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Role of Nrf2 transcription factor in ozone‐induced emphysema in mice
Author(s) -
Limjunyawong Nathachit,
Mitzner Wayne
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.722.7
Subject(s) - oxidative stress , ozone , chemistry , bronchoalveolar lavage , lung , inflammation , transcription factor , andrology , immunology , medicine , biochemistry , organic chemistry , gene
Ozone is a potent air pollutant which is known to cause pulmonary oxidative stress and inflammation. It has been shown that repeated exposure in mice to ozone at high concentration can damage lung parenchymal tissue and lead to emphysema. In the current study, we investigated the protective role of nuclear factor‐erythroid 2‐related factor 2 (Nrf2), a nuclear transcription factor that is induced by oxidative stress and is known to activate production of several antioxidant enzymes. Female wild‐type (WT) C57BL/6 and Nrf2‐deficient (Nrf2−/−) mice were exposed to ozone at a concentration of 2 ppm for 3 hours/day, 2 days/week, for 6 weeks in total. Control mice were exposed to room air. Measurements of lung function were performed one day after the last exposure. Results showed that the total lung capacity (volume at 35 cmH2O) was found to be significantly increased in the WT mice exposed ozone to compared to room air (1.465 ± 0.040 mL and 1.144 ± 0.052 mL, respectively). The effect of O3 was even higher in Nrf2−/− mice (1.784± 0.113 mL vs 1.301 ± 0.082 mL). However, no changes were observed in the diffusion capacity of the lung for carbon monoxide and cell profile in bronchoalveolar lavage fluid in either strain. These results indicate that the role of Nrf2 in ozone exposure is more complex than simple protection. Funding source: NIH HL‐10342