镁离子对阿霉素线粒体毒性的防护作用  

MAGNESIUM CATION CAN ANTAGONIZE THE MITOTOXICITY OF ADRIAMYCIN

作　　者：徐霆[1] 江文[1] 李生广[1] 赵保路[1] 忻文娟[1] 林治焕[1] 

机构地区：[1]中国科学院生物物理研究所

出　　处：《生物物理学报》1995年第4期614-618,共5页Acta Biophysica Sinica

摘　　要：利用ＥＳＲ技术研究了阿霉素与心肌线粒体的相互作用及Ｍｇ２＋的防护作用。结果表明：在线粒体及亚线粒体体系，Ｍｇ２＋可有效地抑制阿霉素半醌自由基产生，在一定浓度范围内抑制效果依赖于Ｍｇ２＋的浓度。另外，Ｍｇ２＋显著抑制阿霉素诱导产生的线粒体脂质过氧化。在亚线粒体体系，我们观察到阿霉素半醌自由基的固定化信号，并发现Ｍｇ２＋能明显延缓固定化信号出现。The effect of Mg2+ on interaction between chchondria inelnbrane and adriamyde (ADM)and the prmbability of using Mg2+ to amuck the mitotoxicity of ADM were investigated.It was found that Mg2+ could signfuntiy inhibit ADM to bind to subchchondriathrough competitive meChanism. It was suggffital that both ADM and Mg2+ intoract with thephosphate moietieS of cardiolipin of rintochondria inner membrane. Our adults shoed that20mol/L Mg2+ drmsed subdschondria-hound ADM by abcut 3 0 %.The signal of ADM swiuinone was mothend with ESR technique. When NADH,ADM, submitochondria were added, the sigul appeals and meched maximun in afew minutes. Mg2+(10-2-10-3mol/L) could dectease the intensity of the signal,The scavengingeffod of Mg2+ was dependent on the Mg2+ concentration. The similar resuits were observed inmitochondria.In addition, in subdechondria and dschodria, it was observed that the symmetric spantrum of ADM semiquinone radical changed into a completely immobiled spectrum andMg2+ could delay this proals.By assaying TBA reaction material, we found that Mg2+ could proal dechondria membrane from lipid peroxidation induce by ADM., and the effect was also relied upon theMg2+ concentration. IC50 was about 20mmol/L

关 键 词：阿霉素 抗癌药 镁离子 线粒体 毒性 

分 类 号：R979.14[医药卫生—药品]