摘要
BACKGROUND:Oxidativestressplaysanimportantroleinthepathophysiologyofepilepsy.Glutathione,knownasoneofthecompoundsofantioxidantdefense,hasbeenshowntoinhibitconvulsions.Nitricoxidehasaproconvulsanteffectonapentylenetetrazole-inducedanimalmodel.OBJECTIVE:Toevaluatetheeffectsofglutathioneadministrationonnitricoxidelevelsinbrainregionsofconvulsiveandkindlingpentylenetetrazole-inducedseizuremodels.DESIGN,TIME,ANDSETTING:Arandomized,controlled,animalexperiment.ThestudywasperformedattheDepartmentofPhysiology,GaziantepUniversityandDepartmentofChemistry-Biochemistry,KahramamarasSutcuImamUniversityin2006.MATERIALS:PentylenetetrazoleandglutathionewerepurchasedfromSigma,USA.METHODS:Atotalof80micewereassignedto8groups(n=10):normalcontrol,salinecontrol(1mLnormalsaline),convulsivepentylenetetrazole(singleintraperitonealadministrationofpentylenetetrazole,60mg/kg),convulsivepentylenetrazoleplusglutathione(singleadministrationof60mg/kgpentylenetetrazoleand200mg/kgglutathione),five-doseglutathione(intraperitonealinjectionof200mg/kgglutathionerespectivelyat1,3,5,7,and10days),single-doseglutathione(singleadministrationof200mg/kgglutathione),pentylenetetrazolekindling(intraperitonealadministrationofpentylenetetrazoleof40mg/kgat1,3,5,7,and10days),andpentylenetetrazolekindlingplusglutathionegroup(intraperitonealinjectionof40mg/kgpentylenetetrazoleand200mg/kgglutathionerespectivelyat1,3,5,7,and10days).MAINOUTCOMEMEASURES:Allmiceweresacrificed1hourafterthelastadministration.Brainnitricoxidelevelsweredeterminedbyspectrophotometry.RESULTS:Therewerenosignificantdifferencesinnitricoxidelevelsbetweenthenormalcontrol,salinecontrol,five-doseglutathione,andsingle-doseglutathionegroups(P>0.05).Nitricoxidelevelsinthecerebralhemisphereandcerebellumweresignificantlylessintheconvulsivepentylenetetrazolegroup,comparedwiththeconvu
出版日期
2009年09月19日（中国期刊网平台首次上网日期，不代表论文的发表时间）
