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3-硝基酪氨酸对HepG2细胞氧化还原状态的影响 被引量:6

The infl uence of 3-Nitrotyrosine to Oxidative Stress in HepG2 Cell
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摘要 为了确定3-硝基酪氨酸是否能促进细胞内产生氧化应激,该文研究了不同浓度3.硝基酪氨酸对HepG2细胞作用不同时间(6-48h)后,其对细胞活力、细胞内ROS(H2O2、O2-)、细胞内总抗氧化能力、细胞内抗氧化酶活力和脂质氧化的影响。结果表明,在高浓度(300μmol/L)3.硝基酪氨酸作用48h后,细胞活力下降至48.5%。同时,3-硝基酪氨酸能显著提升细胞内ROS并降低细胞内抗氧化酶活力,同时造成细胞内脂质过氧化物大量积累,最终使细胞线粒体膜电位去极化,并导致SirT3表达下调。损伤随着3-硝基酪氨酸含量的增加和反应时间的延长而加重。结果发现,3.硝基酪氨酸不仅作为蛋白质氧化产物,还能进一步通过降低机体内抗氧化能力而导致细胞内氧化应激加剧,最终导致细胞凋亡。 In order to determine whether 3-nitrotyrosine can promote oxidative stress in cells, HepG2 cells were treated with 3-nitrotyrosine at different time and concentrations. And the cell viability, intracellular ROS (H2O2, O2-), total antioxidant capacity of cells, intracellular antioxidant enzymes and lipid oxidation were tested. The re- sults showed that, with high concentration (300 μmol/L) of 3-nitrotyrosine, the cell viability decreased to 48.5% when incubated for 48 h. Meanwhile, 3-nitrotyrosine greatly affected intracellular ROS, intracellular antioxidant enzyme activity, and intracellular lipid oxidation of the cells. And it was proportional to 3-nitrotyrosine content and reaction time. In addition, 3-nitrotyrosine reduced mitochondrial membrane potential, and the expression of SirT3. In conclusion, 3-nitrotyrosine acted not only as protein oxidation products, but also could exacerbate oxidative stress of the cells by reducing the antioxidant capacity of the body and eventually lead to apoptosis.
出处 《中国细胞生物学学报》 CAS CSCD 北大核心 2014年第4期509-515,共7页 Chinese Journal of Cell Biology
基金 十二五国家科技支撑项目(批准号:2012BAD33B05) 江苏高校优势学科建设工程资助项目资助的课题~~
关键词 3-硝基酪氨酸 HEPG2 抗氧化能力 细胞凋亡 3-nitrotyrosine HepG2 antioxidant capacity apoptosis
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参考文献17

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