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[目的]研究二氧化硫(SO2)吸入致小鼠肺、心组织蛋白质氧化损伤和对DNA-蛋白质交联(DPC)率的影响。[方法]分别用浓度为14、28、56mg/m3的SO2气体对小鼠动态染毒7d(每天6h),对照组小鼠在同样饲养条件下吸入新鲜空气。用2,4-二硝基苯肼(DNPH)比色法测定蛋白质羰基(PCO)含量,用KCl-SDS法测定DPC率。[结果]SO2各染毒浓度组与对照组相比,均可致小鼠肺、心PCO含量和DPC率升高。雌性小鼠SO2染毒浓度与肺、心PCO含量的回归方程分别为:y=0.1744x+4.192(R2=0.9998),y=0.0420x+3.896(R2=0.9763);雄性小鼠分别为:y=0.0441x+4.204(R2=0.9945),y=0.1553x+4.488(R2=0.9883),均呈现明显的剂量-效应关系。雌性小鼠SO2染毒浓度与肺、心DPC率回归方程分别为:y=0.0395x+1.404(R2=0.9913),y=0.0121x+1.614(R2=0.9902);雄性小鼠分别为:y=0.0132x+1.616(R2=0.9821),y=0.0329x+1.45(R2=0.9922),同样呈现明显的剂量-效应关系。[结论]SO2吸入可致小鼠肺、心PCO含量和DPC率呈剂量依赖性升高。随着SO2浓度的增加,对肺、心蛋白质的氧化损伤加剧,DPC率升高。吸入同浓度SO2小鼠的肺、心PCO含量和DPC率结果表明,对肺的损伤远大于心。
[Objective] To investigate the effects of sulfur dioxide (SO2) inhalation on lung and heart tissue protein oxidative damage and DNA-protein cross-linking (DPC) rate in mice. [Method] The mice were exposed to SO2 gas for 14 days, 8 days and 56 mg / m3, respectively. The mice in the control group were exposed to fresh air for 7 days (6 hours a day). The content of protein carbonyl (PCO) was determined by 2,4-dinitrophenylhydrazine (DNPH) colorimetric method, and the DPC rate was determined by KCl-SDS method. [Result] Compared with the control group, all the concentration of SO2 increased the lung and heart PCO content and DPC rate in mice. The regression equations of SO2 concentration in lungs and PCO in lung and heart of female mice were as follows: y = 0.1744x + 4.192 (R2 = 0.9998), y = 0.0420x + 3.896 (R2 = 0.9763) = 0.0441x + 4.204 (R2 = 0.9945), y = 0.1553x + 4.488 (R2 = 0.9883), respectively. All showed a significant dose-response relationship. The regression equation of SO2 concentration and lung and heart DPC in female mice were: y = 0.0395x + 1.404 (R2 = 0.9913), y = 0.0121x + 1.614 (R2 = 0.9902) 0.0132x + 1.616 (R2 = 0.9821), y = 0.0329x + 1.45 (R2 = 0.9922), also showed a significant dose-response relationship. [Conclusion] SO2 inhalation induced a dose-dependent increase of PCO and DPC in lung and heart of mice. With the increase of SO2 concentration, oxidative damage to lung and heart proteins was exacerbated and DPC rate was increased. Inhalation of lung and heart PCO2 concentration and DPC rate of SO2 mice inhaled at the same concentration showed that lung damage was much greater than that of heart.