Noninvasive detection of hydroxyl radical generation in lung by diesel exhaust particles
Noninvasive detection of hydroxyl radical generation in lung by diesel exhaust particles
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DOI：
10.1016/s0891-5849(00)00501-3
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发表时间：
2001-03-01
影响因子：
7.4
通讯作者：
Utsumi, H
中科院分区：
文献类型：
--
作者：
Han, JY;Takeshita, K;Utsumi, H
柴油机排气颗粒（DEP）在实验动物中诱发肺肿瘤、哮喘样症状等。活性氧（ROS）参与DEP引起的损伤，但尚未证实。本研究首次提供了（OH）-O-存在的直接证据。使用非侵入性的L-带ESR光谱和膜不可渗透的硝酰基探针，在肺内滴注DEP后，在活小鼠的肺中产生。（OH）-O-。通过探针的体内ESR信号衰减速率的增强来证实产生。与溶剂处理的小鼠相比，DEP处理的小鼠胸中部的衰减率显著增强。这种增强作用可被（OH）-O-抑制。清除剂，过氧化氢酶，或去铁胺，而SOD的管理进一步增加的速度。将芬顿试剂注入小鼠肺内也可提高小鼠胸中部探针的衰减率。这些结果清楚地提供了证据，表明小鼠体内暴露于DEP产生（OH）-O-。通过铁催化的超氧化物/H2 O2反应在肺中。这是（OH）-O-的第一个直接证据。在DEP处理的小鼠肺中的产生可以用于确定DEP诱导的肺损伤的治疗。(C)2001 Elsevier Science Inc.
Diesel exhaust particles (DEP) induce pulmonary tumors, asthma-like symptoms, and the like in experimental animals. The involvement of reactive oxygen species (ROS) is suggested in the injuries induced by DEP, though the generation of ROS has not been proven. The present study provided the first direct evidence of (OH)-O-. generation in the lungs of living mice after intratracheal instillation of DEP, using noninvasive L-band ESR spectroscopy and a membrane-impermeable nitroxyl probe. (OH)-O-. generation is confirmed with the enhancement of in vivo ESR signal decay rate of the probe. The decay rate at mid-thorax was significantly enhanced in DEP-treated mice compared to that in vehicle-treated mice. The enhancement was completely suppressed by the administration of either (OH)-O-. scavengers, catalase, or desferrioxamine, while the administration of SOD further increased the rate. The administration of Fenton's reagents into the lung also enhanced the decay rate of the probe at mid-thorax of mice. These results clearly provided evidence that the intratracheal exposure to DEP in mice produced (OH)-O-. in the lung through an iron-catalyzed reaction of superoxide/H2O2. This first direct evidence of (OH)-O-. generation in DEP-treated mice lung may be utilized to determine treatments for DEP-induced lung injury. (C) 2001 Elsevier Science Inc.