Diesel exhaust particles (DEP) induce pulmonary tumors, asthma-like symptom
s, and the like in experimental animals. The involvement of reactive oxygen
species (ROS) is suggested in the injuries induced by DEP, though the gene
ration of ROS has not been proven. The present study provided the first dir
ect evidence of (OH)-O-. generation in the lungs of living mice after intra
tracheal instillation of DEP, using noninvasive L-band ESR spectroscopy and
a membrane-impermeable nitroxyl probe. (OH)-O-. generation is confirmed wi
th 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 desferri
oxamine, while the administration of SOD further increased the rate. The ad
ministration of Fenton's reagents into the lung also enhanced the decay rat
e of the probe at mid-thorax of mice. These results clearly provided eviden
ce that the intratracheal exposure to DEP in mice produced (OH)-O-. in the
lung through an iron-catalyzed reaction of superoxide/H2O2. This first dire
ct evidence of (OH)-O-. generation in DEP-treated mice lung may be utilized
to determine treatments for DEP-induced lung injury. (C) 2001 Elsevier Sci
ence Inc.