肺血栓栓塞患者DNA氧化损伤的研究

目的探讨急性期及病情缓解后肺血栓栓塞（PE）患者氧化应激状态、外周血单个核细胞（PBMcs）DNA氧化损伤情况。方法采用单细胞凝胶电泳法（彗星试验）检测35例急性PE患者（试验组）及33例健康体检者（对照组）PBMCsDNA损伤程度；菲罗啉比色法检测血浆总抗氧化能力（TAC）；硫代巴比妥酸比色法检测血浆丙二醛（MDA）含量；改良Hafeman直接测定法（DNTB）检测血浆谷胱甘肽过氧化物酶（GSH—PX）活力。结果试验组病情缓解后血浆TAC、GSH．PX活性均较急性期明显升高（6．86±1．21）kU／L比（5．18±1．13）kU／L、（165．25±41．96）kU／L比（137．23±38．52）kU／L]，但均显著低于对照组（7．85±1．44），（189．92±51．32）kU／L]，差异有统计学意义（P〈0．01）；试验组病情缓解后血浆MDA含量较急性期明显降低（5．58±1．89）μmol／L比（7．26±2．25）μmol／L]，但均显著高于对照组（3．71±1．52）μmol／L]，差异有统计学意义（P〈0．01）。试验组病情缓解后PBMCsDNA损伤程度（29．01±6．75）较急性期（42．13±8．01）明显减轻，但均显著高于对照组（15．12±4．36），差异有统计学意义（P〈0．01）。试验组病情缓解后及急性期PBMCsDNA损伤均与血浆TAC呈负相关（r=-0．695，P〈0．01；r=-0．536，P〈0．01）、与血浆MDA含量呈正相关（r=0．513，P〈0．01；r=0．628，P〈0．01）；试验组病情缓解后及急性期血浆TAC均与MDA含量呈负相关（r=-0．534，P〈0．01；r=-0．486，P〈0．05）、与GSH．PX活性呈正相关（r=0．512，P〈0．01；r=0．497，P〈0．01）。结论PE患者急性期体内氧化／抗氧化失衡，存在氧化应激及其介导的PBMCsDNA损伤；PE患者病情缓解后，氧化应激及其介导的PBMCsDNA损伤减轻。

DNA oxidative damage of the peripheral blood mononuclear cells in pulmonary embolism patients

Objective To explore the level of the oxidative stress and the DNA oxidative damage of peripheral blood mononuclear cells （PBMCs） in pulmonary embolism （PE） patients after remission and in acute exacerbation. Methods The PBMCs DNA damage in 35 PE patients （test group） after remission and in acute exacerbation respectively and in 33 healthy persons （control group） was detected by single-cell gel electrophoresissingle （Comet assay）. The total antioxidative capacity （TAC） in blood plasma was measured by phenanthroline eolorimetric analysis. The contents of malondialdehyde （MDA） in blood plasma was measured by thiobarbituricacid colorimetric analysis. The capacity of glutathion peroxidase （GSH-PX） in blood plasma was measured by the method of improved Hafeman direct determination method （DNTB）. Results The level of TAC, GSH-PX in test group after remission were significantly higher than those in acute exacerbation （6.86 ± 1.21 ） kU/L vs. （5.18 ± 1.13 ） kU/L, （ 165.25 ±41.96） kU/L vs. （ 137.23 ± 38.52） kU/L] （P 〈0.01）, and they were all significantly lower than those in control group （7.85± 1.44）, （189.92 ± 51.32） kU/L] （P 〈 0.01 ）. The level of MDA in test group after remission was significantly lower than that in acute exacerbation （5.58 ± 1.89） p mol/L vs. （7.26 ± 2.25） μmol/L] （P 〈 0.01 ）, and they were significantly higher than that in control group （3.71 ± 1.52 ） μmol/L ] （P 〈 0.01 ）. The arbitrary units （AU） of PBMCs DNA damage in PE patients after remission （29.01 ± 6.75 ） was significantly lower than that in acute exacerbation （42.13 ± 8.01 ）, and they were all significantly higher than that in control group （ 15.12 ± 4.36）, there were significant differences （P 〈 0.01 ）. There were negative correlations between the PBMCs DNA damage and the level of TAC in PE patients after remission and in acute exacerbation （r = -0.695 ,P 〈 0.01 ;r = -0.536,P 〈 0.01 ）. There were