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时间:2020-04-16
《砷诱导蚕豆气孔保卫细胞死亡的毒性效应-论文.pdf》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、第34卷第5期生态学报Vo1.34.No.52014年3月ACTAECOL0GICASINICAMar.,2014DOI:10.5846/stxb201210171445薛美昭,仪慧兰.砷诱导蚕豆气孔保卫细胞死亡的毒性效应.生态学报,2014,34(5):1134—1139.XueMZ,YiHL.ArsenicinducesguardcelldeathinleafepidermisofViciaba.ActaEcologicaSinica,2014,34(5):1134—1139砷诱导蚕豆气孔保卫细胞死亡的毒性效应薛美昭,仪慧兰(山西大学生命科学学院,太原030006)
2、摘要:采用蚕豆(ViciabaL.)叶面气孔保卫细胞,研究砷对细胞的毒性效应。结果表明,O.3~10mg/L的NaAsO:能降低保卫细胞活性,使部分细胞死亡,死亡率随砷浓度升高而增高。死细胞中呈现核固缩、核崩解等典型程序性死亡特征,且泛caspase抑制剂Z-Asp,CH:一DCB能阻止NaAsO诱发的细胞死亡。过氧化氢清除剂过氧化氢酶与NaAsO共同作用时,细胞死亡率显著低于砷单独处理组,保卫细胞内ca水平降低,具程序性死亡特征的细胞数减少;ca特异性螯合剂EGTA亦能降低NaAsO诱发的细胞死亡。研究结果表明,NaAsO能诱发蚕豆保卫细胞程序性死亡,该过程由胁迫引发
3、的ROS升高引起,ROS可能通过激活质膜ca通道,使胞外ca内流,造成胞内ca浓度升高,进而诱导细胞程序性死亡。关键词:蚕豆保卫细胞;NaAsO2;程序性细胞死亡;ROS;CaArsenicinducesguardcelldeathinleafepidermisofViciafabaXUEMeizhao,YIHuilanSchoolofLifeScience,ShanxiUniversity,Taiyuan030006,ChinaAbstract:Arsenicisahighlytoxicmetalloidforallformsoflifeincludingplants
4、.Arsenicentersinplantsthroughphosphatetransportersasaphosphateanalogueorthroughaquaglycoporins.Uptakeofarsenicinplanttissuescanaffectplantmetabolism,causingvariousphysiologicaldisorders,structuralabnormalitiesandevenplantdeath.Oxidativestressisconsideredtobeakeymechanismofarsenictoxicity
5、.Inthisstudy,theeffectofsodiumarsenite(NaAsO2)Oilguardcellviabilitywasinvestigatedindetachedepidermisof、.缸baleaves.Epidermalstripswereobtainedfrom4-week-oldplantsbypeelingofthelowerepidermisof、.缸baleavesandincubatedin2-(N—morpholino)ethanesulfonicacid(MES)buffercontainingsomechemicals(Na
6、AsO2withorwithoutsomeantagonists)for3hinwhitelightat23℃asthetreatments.Aftertreatment,theepidermalstripswerestainedwithfluoresceindiacetate(FDA)toshowcellviability,orwith2,7'-dichlorofluoresceindiacetate(DCFH—DA)andfluo一3acetomethoxyester(Fluo一3AM)respectivelytoindicateintracellularreact
7、iveoxygenspecies(ROS)andcalciumion(Ca)levels.TheresultsofourexperimentsshowedthatNaAsO2treatmentsignificantlydecreasedcellviabilityandinducedcelldeathintheconcentrationrangeof0.3to10mg/L.ArsenicprovokessynchronousincreasesincelldeathrateandintraeellularlevelsofROSandCainb
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