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1 Department of Environmental Medicine, The University of Rochester, Rochester, NY, USA
2 Department of Pathology and Laboratory Medicine, The University of Rochester, Rochester, NY, USA
3 Department of Pediatrics, The University of RochesterThe University of Rochester, Rochester, NY, USA
4 Department of Radiation Oncology, The University of Rochester, Rochester, NY, USA
* To whom correspondence should be addressed. E-mail: michael_oreilly{at}urmc.rochester.edu.
It is well established that hyperoxia injures and kills alveolar endothelial and type I epithelial cells of the lung. Although type II epithelial cells remain morphologically intact, it remains unclear whether they are also damaged. DNA integrity was investigated in adult mice whose type II cells were identified by their endogenous expression of proSP-C or transgenic expression of enhanced green fluorescent protein (EGFP). In mice exposed to room air, punctate perinuclear 8-oxoguanine staining was detected in approximately 4% of all alveolar cells and in 30% of type II cells. After 48 or 72 hours of hyperoxia, 8-oxoguanine was detected in 11% of all alveolar cells and in greater than 60% of type II cells. 8-oxoguanine co-localized by confocal microscopy with the mitochondrial transmembrane protein cytochrome oxidase subunit 1. Type II cells isolated from hyperoxic lungs exhibited nuclear DNA strand breaks by comet assay even though they were viable and morphologically indistinguishable from cells isolated from lungs exposed to room air. These data reveal that type II cells exposed to in vivo hyperoxia have oxidized and fragmented DNA. Because type II cells are essential for lung remodeling, our findings raise the possibility that they are proficient in DNA repair.
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