摘要:
轻稀土元素进入生物体后主要累积于肝脏,进入肝细胞,除蓄积在细胞核中,还存在于线粒体中。为探讨轻稀土元素对小鼠肝细胞线粒体的氧化损伤作用,选用5周龄雄性ICR小鼠分别以10、20和40 mg·kg-1的镧(La)、铈(Ce)和钕(Nd)灌胃,6周后测定小鼠肝细胞线粒体中超氧化物岐化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)的活性,以及谷胱甘肽(GSH)和丙二醛(MDA)的含量。结果显示,与对照组相比,La中剂量组和Ce低剂量组SOD活性显著升高,La高剂量组和Nd中、高剂量组中SOD活性显著降低(P < 0.05,P < 0.01);除个别剂量组外,各染毒组CAT和GPx活性与GSH含量显著降低(P < 0.05,P < 0.01);Nd各剂量组、La高剂量组和Ce高剂量组的MDA含量显著升高(P < 0.05,P < 0.01)。研究表明,La、Ce和Nd所导致的CAT和GPx活性以及GSH含量降低可能是造成肝细胞线粒体氧化损伤的主要原因。
Abstract:
Light rare earth elements are found to mainly accumulate in the livers of receiving organisms. They can enter into hepatocytes and are mainly distributed in the mitochondria besides nuclei. To investigate the oxidative damage effects of light rare earth elements on the mitochondria isolated from the mouse liver, five-week-old male ICR mice were exposed to lanthanum (La), cerium (Ce) and neodymium (Nd) at different doses (10, 20 and 40 mg·kg-1) by oral gavage for 6 weeks. The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were determined as well as the contents of glutathione (GSH) and malondialdehyde (MDA). Results showed that compared with the control group, SOD activity was significantly elevated in the La middle-dosage and Ce low-dosage groups, while SOD activity significantly decreased in the La highdosage, Nd middle-dosage and Nd high-dosage groups (P < 0.05, P < 0.01); the activities of CAT and GPx, and GSH level significantly decreased (P < 0.05, P < 0.01) with only a few exceptions; MDA level significantly increased in the La high-dosage, Ce high-dosage and all Nd exposure groups (P < 0.05, P < 0.01). It is indicated that La, Ce and Nd decreased the activities of CAT and GPx and the level of GSH, which might be the main reason for inducing oxidative damage in hepatic mitochondria.
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