红葡萄酒中英文对照外文翻译文献

中英文对照外文翻译文献(文档含英文原文和中文翻译)英文文献: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,Co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大量的证据表明自由基的多少，在涉及到细胞过程的动脉粥样硬化和CVD时，可直接或间接地发挥重要作用。因此本研究的目的是先了解两周内适度消费红葡萄酒（400毫升/天），对流动脂质在抗氧化水平和总抗氧化能力循环中的影响；其次评估年轻人和老年人的人口在红葡萄酒中的生物学效价的差异。方法招募志愿者

本研究议定书经过人类研究维多利亚大学伦理委员会的批准。根据对一份一般健康问卷的答复，筛选出四十名志愿者，然后发出书面知情同意书。将那些服用任何抗凝血剂或抗发炎的药物或有心血管或肝脏疾病病史的排除。选取两个年龄组，20名志愿者是18-30岁之间（青年组），另一组的志愿者比前一组志愿者年龄大了50岁（老年组）。志愿者们开始被随机分配到红葡萄酒或对照组在各自的年龄组（图1）。

因素设计在此之前喝红葡萄酒或控制阶段的志愿者被要求一个星期内放弃饮用任何酒精，葡萄或葡萄产品。一周后的项目是通过静脉穿刺收集3管10ml的血液，进行基准测量来确定丙二醛、谷胱甘肽、总抗氧化能力和体重指数(kg/m2)，在他们开始了饮用红葡萄酒或控制阶段之后。在经过连续的两周内不饮用酒类、葡萄或葡萄产品，之后进入每天饮用400ml的红葡萄酒（赤霞珠）的时期。所谓安慰剂，不使用诸如无酒精葡萄酒是因为它不同的相匹配的风味和口感。相反，采用交叉设计完成后，即无论是红葡萄酒还是控制阶段志愿者分别在进入另一组前都要经过两个星期的洗脱期。控制期的志愿者要求在两个星期内不饮用任何酒精来源的食品、葡萄和葡萄产品。在治疗或控制阶段之后再次收集三管10ml的空腹血样。还鼓励志愿者们在整个学习阶段保持平时的饮食和锻炼习惯，监测他们在研究之前和研究期间的饮食和活动记录。就像前面所描述的那样，没有具体指明要求避免食物中含有大量的酚类化合物，其他的任何酒精、葡萄或葡萄产品。葡萄酒的饮用在本研究使用的红酒是一赤霞珠干红，用一个木桶来提供，以防止葡萄酒的氧化。选中这种酒是因为它适合大多数人的胃口，包括这些研究中的志愿者。志愿者们可以在一天当中的任何时候饮用红葡萄酒，然而，会有人建议他们在经常饮用的时候做，例如晚饭的时候。重要的是，在志愿者们的补充期间被要求不要食用酒精，葡萄或任何其他来源的葡萄产品。葡萄酒的组成总花青素浓度、程度电离花青素、总酚类化合物、红葡萄酒的颜色（密度和色调）和提供两个指数用分光光度法测定单体的聚合形式（化学年龄指数1和2）。用朗肯和波科克方法测定红酒中游离和混合状态的二氧化硫。葡萄酒中的酒精含量是葡萄酒生产商提供的。在这项研究中所用的酒成分可以在表1中看到。在这个研究中用到的所有成分，除了红葡萄酒的颜色-色调和游离的二氧化硫，都略高于Greenrod等在相似研究里使用的红酒。分析谷胱甘肽由于谷胱甘肽在循环体系中是一个重要的抗氧化剂，它的侧定是使用市售的比色试剂盒（西北生命科学），依据Teitze方法、按其生产说明来测定的。通过静脉穿刺采血用EDTA涂层管在4°C条件下储存，然后全血样本经脱蛋白后，等份混合，加入5%的冷偏酸在1500r每分钟离心5分钟，再取出上清液并储存在-20°C条件下，有待进一步分析。然后所有样品检测到在一个批次里减少谷胱甘肽。这涉及混合50μL的定标液或50ulDTNB法试剂的样品和50μl谷胱甘肽还原酶的微孔板井试剂。当这种反应在环境温度混合培养3分钟后，加入50微升的NADPH试剂板孔，在3分钟内每隔15秒在吸光度值在405nm时读取和收集数据。之后以作为对每个校准器和样品的吸光度值和时间绘图。标准曲线绘制当时构建了每个表准作为谷胱甘肽功能A405/min浓度和校准曲线方程，用来计算所有样品中GSH的含量。分析丙二醛血浆丙二醛作为脂质过氧化的标记，按以下的生产指令使用市售的比色试剂盒（西北生命科学）。血液通过静脉穿刺法采集置于EDTA的涂层管，储存于4°C条件下，2小时内在室温下以3000r每分钟离心10分钟，进行血浆分离。然后将血浆样品储存在-20°C，等待进一步分析。然后测定的所有样品的MDA为一批。这包括250μL的定标液或样品和10μL的二叔丁基对甲酚试剂，250μL的磷酸试剂和250μL及二硫代巴比妥酸剂的混合。混合反应，在10000r每分钟离心3分钟，然后保持温度在60℃条件60分钟。之后在532nm时用分光光度计读取校准品和样品的吸光度。为校准吸光度值，用来构建一个校准曲线和方程，然后用校准曲线来计算所有样本中MDA浓度。总抗氧化状态分析血清总抗氧化水平（TAS）为定量评价体内抗氧化状态，使用市售的套件（英国朗道），按照米勒的测定总抗氧化能力方法制造说明的基础上测定出来的。通过静脉穿刺采血应用血清分离管分装，储存于4°C和在2小时内分离血清。然后将血清样本储存在-20°C有待进一步分析。检测所有样品的血清总抗氧化水平作为一个批次。这包括20μL的混合定标液（1.79mmol/L的6-羟基-2，5,7,8-四甲基二氢吡喃-2-羧酸）或1毫升的样品显色液（6.1μmol/L的肌红蛋白，610μmol/L的ABTS），在37℃反应3分钟。然后用分光光度计在600nm处读取其初始吸光度值。加入200µL的基板（250μmol/L的过氧化氢）至定标液和样品后，在37℃下反应3分钟。最后读取在600nm处得吸光度值。该样品的吸光度值变化相对于标准液的吸光度而改变，然后计算所有样本的血清总抗氧化水平。在本研究中使用的红葡萄酒（赤霞珠）的总抗氧化水平也使用相同的测量法测定。分析血清葡萄糖和血脂血糖测定采用商业的葡萄糖氧化酶试剂和标准（热电公司）。这包括3μL的定标液或样品和450μL葡萄糖氧化酶试剂混合，于37℃下反应5分钟。用分光光度计在500nm时读取定标液和样品的吸光度值。样品的吸光度值与标准液的吸光度值变化是相联系的，然后计算所有样本中葡萄糖的水平。血浆甘油三酯的测定是使用市售的比色试剂盒（热电公司）。这包括6µL定标液或样品和600μL的甘油三酯试剂混合，在37℃时反应3分钟。然后用分光光度计在500nm时读取校准品和样品吸光度值。样品的吸光度值和定标液的吸光度值相对应，然后计算出在所有样本甘油三酯的水平。总胆固醇的测定是使用市售比色试剂盒（热电公司）。这包括6µL定标液或样品和600µL的胆固醇试剂混合，在37℃的条件下反应3分钟。用分光光度计在500nm时读取校准品和样品吸光度值。然后根据样品和定标液的吸光度值的相对关系，计算所有样本的胆固醇水平。高密度脂蛋白胆固醇的测定是使用商用比色法试剂盒（热电公司）。这包括4μL定标液或样品和300μL高密度脂蛋白胆固醇试剂1混合，在37℃反应5分钟。将100µL的高密度脂蛋白胆固醇试剂2添加到定标液和样品中后，在37°C时反应3分钟。用分光光度计在600nm时读取校准品和样品吸光度。依据样品和标准液吸光度值的相对关系，然后再计算出所有样本的甘油三酯水平。在总胆固醇中，低密度脂蛋白胆固醇是心血管疾病的危险因素，它是减去对心血管疾病具有负面影响的高密度脂蛋白胆固醇值而计算得到的。统计分析采用SPSS统计软件包（版本12.0，SPSS公司）进行统计分析。所有数据进行正态分布，并表示为平均值±平均标准（扫描电镜）的误差。年轻人和老年人的个人数据采用三因素方差分析，以确定葡萄酒消费的影响在年轻和年老组，年轻人和老年人之间的任何团体及每个样本的差异。由于以上的交叉研究设计之间的任何差异分析，本研究的主要重点是确定红葡萄酒消耗的影响。在所有情况下，P值<0.05有统计学意义。结论测定全血谷胱甘肽，因为它是循环系统的一个重要的抗氧化剂。前后红葡萄酒的消耗量GSH水平，老年志愿者比青年志愿者更高（P<0.001,图2）。尽管年轻人和老年人志愿者之间的这种差异，在青年群体和老年群体的红酒消耗量具有两个同样的效果，在饮用红葡萄酒后导致GSH水平显著下降，青年饮酒后（P=0.004）和老年人饮酒期间（P<0.001，图2）。而在没有饮用红葡萄酒的青年和老年群体中的GSH水平则无显著变化。血浆丙二醛作为生物脂质过氧化作用的标志来测定。老年志愿者相对于青年志愿者在饮用红葡萄酒前后其MDA水平减少了(P<0.05,图3)。尽管年轻人和老年人志愿者之间的这种差异，在青年群体和老年群体的红酒消耗量具有两个同样的效果，在饮用红葡萄酒后导致MDA水平显着降低，青年饮酒后(P<0.001)，老年饮酒期(P<0.001,图3）。在没有饮用红葡萄酒的青年和老年群体中的MDA水平则无显著变化。每个研究小组以样本计算出血清总抗氧化水平。在饮用红葡萄酒前，老年志愿者相对于青年志愿者的总抗氧化水平降低(P<0.001,图4)。尽管年轻人和老年人志愿者之间的这种差异，在青年群体和老年群体的红酒消耗量具有两个