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Am J Physiol Lung Cell Mol Physiol 260: L318-L325, 1991;
1040-0605/91 $5.00
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AJP - Lung Cellular and Molecular Physiology, Vol 260, Issue 4 318-L325, Copyright © 1991 by American Physiological Society


ARTICLES

Injury of rat pulmonary alveolar epithelial cells by H2O2: dependence on phenotype and catalase

R. H. Simon, J. A. Edwards, M. M. Reza and R. G. Kunkel
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109.

In a variety of inflammatory lung diseases, type I alveolar epithelial cells are more likely to be injured than are type II cells. Because oxidants have been implicated as a cause of injury in various inflammatory lung diseases, we evaluated the effects of differentiation on alveolar epithelial cell susceptibility to H2O2-induced injury. With the use of isolated rat type II cells in culture, we found that the cytotoxic effect of H2O2 increased between days 2 and 7, when type II cells are known to lose their distinctive type II properties and assume a more type I-like appearance. We previously reported that type II cells utilized both intracellular catalase and glutathione-dependent reactions to protect against H2O2. We therefore examined whether alterations in either of these protective mechanisms were responsible for the differentiation-dependent changes in sensitivity to H2O2. We found that catalase activity within alveolar epithelial cells decreased between 2 and 7 days in culture, whereas no changes were detected in glutathione-dependent systems. We then used a histochemical technique that detects catalase activity and found that type II cells within rat lungs possessed numerous catalase-containing peroxisomes, whereas very few were detected in type I cells. These findings demonstrate that as type II cells assume a type I-like phenotype, they become more susceptible to H2O2-induced injury. This increased susceptibility is associated with reductions in intracellular catalase activity, both in vitro and in vivo.


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