The oxidant ozone is a well-known air pollutant, inhalation of which is associated with respiratory tract inflammation and functional alterations of the lung. It is well established as an inducer of intracellular oxidative stress. We investigated whether Cockayne syndrome B, transcription-coupled, repair-deficient mice ( Csb−/−), known to be sensitive to oxidative stressors, respond differently to ozone than repair-proficient controls ( Csb+/−). Mice were exposed to 0.8 parts/million ozone for 8 h, and we examined a wide range of biological parameters in the lung at the gene expression, protein, and cellular level 4 h after the ozone exposure. Relevant biological responses to ozone for both repair-deficient Csb−/− and repair-proficient Csb+/− mice, as determined by biochemical analysis of bronchoalveolar lavage fluid (e.g., increases of polymorphonuclear neutrophils, alkaline phosphatase, macrophage-inflammatory protein-2, and tumor necrosis factor-α), pathological examinations, and gene expression (upregulation of oxidative-stress-related genes) analyses were observed. The bronchoalveolar lavage fluid showed significantly more tumor necrosis factor-α in repair-deficient Csb−/− mice than in repair-proficient Csb+/− mice after ozone exposure. In addition, a clear trend was observed toward fewer differentially expressed genes with a lower fold ratio in repair-deficient Csb−/− mice than in repair-proficient Csb+/− mice. However, repair-deficient Csb−/− mice do not respond significantly more sensitively to ozone compared with repair-proficient Csb+/− mice at the level of gene expression. We conclude that, under the conditions employed here, although small differences at the transcriptional level exist between repair-proficient Csb+/− mice and transcription-coupled repair defective Csb−/− mice, these do not have a significant effect on the ozone-induced lung injury.
Influence of Autologous and Homologous Blood Transfusion on Interleukins and Tumor Necrosis Factor-α in Peri-operative Patients with Esophageal Cancer
