资源描述：
《Atomic Force Microscope-Related Study Membrane-Associated Cytotoxicity in Human》由会员上传分享，免费在线阅读，更多相关内容在学术论文-天天文库。
1、J.Phys.Chem.B2010,114,3833–38393833AtomicForceMicroscope-RelatedStudyMembrane-AssociatedCytotoxicityinHumanPterygiumFibroblastsInducedbyMitomycinCXiaofangCai,†XiaoxiYang,‡JiyeCai,*,†ShixianWu,andQianChen†DepartmentofChemistry,TheFirstAffiliatedHospital,JinanUniVersity,Guangzhou,Guangdong510632,Peo
2、ple’sRepublicofChina,ReceiVed:NoVember10,2009;ReVisedManuscriptReceiVed:January9,2010MitomycinC(MMC)hasbeenshowntohaveatherapeuticeffectagainsthumanpterygiumfibroblasts(HPFs)byinducingapoptosis.However,thereislittledataabouttheeffectofitonplasmamembrane.Inthepresentstudy,thecytotoxicityofMMCtoHPFs
3、includinginhibitingcellgrowth,inducingapoptosisandbringingaboutmembranetoxicitywasinvestigated.ItwasfoundthatMMCcouldsignificantlysuppresstheproliferationofHPFsinadose-dependentmannerbyCCK-8assay.FlowcytometricanalysisalsorevealedthattreatmentwithMMCresultedinincreasedpercentagesofapoptoticcellsin
4、adose-dependentmanner.Membranelipidperoxidationlevel,lactatedehydrogenase(LDH)leakage,membranesurfacetopography,andmembranerigidityalterationswereinvestigatedtoassessthemembranetoxicityinducedbyMMC.TreatmentwithMMCatdifferentconcentrationsacceleratedmembranelipidperoxidationandpotentiatedLDHleaka
5、ge,whichwasconsistentwithdisturbanceofmembranesurfaceanddecreaseofmembraneelasticitydetectedbyatomicforcemicroscopy.AlltheabovechangesledtothedisturbedintracellularCa2+homeostasis,whichwasanimportantsignaltriggeringapoptosis.Hence,themembranetoxicityinducedbyMMCmightplayanimportantroleintheproces
6、sofapoptoticinductionandthecalciumchannelmaybeoneoftheapoptosismechanisms.IntroductionPreviousdataalsoshowedthatthemechanicswerealsorelatedtocellsurfacebrush.22MitomycinC(MMC)isanantimitoticagent.ItpreventscellPlasmamembraneconstitutestheboundarybetweenalivingreplicationbyformingirreversiblebonds
7、betweenthetwo1cellanditsenvironmentandplaysanimportantfunctioninstrandsoftheDNAhelixandinducesapoptosis.Itsuseisbasedcontrollingthetransportofions.Disturbanceofthemembraneonitsabilitytosuppressocularfibroblasticactivity
