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机构地区:[1]北京大学医学部 药学院 化学生物学系,北京100191
出 处:《Journal of Chinese Pharmaceutical Sciences》2013年第1期77-80,共4页中国药学(英文版)
基 金:National Natural Science Foundation of China(Grant No. 20871008 and 21171011)
摘 要:In this study, we aimed to clarify the source of the reactive oxygen species (ROS) generation induced by vanadium compounds. We used vanadyl acetylacetonate (VO(acac)2), a highly effective agent in controlling hyperglycemia, to determine the source of ROS generation in two renal cell lines LLC-PK1 and MDCK. Four commonly fluorescent dyes were used to assess VO(acac)2-induced H202 and "02 production and their location. It demonstrated that VO(acac)2 can induce significant ROS generation in both LLC-PKI and MDCK cells, which were primarily derived from mitochondria. The results obtained in this study raised the possibility to reduce ROS level induced by vanadium compounds locally and thus avoid affecting its activity.本研究利用具有降糖效应的双乙酰丙酮氧钒确定其在两种肾上皮细胞系LLC-PK1和MDCK中诱导产生活性氧物种的来源。利用四种常用的荧光试剂分别检测了VO(acac)2诱导产生的过氧化氢(H2O2)和超氧阴离子(·O2)的水平并确定了它们在细胞内的主要来源部位。实验结果表明,VO(acac)2在LLC-PK1和MDCK两种肾细胞系中均能显著诱导ROS的生成,并且ROS主要来源于线粒体。本研究结果提示,可通过局部降低线粒体部位ROS的水平来减少钒化合物的毒性损伤,同时不影响钒化合物的活性。
关 键 词:VO(acac)2 MITOCHONDRIA Reactive oxygen species LLC-PK1 cells MDCK cells
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