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Study on the Mechanism of Oxidative Damage and Genotoxicity induced by BBP in Hepatic cells of Mice

机译:BBP诱导的小鼠肝细胞氧化损伤和遗传毒性的机制研究

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摘要

To illustrate the possible function of genotoxicity of BBP on DNA, this study took mice livers as experimental materials to detect the levels of DNA-protein crosslinks (DPC), the activity of surperoxide dismutase (SOD), and the contents of malondialdehyde (MDA) with intraperitioneal injection of different doses of BBP for two consecutive 14 days. DPC levels in hepatic cells showed a dose-dependent enhancement after administration of BBP. Significant DPC was observed in the 500 and 1000 mg/(kg·d) (P<0.01) groups, compared to the control group. A decrease in the activities of SOD, companied by a increase in the MDA contens, was observed. Significant changes of SOD activity could be observed in 250, 500 and 1000mg/(kg·d) (P<0.01) groups. When the exposure doses were 250, 500 and 1000mg/(kg·d), there were dramatic changes in the levels of MDA (P<0.01). To conclusion, high levels BBP induced significant oxidative damage, then caused damage to DNA.
机译:为了说明BBP对DNA的遗传毒性的可能功能,本研究以小鼠肝脏为实验材料,检测DNA-蛋白质交联(DPC)的水平,超氧化物歧化酶(SOD)的活性和丙二醛(MDA)的含量连续两个14天腹膜内注射不同剂量的BBP。给予BBP后,肝细胞中的DPC水平显示出剂量依赖性的增强。与对照组相比,在500和1000 mg /(kg·d)组中观察到了显着的DPC(P <0.01)。观察到SOD活性下降,同时MDA含量增加。 250、500和1000mg /(kg·d)组的SOD活性发生了显着变化(P <0.01)。当暴露剂量分别为250、500和1000mg /(kg·d)时,MDA水平发生了显着变化(P <0.01)。结论是,高水平的BBP会引起明显的氧化损伤,然后对DNA造成损伤。

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