3-硝基酪氨酸对HepG2细胞氧化还原状态的影响

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。

The influence of 3-Nitrotyrosine to Oxidative Stress in HepG2 Cell

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.