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目的探讨hOGG1基因在Cr(Ⅵ)诱导线粒体DNA氧化损伤中的修复作用。方法取不同浓度的Cr(Ⅵ)(0、2、8和32μmol/L)处理L-02肝细胞24h,分别测定细胞内活性氧簇(ROS)与hOGG1 mRNA表达水平和线粒体内8-羟基脱氧鸟苷(8-OHdG)与hOGG1基因表达的人类8-羟基鸟嘌呤DNA糖苷酶蛋白(hOGG1蛋白)水平。结果 8μmol/L和32μmol/L剂量组与对照组比较,细胞内ROS平均水平及线粒体内8-OhdG平均水平均明显增加(P<0.05),而hOGG1基因mRNA水平和线粒体内hOGG1蛋白水平,与对照组比较,2μmol/L剂量组两者水平均上升(P<0.05),32μmol/L剂量组两者水平均降低(P<0.05)。结论 Cr(Ⅵ)可诱导细胞内ROS水平增加,引起线粒体DNA氧化损伤,而hOGG1基因表达水平的改变,影响了线粒体DNA的修复能力。hOGG1基因在Cr(Ⅵ)诱导线粒体DNA氧化损伤中起到了重要的作用。
Objective To investigate the repair effect of hOGG1 gene on mitochondrial DNA oxidative damage induced by Cr (Ⅵ). Methods L-02 hepatocytes were treated with different concentrations of Cr (Ⅵ) (0, 2, 8 and 32 μmol / L) for 24 h. The levels of reactive oxygen species (ROS) and hOGG1 mRNA in mitochondria and the levels of 8- Guanosine (8-OHdG) and hOGG1 gene expression of human 8-oxoguanine DNA glycosidase protein (hOGG1 protein) levels. Results Compared with the control group, the average level of intracellular ROS and the average level of 8-OhdG in mitochondria increased significantly (P <0.05), while the mRNA levels of hOGG1 and hOGG1 in mitochondria were significantly increased in 8μmol / L and 32μmol / Compared with the control group, both the 2 μmol / L dose group and the 32 μmol / L dose group both increased (P <0.05). Conclusion Cr (Ⅵ) can induce an increase of intracellular ROS levels and cause oxidative damage to mitochondrial DNA. The change of hOGG1 gene expression affects the repair ability of mitochondrial DNA. The hOGG1 gene plays an important role in Cr (VI) -induced mitochondrial DNA oxidative damage.