaspectrophotometer(Biorad).Theabsorbancevalueofsamplesrelativetotheabsorbanceofthecalibratorwasthentocalculatethetriglyceridelevelinallsamples.LDLcholesterol,ariskfactorforcardiovasculardisease,wascalculatedbysubtractingHDLcholesterolvalues,anegativeriskfactorforcardiovasculardisease,fromtotalcholesterol.StatisticalanalysisStatisticalanalysiswasperformedusingtheSPSSstatisticalpackage(version12.0,SPSSInc.).Alldataweredistributednormallyandexpressedasmean±standarderrorofthemean(SEM).DatafromyoungandolderindividualswereanalyzedusingathreewayANOVAtodeterminetheeffectofwineconsumptionwithintheyoungoroldgroup,anydifferencebetweenyoungandoldgroupsandanydifferencebetweenpresampleswiththeyoungoroldgroup.Duetothecrossoverdesignofthestudyanydifferencebetweenarenotincludedintheanalysisstheprimaryfocusoftheresearchwastodeterminetheeffectofredwineconsumption.InallcasesaPvalueof<0.05wasconsideredstatisticallysignificant.ResultsWholebloodglutathionewasmeasuredasitisanimportantcirculatingantioxidant.BeforeandafterredwineconsumptionGSHlevelswereelevatedinoldervolunteerscomparedtoyoungvolunteers(P<0.001,Figure2).DespitethisdifferencebetweenyoungandoldvolunteersconsumptionofredwinehadthesameeffectwithboththeyoungandoldgroupscausingsignificantreductionsinGSHlevelsafterredwineconsumption,youngwithwine(P=0.004)andolderwithwineperiods(P<0.001,Figure2).NosignificantchangesinGSHlevelwereobservedinyoungandoldergroupswithoutredwine.Plasmamalondialdehydewasmeasuredasabiomarkeroflipidperoxidation.BeforeandafterredwineconsumptionMDAlevelswerereducedinoldervolunteerscomparedtoyoungvolunteers(P<0.05,Figure3).DespitethisdifferencebetweenyoungandoldvolunteersconsumptionofredwinehadthesameeffectwithinboththeyoungandoldgroupcausingsignificantreductionsinMDAlevelsafterredwineconsumption,youngwithwine(P<0.001)andolderwithwineperiods(P<0.001,Figure3).NosignificantchangesinMDAlevelwereobservedinyoungandoldergroupswithoutredwine.Serumtotalantioxidantstatuswascalculatedforsamplesfromeachstudygroup.BeforeredwineconsumptionTASlevelsweredecreasedinoldervolunteerscomparedtoyoungvolunteers(P<0.001,Figure4).Despitethisdifferencebetweenyoungandoldvolunteersconsumptionofredwinehadthesameeffectwithinboththeyoungandoldgroupdemonstratingasignificantincreaseintotalantioxidantstatusafterredwineconsumption,youngwithwine(P=0.026)andolderwithwineperiods(P=0.01,Figure4).ThesechangescorrespondtothechangesinGSHandMDAwithredwineconsumptionforbothyoungandoldergroups.Thetotalantioxidantstatusoftheredwineconsumedbyalltreatmentsubjectsinthisstudycontained1.53±0.027mmol/Lofantioxidantcapacity(Figure4).Therewasnosignificantdifferenceinbothage(yrs)andBMI(kg/m2)betweenredwineandabstinenceperiodsforbothyoungandolderpopulationgroups(Table2).Similarlytherewerenodifferencesinserumglucoseconcentrationsbetweenpreandpostsamplesforbothyoungandoldercontrolandtreatmentgroups(Table2).Plasmalipidprofilesforeachstudygroupwereexaminedthroughthedeterminationofplasmacholesterol,plasmatriglycerides,plasmaHDL-cholesterolandplasmaLDL-cholesterolvalues.Nostatisticalsignificancewasfoundforanyofthebloodlipidprofileswithineachstudygroup(Table2).References1.MortonLW,Abu-AmshaCaccettaR,PuddeyIB,CroftKD:Chemistryandbiologicaleffectsofdietaryphenoliccompounds：relevancetocardiovasculardisease.ClinExpPharmacolPhysiol2000,27(3):152-9.2.Rice-EvansCA,MillerNJ,BolwellPG,BramleyPM,PridhamJB:Therelativeantioxidantactivitiesofplant-derivedpolyphenolicflavonoids.FreeRadicRes1995,22(4):375-83.3.GermanJB,WalzemRL:Thehealthbenefitsofwine.AnnuRevNutr2000,20:561-93.4.RenaudS,deLorgerilM:Wine,alcohol,platelets,andtheFrenchparadoxforcoronaryheartdisease.Lancet1992339(8808):1523-6.5.GronbaekM:Factorsinfluencingtherelationbetweenalcoholandmortality–withfocusonwine.JInternMed2001,250(4):291-308.6.RificiVA,StephanEM,SchneiderSH,KhachadurianAK:Redwineinhibitsthecell-mediatedoxidationofLDLandHDL.JAmCollNutr1999,18(2):137-43.7.GreenrodW,FenechM:Theprincipalphenolicandalcoholiccomponentsofwineprotecthumanlymphocytesagainsthydrogenperoxide-andionizingradiation-inducedDNAdamageinvitro.Mutagenesis2003,18(2):119-26.8.SzetoYT,BenzieIF:EffectsofdietaryantioxidantsonhumanDNAexvivo.FreeRadicRes2002,36(1):113-8.9.TosukhowongP,SangwatanarojS,JatupornS,PrapunwattanaP,SaengsiriA,RattanapruksS,SrimahachotaS,UdayachalermW,TangkijvanichP:ThecorrelationbetweenmarkersofoxidativestressandriskfactorsofcoronaryarterydiseaseinThaipatients.ClinHemorheolMicrocirc2003,29(3–4):321-9.10.JefferiesH,CosterJ,KhalilA,BotJ,McCauleyRD,HallJC:Glutathione.ANZJSurg2003,73(7):517-22.11.DjuricZ,PotterDW,TaffeBG,StrasburgGM:Comparisonofiron-catalyzedDNAandlipidoxidation.JBiochemMolToxicol2001,15(2):114-9.12.LasherasC,HuertaJM,GonzalezS,BranaAF,PattersonAM,FernandezS:Independentandinteractiveassociationofbloodantioxidantsandoxidativedamageinelderlypeople.FreeRadicRes2002,36(8):875-82.13.WestIC:Radicalsandoxidativestressindiabetes.DiabetMed2000,17(3):171-80.14.HalliwellB,GutteridgeJ,editors:Freeradicalsinbiologyandmedicine.Oxford:ClarendonPress;1989.15.SomersT,VéretteE:Phenoliccompositionofnaturalwinetypes.InModernMethodsofPlantAnalysis:WineAnalysisEditedbyLinskensH,JacksonJ.Berlin:Springer-Verlag;1988:219-57.16.SomersT,EvansM:Spectralevaluationofyoungredwines:anthocyaninequilibria,totalphenolics,freeandmolecularSO2chemicalage.JSciFoodAgric1977,28:279-87.譯文:飲用紅葡萄酒能增加抗氧化狀態(tài)并減少氧化應(yīng)激在年輕和老年人體內(nèi)的循環(huán)摘要背景：紅葡萄酒中含有豐富的抗氧化劑天然來(lái)源，這可以保護(hù)免受氧化應(yīng)激，一個(gè)與年齡有關(guān)的疾病決定因素身體。目前的研究要確定適度飲用紅葡萄酒對(duì)體內(nèi)抗氧化狀態(tài)及氧化應(yīng)激的循環(huán)。方法：20名青年（18-30歲）和20個(gè)老年人（≥50歲）志愿者招募。每個(gè)年齡組隨機(jī)分為治療科目，在兩星期內(nèi)消耗的紅葡萄酒為400毫升/天;或控制科目，即放棄飲用紅葡萄酒兩周，之后他們相互交換，進(jìn)入另一組進(jìn)行實(shí)驗(yàn)。收集血液樣本前、后的紅葡萄酒的消耗量并用于分析全血谷胱甘肽（GSH），血漿丙二醛（MDA）和血清總抗氧化狀態(tài)。結(jié)果：本研究顯示，在年輕人和老年人科目中，紅酒飲用的結(jié)果引起的血漿總抗氧化狀態(tài)（P<0.03）顯著增加，血漿丙二醛性（P<0.001）和GSH性（P<0.004）顯著降低。結(jié)果表明：400毫升/天紅葡萄酒消耗量?jī)蓚€(gè)星期，大大增強(qiáng)了抗氧化狀態(tài)，降低氧化應(yīng)激反應(yīng)的循環(huán)。結(jié)論：這可能是通過(guò)此數(shù)據(jù)來(lái)暗示紅葡萄酒提供一般氧化保護(hù)，并在循環(huán)中的脂質(zhì)系統(tǒng)增加抗氧化狀態(tài)。背景致力于界定在健康的營(yíng)養(yǎng)作用的抗氧化劑，已經(jīng)引起了研究者的興趣，它們可以以防止氧化應(yīng)激反應(yīng)損傷身體。廣泛的研究已經(jīng)證明，抗氧化劑的這種能清除活性氧自由基（ROS）及其前體，以及參與上調(diào)在細(xì)胞損傷修復(fù)酶的保護(hù)性能。紅葡萄酒中含有大量豐富抗氧化劑來(lái)源，即酚酸類和多酚類物質(zhì)，它提供其氧化還原電位保護(hù)。流行病學(xué)研究表明，盡管一些人飲食內(nèi)的高飽和脂肪酸攝入量較高，根據(jù)'法國(guó)悖論'，來(lái)自心血管疾病死亡率會(huì)降低是歸因于高消耗量的紅葡萄酒，無(wú)關(guān)其酒精含量。研究還表明，溫和的飲用葡萄酒，在冠心病的高危亞群還可能會(huì)遇到更大的潛在有利的影響。適度消費(fèi)紅葡萄酒也被證明可以阻礙或延緩血漿清除高密度脂蛋白（HDL），一種對(duì)于心血管疾?。–VD）發(fā)展不利的危險(xiǎn)因素。在這樣做時(shí)，高密度和中度的脂蛋白粒子之間的紅酒攝入正相關(guān)關(guān)系變得很明顯。此外，低密度脂蛋白（LDL）在紅、白葡萄酒的發(fā)酵過(guò)程中，在氧化50％左右時(shí)，濃度0.7毫克/乙醇/毫升，呈現(xiàn)0.04％的跌幅，最多為1.0毫克/毫升的濃度。這些結(jié)果表明，紅葡萄酒能以低得多的濃度，比白葡萄酒更高效的抑制細(xì)胞介導(dǎo)的??低密度脂蛋白的氧化。為了進(jìn)一步調(diào)查人們的紅葡萄酒飲用量和氧化損傷之間的關(guān)系，Greenrod和Fenech研究了在體外和體外研究設(shè)計(jì)系列。他們說(shuō)明了飲用了300ml的紅葡萄酒一小時(shí)后，表現(xiàn)出了強(qiáng)烈的過(guò)氧化氫誘導(dǎo)的遺傳損傷（>70％）減少的現(xiàn)象。這些發(fā)現(xiàn)也支持了Szeto和Benzie的類似的研究，表明DNA損傷在經(jīng)過(guò)咖啡酸的處理，即在紅酒中發(fā)現(xiàn)一種多酚，顯著減少了過(guò)氧化氫的傷害。研究人員特別感興趣的是生物分子氧化損傷的的范圍。GSH作為一種抗氧化劑，它的作用是讓腐質(zhì)物中的自由基循環(huán)。GSH是谷胱甘肽過(guò)氧化酶的氧化酶，可以催化降解過(guò)氧化氫。越來(lái)越多的證據(jù)表明，谷胱甘肽在中的抗氧循環(huán)化應(yīng)激保護(hù)作用中是一個(gè)一個(gè)不可或缺的角色，是因?yàn)樗苑奖慊厥昭趸?維生素E和維生素C的能力。它們是兩種重要的抗氧化劑，廣泛應(yīng)用為在抗氧化劑水平的循環(huán)的生物標(biāo)志物。在血漿脂肪酸種的磷脂酸殘基和低密度脂蛋白，是非常容易被自由基氧化損傷的，氧化脂肪酸和脂質(zhì)過(guò)氧化造成的副產(chǎn)品而產(chǎn)生的中間體，如CD和MDA的衍生物。MDA似乎是通過(guò)細(xì)胞膜的脂質(zhì)里的多不飽和脂肪酸氧化而產(chǎn)生最具毒性、最易使其它物種突變的醛之一。這也是一個(gè)受歡迎的測(cè)試，用于定量分析自由基損傷對(duì)細(xì)胞血脂的影響。

大量的證據(jù)表明自由基的多少，在涉及到細(xì)胞過(guò)程的動(dòng)脈粥樣硬化和CVD時(shí)，可直接或間接地發(fā)揮重要作用。因此本研究的目的是先了解兩周內(nèi)適度消費(fèi)紅葡萄酒（400毫升/天），對(duì)流動(dòng)脂質(zhì)在抗氧化水平和總抗氧化能力循環(huán)中的影響；其次評(píng)估年輕人和老年人的人口在紅葡萄酒中的生物學(xué)效價(jià)的差異。方法招募志愿者

本研究議定書經(jīng)過(guò)人類研究維多利亞大學(xué)倫理委員會(huì)的批準(zhǔn)。根據(jù)對(duì)一份一般健康問(wèn)卷的答復(fù)，篩選出四十名志愿者，然后發(fā)出書面知情同意書。將那些服用任何抗凝血?jiǎng)┗蚩拱l(fā)炎的藥物或有心血管或肝臟疾病病史的排除。選取兩個(gè)年齡組，20名志愿者是18-30歲之間（青年組），另一組的志愿者比前一組志愿者年齡大了50歲（老年組）。志愿者們開(kāi)始被隨機(jī)分配到紅葡萄酒或?qū)φ战M在各自的年齡組（圖1）。

因素設(shè)計(jì)在此之前喝紅葡萄酒或控制階段的志愿者被要求一個(gè)星期內(nèi)放棄飲用任何酒精，葡萄或葡萄產(chǎn)品。一周后的項(xiàng)目是通過(guò)靜脈穿刺收集3管10ml的血液，進(jìn)行基準(zhǔn)測(cè)量來(lái)確定丙二醛、谷胱甘肽、總抗氧化能力和體重指數(shù)(kg/m2)，在他們開(kāi)始了飲用紅葡萄酒或控制階段之后。在經(jīng)過(guò)連續(xù)的兩周內(nèi)不飲用酒類、葡萄或葡萄產(chǎn)品，之后進(jìn)入每天飲用400ml的紅葡萄酒（赤霞珠）的時(shí)期。所謂安慰劑，不使用諸如無(wú)酒精葡萄酒是因?yàn)樗煌南嗥ヅ涞娘L(fēng)味和口感。相反，采用交叉設(shè)計(jì)完成后，即無(wú)論是紅葡萄酒還是控制階段志愿者分別在進(jìn)入另一組前都要經(jīng)過(guò)兩個(gè)星期的洗脫期。控制期的志愿者要求在兩個(gè)星期內(nèi)不飲用任何酒精來(lái)源的食品、葡萄和葡萄產(chǎn)品。在治療或控制階段之后再次收集三管10ml的空腹血樣。還鼓勵(lì)志愿者們?cè)谡麄€(gè)學(xué)習(xí)階段保持平時(shí)的飲食和鍛煉習(xí)慣，監(jiān)測(cè)他們?cè)谘芯恐昂脱芯科陂g的飲食和活動(dòng)記錄。就像前面所描述的那樣，沒(méi)有具體指明要求避免食物中含有大量的酚類化合物，其他的任何酒精、葡萄或葡萄產(chǎn)品。葡萄酒的飲用在本研究使用的紅酒是一赤霞珠干紅，用一個(gè)木桶來(lái)提供，以防止葡萄酒的氧化。選中這種酒是因?yàn)樗m合大多數(shù)人的胃口，包括這些研究中的志愿者。志愿者們可以在一天當(dāng)中的任何時(shí)候飲用紅葡萄酒，然而，會(huì)有人建議他們?cè)诮?jīng)常飲用的時(shí)候做，例如晚飯的時(shí)候。重要的是，在志愿者們的補(bǔ)充期間被要求不要食用酒精，葡萄或任何其他來(lái)源的葡萄產(chǎn)品。葡萄酒的組成總花青素濃度、程度電離花青素、總酚類化合物、紅葡萄酒的顏色（密度和色調(diào)）和提供兩個(gè)指數(shù)用分光光度法測(cè)定單體的聚合形式（化學(xué)年齡指數(shù)1和2）。用朗肯和波科克方法測(cè)定紅酒中游離和混合狀態(tài)的二氧化硫。葡萄酒中的酒精含量是葡萄酒生產(chǎn)商提供的。在這項(xiàng)研究中所用的酒成分可以在表1中看到。在這個(gè)研究中用到的所有成分，除了紅葡萄酒的顏色-色調(diào)和游離的二氧化硫，都略高于Greenrod等在相似研究里使用的紅酒。分析谷胱甘肽由于谷胱甘肽在循環(huán)體系中是一個(gè)重要的抗氧化劑，它的側(cè)定是使用市售的比色試劑盒（西北生命科學(xué)），依據(jù)Teitze方法、按其生產(chǎn)說(shuō)明來(lái)測(cè)定的。通過(guò)靜脈穿刺采血用EDTA涂層管在4°C條件下儲(chǔ)存，然后全血樣本經(jīng)脫蛋白后，等份混合，加入5%的冷偏酸在1500r每分鐘離心5分鐘，再取出上清液并儲(chǔ)存在-20°C條件下，有待進(jìn)一步分析。然后所有樣品檢測(cè)到在一個(gè)批次里減少谷胱甘肽。這涉及混合50μL的定標(biāo)液或50ulDTNB法試劑的樣品和50μl谷胱甘肽還原酶的微孔板井試劑。當(dāng)這種反應(yīng)在環(huán)境溫度混合培養(yǎng)3分鐘后，加入50微升的NADPH試劑板孔，在3分鐘內(nèi)每隔15秒在吸光度值在405nm時(shí)讀取和收集數(shù)據(jù)。之后以作為對(duì)每個(gè)校準(zhǔn)器和樣品的吸光度值和時(shí)間繪圖。標(biāo)準(zhǔn)曲線繪制當(dāng)時(shí)構(gòu)建了每個(gè)表準(zhǔn)作為谷胱甘肽功能A405/min濃度和校準(zhǔn)曲線方程，用來(lái)計(jì)算所有樣品中GSH的含量。分析丙二醛血漿丙二醛作為脂質(zhì)過(guò)氧化的標(biāo)記，按以下的生產(chǎn)指令使用市售的比色試劑盒（西北生命科學(xué)）。血液通過(guò)靜脈穿刺法采集置于EDTA的涂層管，儲(chǔ)存于4°C條件下，2小時(shí)內(nèi)在室溫下以3000r每分鐘離心10分鐘，進(jìn)行血漿分離。然后將血漿樣品儲(chǔ)存在-20°C，等待進(jìn)一步分析。然后測(cè)定的所有樣品的MDA為一批。這包括250μL的定標(biāo)液或樣品和10μL的二叔丁基對(duì)甲酚試劑，250μL的磷酸試劑和250μL及二硫代巴比妥酸劑的混合。混合反應(yīng)，在10000r每分鐘離心3分鐘，然后保持溫度在60℃條件60分鐘。之后在532nm時(shí)用分光光度計(jì)讀取校準(zhǔn)品和樣品的吸光度。為校準(zhǔn)吸光度值，用來(lái)構(gòu)建一個(gè)校準(zhǔn)曲線和方程，然后用校準(zhǔn)曲線來(lái)計(jì)算所有樣本中MDA濃度?？偪寡趸癄顟B(tài)分析血清總抗氧化水平（TAS）為定量評(píng)價(jià)體內(nèi)抗氧化狀態(tài)，使用市售的套件（英國(guó)朗道），按照米勒的測(cè)定總抗氧化能力方法制造說(shuō)明的基礎(chǔ)上測(cè)定出來(lái)的。通過(guò)靜脈穿刺采血應(yīng)用血清分離管分裝，儲(chǔ)存于4°C和在2小時(shí)內(nèi)分離血清。然后將血清樣本儲(chǔ)存在-20°C有待進(jìn)一步分析。檢測(cè)所有樣品的血清總抗氧化水平作為一個(gè)批次。這包括20μL的混合定標(biāo)液（1.79mmol/L的6-羥基-2，5,7,8-四甲基二氫吡喃-2-羧酸）或1毫升的樣品顯色液（6.1μmol/L的肌紅蛋白，610μmol/L的ABTS），在37℃反應(yīng)3分鐘。然后用分光光度計(jì)在600nm處讀取其初始吸光度值。加入200μL的基板（250μmol/L的過(guò)氧化氫）至定標(biāo)液和樣品后，在37℃下反應(yīng)3分鐘。最后讀取在600nm處得吸光度值。該樣品的吸光度值變化相對(duì)于標(biāo)準(zhǔn)液的吸光度而改變，然后計(jì)算所有樣本的血清總抗氧化水平。在本研究中使用的紅葡萄酒（赤霞珠）的總抗氧化水平也使用相同的測(cè)量法測(cè)定。分析血清葡萄糖和血脂血糖測(cè)定采用商業(yè)的葡萄糖氧化酶試劑和標(biāo)準(zhǔn)（熱電公司）。這包括3μL的定標(biāo)液或樣品和450μL葡萄糖氧化酶試劑混合，于37℃下反應(yīng)5分鐘。用分光光度計(jì)在500nm時(shí)讀取定標(biāo)液和樣品的吸光度值。樣品的吸光度值與標(biāo)準(zhǔn)液的吸光度值變化是相聯(lián)系的，然后計(jì)算所有樣本中葡萄糖的水平。血漿甘油三酯的測(cè)定是使用市售的比色試劑盒（熱電公司）。這包括6μL定標(biāo)液或樣品和600μL的甘油三酯試劑混合，在37℃時(shí)反應(yīng)3分鐘。然后用分光光度計(jì)在500nm時(shí)讀取校準(zhǔn)品和樣品吸光度值。樣品的吸光度值和定標(biāo)液的吸光度值相對(duì)應(yīng)，然后計(jì)算出在所有樣本甘油三酯的水平?？偰懝檀嫉臏y(cè)定是使用市售比色試劑盒（熱電公司）。這包括6μL定標(biāo)液或樣品和600μL的膽固醇試劑混合，在37℃的條件下反應(yīng)3分鐘。用分光光度計(jì)在500nm時(shí)讀取校準(zhǔn)品和樣品吸光度值。然后根據(jù)樣品和定標(biāo)液的吸光度值的相對(duì)關(guān)系，計(jì)算所有樣本的膽固醇水平。高密度脂蛋白膽固醇的測(cè)定是使用商用比色法試劑盒（熱電公司）。這包括4μL定標(biāo)液或樣品和300μL高密度脂蛋白膽固醇試劑1混合，在37℃反應(yīng)5分鐘。將100μL的高密度脂蛋白膽固醇試劑2添加到定標(biāo)液和樣品中后，在37°C時(shí)反應(yīng)3分鐘。用分光光度計(jì)在600nm時(shí)讀取校準(zhǔn)品和樣品吸光度。依據(jù)樣品和標(biāo)準(zhǔn)液吸光度值的相對(duì)關(guān)系，然后再計(jì)算出所有樣本的甘油三酯水平。在總膽固醇中，低密度脂蛋白膽固醇是心血管疾病的危險(xiǎn)因素，它是減去對(duì)心血管疾病具有負(fù)面影響的高密度脂蛋白膽固醇值而計(jì)算得到的。統(tǒng)計(jì)分析采用SPSS統(tǒng)計(jì)軟件包（版本12.0，SPSS公司）進(jìn)行統(tǒng)計(jì)分析。所有數(shù)據(jù)進(jìn)行正態(tài)分布，并表示為平均值±平均標(biāo)準(zhǔn)（掃描電鏡）的誤差。年輕人和老年人的個(gè)人數(shù)據(jù)采用三因素方差分析，以確定葡萄酒消費(fèi)的影響在年輕和年老組，年輕人和老年人之間的任何團(tuán)體及每個(gè)樣本的差異。由于以上的交叉研究設(shè)計(jì)之間的任何差異分析，本研究的主要重點(diǎn)是確定紅葡萄酒消耗的影響。在所有情況下，P值<0.05有統(tǒng)計(jì)學(xué)意義。結(jié)論測(cè)定全血谷胱甘肽，因?yàn)樗茄h(huán)系統(tǒng)的一個(gè)重要的抗氧化劑。前后紅葡萄酒的消耗量GSH水平，老年志愿者比青年志愿者更高（P<0.001,圖2）。盡管年輕人和老年人志愿者之間的這種差異，在青年群體和老年群體的紅酒消耗量具有兩個(gè)同樣的效果，在飲用紅葡萄酒后導(dǎo)致GSH水平顯著下降，青年飲酒后（P=0.004）和老年人飲酒期間（P<0.001，圖2）。而在沒(méi)有飲用紅葡萄酒的青年和老年群體中的GSH水平則無(wú)顯著變化。血漿丙二醛作為生物脂質(zhì)過(guò)氧化作用的標(biāo)志來(lái)測(cè)定。老年志愿者相對(duì)于青年志愿者在飲用紅葡萄酒前后其MDA水平減少了(P<0.05,圖3)。盡管年輕人和老年人志愿者之間的這種差異，在青年群體和老年群體的紅酒消耗量具有兩個(gè)同樣的效果，在飲用紅葡萄酒后導(dǎo)致MDA水平顯著降低，青年飲酒后(P<0.001)，老年飲酒期(P<0.001,圖3）。在沒(méi)有飲用紅葡萄酒的青年和老年群體中的MDA水平則無(wú)顯著變化。每個(gè)研究小組以樣本計(jì)算出血清總抗氧化水平。在飲用紅葡萄酒前，老年志愿者相對(duì)于青年志愿者的總抗氧化水平降低(P<0.001,圖4)。盡管年輕人和老年人志愿者之間的這種差異，在青年群體和老年群體的紅酒消耗量具有兩個(gè)