Differential Changes In Caveolin Levels In Lung And Heart From Ozone Exposed Adult Healthy Rats

The WHO estimates that air pollution is responsible for approximately 2 million premature deaths worldwide annually. The current study is a continuation of the previous research work and proposes to investigate change in the lung function compared to cardiac injury after exposure to chronic levels of Ozone (O3). We hypothesized differential changes in the pulmonary system compared to cardiovascular system after chronic exposure to O3. Twenty age/weight matched male Sprague Dawley rats were divided into two groups that were exposed to air (0 ppm O3) or 0.8 ppm O3 for 8 hours/day for 28 days. Animals were sacrificed and the lungs and left ventricles were analyzed. Western blot analysis was performed on lung and heart tissue from both groups to quantify the differential levels of caveolin-1, p38MAPK in the membrane fraction, and P-p38 activity in the cytosolic fraction. Upon chronic O3 exposure, we found: a) 4 week O3-exposed rat lung expressed increased levels of caveolin-1 in membrane compared to 4 week O3-exposed rat heart, b) although cytoplasmic levels of p38 MAPK alpha expression were increased in lung and heart, this increase was less in lung compared to heart, and P-p38 activity was significantly decreased in lung compared to heart, suggesting decreased death signaling in lung. We conclude that differential expression of cell death signaling is leading to progressive deterioration of cardiac muscle and progressive repair of lung tissue after chronic ozone exposure. These findings indicate a regulatory role of caveolin-1 in O3-induced pulmonary and cardiac toxicity.