Khodayar Mohammad Javad, Javadipour Mansoureh, Keshtzar Elham, Rezaei Mohsen
J Environ Biol. 2016 Mar;37(2):285-90.
The aim of the present study was to assess the protective role of berberine against toxicity induced by arsenic in mitochondria from liver of rat. The level of reactive oxygen species and mitochondrial membrane potential changes were evaluated spectrofluorometrically. 20, 40 and 100 μM arsenic concentration increased ROS level approximately by 13.5, 21.3 and 29 %. However, when pretreated mitochondria with berberine (10, 25, 50 μM) were exposed to arsenic (20, 40 and 100 μM), ROS production diminished. Also, for all arsenic concentration mitochondrial membrane damage was detected to be 2.5, 4.8 and 7.26 % respectively. Pretreatment with berberine even at highest concentration (50μM) was not able to retain membrane potential as compared to control. These results showed that mitochondria were significantly affected when exposed to arsenic, forcedly directed toward excess ROS production and mitochondrial membrane disruption. Pretreatment with berberine, reduced ROS generation but did not restore mitochondrial membrane integrity.
本研究的目的是评估小檗碱对大鼠肝脏线粒体中砷诱导的毒性的保护作用。通过荧光分光光度法评估活性氧水平和线粒体膜电位变化。20、40和100μM的砷浓度分别使活性氧水平升高了约13.5%、21.3%和29%。然而，当用小檗碱（10、25、50μM）预处理的线粒体暴露于砷（20、40和100μM）时，活性氧的产生减少。此外，对于所有砷浓度，检测到线粒体膜损伤分别为2.5%、4.8%和7.26%。与对照组相比，即使在最高浓度（50μM）下用小檗碱预处理也不能维持膜电位。这些结果表明，线粒体暴露于砷时受到显著影响，被迫产生过量的活性氧并导致线粒体膜破坏。用小檗碱预处理可减少活性氧的产生，但不能恢复线粒体膜的完整性。
