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镉致心肌细胞线粒体损伤的研究

发布时间 2009-10-08 浏览量 作者: 无 来源: 无
    镉是一种十分重要的工业和环境污染物,动物实验和人群流行病学资料表明镉可产生复杂的毒性效应.长期以来,人们就其对肝、肾、睾丸等器官及其线粒体损伤的研究较多,但对心肌细胞及其线粒体损伤报道却很少.
    本次实验主要针对氯化镉致心肌细胞线粒体的损伤进行研究,实验结果表明5μM 的氯化镉即可引起大鼠心肌细胞线粒体的损伤,并且随着给予氯化镉剂量的增加,损伤程度逐渐加重.
    MTT 实验结果显示,镉能降低心肌细胞存活率,并呈现明显的剂量效应关系.镉可影响心肌细胞与能量代谢相关酶的活性,受试组细胞ATP 酶和LDH 的活性明显低于对照组,随着剂量加大,其活性逐渐降低,与对照组相比较差异具有显著性.采用流式细胞仪检测分析线粒体膜电位变化,受试组线粒体膜电位减低显著.分光光度法测定线粒体膜通透性变化(MPT),吸光度呈下降趋势.实验结果表明,氯化镉可影响心肌细胞能量代谢、损伤线粒体膜结构,从而进一步导致心肌细胞受损.此项研究的意义在于证明氯化镉可以对心肌细胞线粒体造成损伤,从而可能导致相关心血管疾病的发生,该项研究为镉中毒以及心血管疾病的防治工作提供了新的思路.
    In the study, we use toxicological and cytobiocological methods todetermine the things of damage on myocytes induced by CdCl2.The results inmy study showed as follows :1. The effects of CdCl2 on living-rate of myocytesWe use MTT method to examine the living-rate of myocytes . As results , afew of dead myocytes were observed in 5uM group. And death-rate increasedfollowing doses increased, there were significant differences between controlgroup and exposure groups. It indicated that CdCl2 could influent the living-rateof myocytes.2. The effects of CdCl2 on activity of LDHIt’s showed that the LDH activities of exposure groups had decreased thanthat of control group , following increased doses. There were significantdifferences between exposure groups and control group, and also among theexposure groups. It indicated that CdCl2 could decreased the activity of LDH.3. The effects of CdCl2 on activity of ATP-enzymeIt was found that the ATP activities of exposure groups were low than thatof control group. And there were significant differences beween control groupand exposure groups, and also among the exposure groups. It indicated thatCdCl2could also decreased the activity of ATP-enzyme.4. CdCl2 could affect the MMPWe use FCM to determine the MMP of myocytes. In the way of bindingRh123 to mitochondria , we could see that the MMP have decreased followedthe CdCl2 doses increased. There was dose-effect correlationship existed.Determination of Rh123-PI double binding, the Rh123-binding rates of cells ofexposure groups has decreased, and PI-binding rates of cells of exposure groups

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