微囊藻毒素LR诱导无DNA片断化的细胞凋亡  

Microcystin-LR Induces Apoptosis with the Absence of DNA Fragmentation

作　　者：雷腊梅[1] 宋立荣[2] 韩博平[1] 

机构地区：[1]暨南大学水生生物研究中心,广州510632 [2]中国科学院水生生物研究所,武汉430072

出　　处：《热带医学杂志》2006年第7期749-751,784,共4页Journal of Tropical Medicine

基　　金：国家重点基础研究发展规划项目(No.2002CB412306);广东省自然科学基金(No.5300418)

摘　　要：目的研究微囊藻毒素(microcystin,MC)损伤肝细胞的毒性机制。方法以不同浓度的微囊藻毒素LR(MCLR)处理L-02肝细胞,通过光镜和电镜下的形态观察、DNA片断化分析、线粒体膜电位变化等了解MCLR对肝细胞的毒性效应。结果光镜下观察表明,50!g/mlMCLR处理可使细胞变圆、萎缩、不贴壁生长,电镜下L-02细胞呈现皱缩、膜发泡及染色质凝聚并边缘化等变化,这是典型的细胞凋亡形态特征,但电镜下没有观察到凋亡小体的形成;DNA电泳表明凋亡细胞没有出现明显的DNAladder,与电镜观察的结果一致。流式细胞仪检测发现以50!g/mlMCLR处理60h后,细胞的线粒体膜电位显著下降。结论微囊藻毒素损伤线粒体可能是其损伤细胞的途径之一,这种微囊藻毒素诱导的无DNA片段断裂的凋亡现象属首次报道,具体机制有待进一步阐明。Objective To study the mechanism of hepatocyte damage caused by micrecystins. Methods In this study,a human normal liver cell line L-02 was treated with different concentrations of MCLR for toxicological investigation such as morphological changes, DNA fragmentation and mitochmndria membrane potential. Results It was found that L-02 cells treated with 50 μg/ml of MCLR underwent cell rounding-up, detachment from the substrate and cell shrinkage. Ultrastructural investigation showed the treated cells were shrunken, and with membrane blebbling and condensed and marginated chromatin, which were typical morphological changes of apoptosis. However, no obvious DNA degradation occurred according to electron microscopic and DNA gel clectrophoresis analysis. The results also showed that mitochondria membrane potential of the treated L-02 ceils obviously decreased. Conclusion Microcystin-induced cell damage may be cause by decreasing the mitochondria membrane potential. The mechanism of apoptosis without DNA fragmentation induced by MCLR needed to be further demonstrated.

关 键 词：微囊藻毒素 细胞凋亡 DNA片断化 

分 类 号：Q949.222[生物学—植物学]