Ozone adaptation in mice and its association with ascorbic acid in the lung

We have previously shown that ozone (O-3) adaptation occurred in rats after daily exposure to an "urban-type" concentration. The adaptation was positi vely associated with an excess of ascorbic acid (AA) in bronchoalveolar lav age fluid (BALF), suggest ing that AA may play a role in the adaptation mec hanism. This relationship was not seen at higher and more toxic exposures. The present work exposed mice to low and high levels of O-3 to see if the a daptation-AA relationship is common among rodent species. Male CD-1 mice we re studied during repeated 6-h/day exposures to 0.0 or 0.25 ppm O-3 for 10 days and 10 days of recovery in air (experiment 1) and to 0.0, 0.5, or 1.0 ppm O-3 for 5 days (experiment 2). Approximately 20 h after each daily expo sure, groups of mice Mere randomly selected from each concentration type an d examined for patterns of response. They were anesthetized (urethane, ip), incubated, and the lungs were lavaged with 37 degrees C saline. BALF was a ssayed for cells, cell differential protein, albumin, lactate dehydrogenase , lysozymes, N-acetyl-beta-D-glucosaminidase, gamma-glutamyl transferase, u ric acid, glutathione, and AA. Body weight and total lung capacity were als o measured. Mice from experiment 1 (10/exposure) were tested for adaptation on day 12 by challenging them with 1.0 ppm O-3 for 6 h and collecting BALF 20 h later. In experiment 2, adaptation was assessed by evaluating the att enuation in response to continued exposure. There was only minimal response to the daily O-3 exposures in experiment 1 except for AA, which was signif icantly increased in BALF by day 3 and remained elevated well into the reco very period. The O-3-preexposed mice demonstrated adaptation when compared to their O-3-naive counterparts. Daily exposure to 1.0 ppm O-3 in experimen t 2 caused weight loss and changes in BALF consistent with toxicity, and ne ither adaptation nor an excess quantity of AA was seen. The findings in mic e were in agreement with those seen in rats and suggest that there may be a common O-3 adaptation mechanism among rodents that involves the regulation of AA in lung lining fluid.