Ozone is a well-known
oxidant air pollutant, inhalation of which can result in oxidative stress, and lead to
pulmonary inflammation. The aim of this study was to evaluate the time-course events after a single
ozone exposure in transcription-coupled repair defective Csb and wild type mice. Mice were exposed for 3 h to 2 ppm
ozone and biological parameters related to oxidative stress and
inflammation were examined in the lungs at 0, 4, 9, 24 and 48 h after exposure. In addition the procoagulant and
thrombomodulin activities were explored by a combination of assays for
tissue factor and
thrombin generation. This study revealed a significant biological response to
ozone, for both Csb and wild type mice. The onset of
inflammation in Csb mice, as indicated by an increase in
interleukin-6,
tumor necrosis factor-alpha and total cell influx, occurred earlier compared with those seen in wild type mice. On the other hand, Csb mice showed a delayed
antioxidant reaction compared with wild type mice. Both genotypes developed a procoagulant reaction characterized by a stably increased
tissue factor activity and a progressive increase in
thrombin generation after 2 days. These experiments have shown that
ozone, a well-known toxic substance from the environment, induces not only
inflammation, but also procoagulant reactions in the lungs of mice. These results have implications for understanding the systemic effects induced by
oxidant air pollutants.