镁离子对阿霉素线粒体毒性的防护作用

利用ＥＳＲ技术研究了阿霉素与心肌线粒体的相互作用及Ｍｇ＾２＋的防护作用。结果表明：在线粒体及亚线粒体体系，Ｍｇ＾２＋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Ｍｇ＾２＋的浓度。另外，Ｍｇ＾２＋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Ｍｇ＾２＋能明显延缓固定化信号出现。

MAGNESIUM CATION CAN ANTAGONIZE THE MITOTOXICITY OF ADRIAMYCIN

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