Abstract
Earlier studies from our laboratory have shown myocardial dysfunction subsequent to chronic O3 exposure in rats may be associated with a decrease in antioxidant reserve and increased activity of inflammatory mediators. The present study tested the hypothesis that O3-induced cardiac dysfunction in healthy adult rats may be due to changes in caveolin-1 and caveolin-3 levels. Sprague–Dawley rats were exposed 8 h/day for 28 and 56 days to filtered air or 0.8 ppm O3. In order to assess the chronic effects to O3, in vivo cardiac function was assessed by measuring LVDP, 24 h after termination of O3 exposure. Compared to rats exposed to filtered air, LVDP values significantly decreased in all O3-exposed animals. This attenuation of cardiac function was associated with increased myocardial TNF-α levels and decreased myocardial activities of superoxidase dismutase. Progressive increases in the expression of myocardial TNF-α in 28 days and 56 days O3-exposed animals were followed by decreases in cardiac caveolin-1 levels. On the other hand, differential changes in the expression of caveolin-3 in hearts from 28 and 56 days O3-exposed animals were independent of intra-cardiac TNF-α levels. These novel findings suggest the interesting possibility that a balance between caveolin-1 and caveolin-3 may be involved in O3-mediated cardiac toxicity.
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Acknowledgments
This work was made possible by the United States Environmental Protection Agency Grant (USEPA Grant # IT-83404401-0), Texas A&M Health Science Research Development Grant (Act # 134403-35402), and funds from TAMHSC Research Startup (Act # 13100-35488). The authors would like to thank Ms. Maggie Ramirez from the TAMUK—Department of Biology and Health Sciences, Dr. Dennis Miller and Mr. Pranjal Manchanda from UT Dallas, and Mr. Vishal Sethi from UT-Pan American for reference checks, literature searches, technical help, software support, and proof reading.
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Sethi, R., Manchanda, S., Perepu, R.S.P. et al. Differential expression of caveolin-1 and caveolin-3: potential marker for cardiac toxicity subsequent to chronic ozone inhalation. Mol Cell Biochem 369, 9–15 (2012). https://doi.org/10.1007/s11010-012-1363-2
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DOI: https://doi.org/10.1007/s11010-012-1363-2