微囊藻毒素-LR致肝细胞连接通讯下调的研究  

Studies on the downregulation of gap-junctional in hepatocyte by microcystin-LR

作　　者：毛国根[1] 徐立红[1] 叶少菁[2] 

机构地区：[1]浙江大学劳动卫生与环境卫生研究所,浙江杭州310031 [2]浙江大学医学院,浙江杭州310031

出　　处：《中国环境科学》2003年第1期34-37,共4页China Environmental Science

基　　金：国家自然科学基金资助项目(20137010)

摘　　要：不同剂量(0, 10, 50,100, 200, 500, 1000nmol/L)的微囊藻毒素-LR作用于肝细胞株BRL-3A 24 h.采用激光扫描共焦显微镜,按荧光光漂白后再恢复技术测定BRL-3A的间隙连接细胞间通讯功能,四唑盐法测定BRL-3A细胞增殖,同时分析胆汁酸运输系统抑制剂利福平对两者的阻滞作用.结果表明,微囊藻毒素-LR可以显著地抑制BRL-3A细胞GJIC功能,并促进BRL-3A细胞增殖,两者均呈剂量效应关系.利福平(30靘ol/L)对微囊藻毒素-LR诱导的BRL-3A细胞GJIC功能下调和增殖有明显的抑制作用.微囊藻毒素-LR可诱导BRL-3A细胞膜泡形成.说明微囊藻毒素-LR肝脏毒性及致癌性可能与抑制肝细胞GJIC功能有关.Different amounts (0, 10, 50, 100, 200, 500, 1000nmol/L) of microcystin-LR reacted on hepatocyte BRL-3A, 24h. The function of microcystin-LR on gap-junction intercellular communication (GJIC) and the proliferation of the hepatocyte BRL-3A were determined using the fluorescence redistribution after photobleaching (FRAP) and MTT techniques, respectively; meanwhile, bill acid transport system inhibitor (rifampicin) was analyzed. The results showed that 10~1000 nmol/L microcystin-LR could significantly increase proliferation and downregulate GJIC of BRL-3A cells in a dose-dependent manner, which could be inhibited significantly in the presence of rifampicin (30靘ol/L). The study also showed the effect of microcystin-LR to induce the BRL-3A plasma membrane blebbing (named blebs). These results suggest that the downregulation of GJIC in heptocytes may play a key role in hepatotoxicity and carcinogenesis of microcystin.

关 键 词：微囊藻毒素 肝细胞 间隙连接 细胞间通讯 细胞增殖 

分 类 号：X503.2[环境科学与工程—环境工程] X171.5