氢醌/Cu2+对小鼠骨髓细胞线粒体氧化损伤的研究

目的 研究在Cu^2 存在的条件下，氢醌（HQ）对小鼠骨髓细胞线粒体的氧化损伤。方法 染毒：（1）在1μmol/LCu^2 存在的条件下，小鼠骨髓细胞用0、10、20和40μmol/LHQ染毒30min；（2）1μmol/LCu^2 存在的条件下，20μmol/LHQ染毒30、60、120min。观察骨髓细胞死亡率（CDR）、活性氧（ROD）生成、线粒体酶活力和线粒体电位（MMP）的改变。结果 在1μmol/LCu^2 存在的条件,HQ正最低剂量组（10μmol/L)和最染毒时间（30min，20μmol/L）即表现出ROS生成增加（为对照组的374％和541％）、CDR增加（为对照组的115％和117％）、线粒体酶活力下降（为对照组的54％和30％）和存在剂量、时间的依赖关系（ROS：r=0.941,r=-0.981；CDR:r=0.886,r=0.886；线粒体酶活力：r=-0.842,r=-0.902；MMP：r=-0.844,r=-0.961)，ROS生成与MMP、CDR和线粒体酶活力间相关密切（r分别为－0。902，0。943，－0。977）。结论 在Cu^2 存在的情况下，HQ可导致小鼠骨髓细胞线粒体氧化损伤。细胞内ROS生成增加致线粒体氧化损伤可能是HQ诱导小鼠骨髓细胞毒性的重要途径之一。

Study on mitochondrial oxidative damage induced by hydro quinone/Cu2+ in mice bone marrow cells

Objective　To study hydroquinone(HQ) induced mitochondrial oxidative injury in mice bone marrow cells in the presence of Cu 2+. Methods　In the presence of 1 μmol/L Cu 2+,bone marrow cells isolated from mice were treated with 0,10,20 and 40 μmol/L HQ for 30 min for the dose-effect study,or treated with the combination of 1 μmol/L Cu2+ and 20 μmol/L HQ for 0,30,60 and 120 min for time -course study.Cell death rate(CDR),reactive oxygen species(ROS),mitochondrial e nzyme activity(MEA) and mitochondrial membrane potential(MMP) were observed. Results　In the presence of 1 μmol/L Cu2+,the lowest dosage of HQ (10 μmol/L) and the shoytest exposure time(30 min,20 μmol/ L) caused increase of CDR(115% and 117% of control respectively) and ROS generat ion(374% and 541% of control respectively) as well as de crease of MEA(54% and 30% of control respectively) and MMP(67% and 71% of contro l respectively) in dose- and time-dependent manner(ROS:r=0.941,0.981;CDR: r=0.866,0.866;MEA:r=-0.842,-0.902,respectively).All data were statistica lly different when compared with the control(P<0.05).In addition,ROS appeare d to have a close relationship with CDR(r=0.943),MEA(r=-0.977) and M MP(r=-0.902). Conclusion　In the presence of 1 μmol/L Cu2+,H Q could definitely cause mitochondrial oxidative injury in mice bone marrow cell s.Mitochondrial oxidative injury induced by ROS generation might be one of impor tant pathways leading to cytotoxicity of HQ.