AJP - Lung Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 257: L217-L220, 1989;
1040-0605/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Warburton, D.
Right arrow Articles by Forman, H. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Warburton, D.
Right arrow Articles by Forman, H. J.

AJP - Lung Cellular and Molecular Physiology, Vol 257, Issue 4 217-L220, Copyright © 1989 by American Physiological Society

ARTICLES

Sublethal oxidant injury inhibits signal transduction in rat type II pneumocytes

D. Warburton, S. Buckley, L. Cosico and H. J. Forman
Developmental Lung Biology Research Center, Children's Hospital of Los Angeles, California.

The production of reduced forms of O2 in oxidant injury can lead to lipid peroxidation, which would pose a threat to cell membrane integrity and therefore to signal transduction pathways located in the membrane. We studied the effects of oxidant injury with t-butyl hydroperoxide (tBOOH) on signal transduction in rat type II pneumocytes in culture. Exposure of 1 x 10(6) type II pneumocytes to tBOOH concentrations less than or equal to 100 microM did not cause significant release of lactate dehydrogenase and was therefore termed sublethal. Exposure to sublethal concentrations of tBOOH caused a dose-dependent inhibition of surfactant secretion stimulated both by terbutaline (10(-4)M) and by extracellular ATP (10(-5)M). Adenosine 3',5'-cyclic monophosphate production in response both to terbutaline and to extracellular ATP was also inhibited by exposure to 100 microM tBOOH. In addition, exposure to 100 microM tBOOH inhibited inositol phosphate formation in response to extracellular ATP. We conclude that sublethal oxidant injury inhibits not only receptor-mediated agonist stimulation of surfactant secretion but also receptor-mediated agonist stimulation of second messenger formation in type II pneumocytes in culture. Such inhibition may be important in the pathogenesis of both the adult and neonatal forms of respiratory distress syndrome, in which alveolar surfactant deficiency may be exacerbated by oxidant injury.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
E. Matthew, R. Pun, M. Simonich, H. Iwamoto, and J. Dedman
Cyclosporin A protects lung function from hyperoxic damage
Am J Physiol Lung Cell Mol Physiol, May 1, 1999; 276(5): L786 - L795.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
M. E. ERASMUS, G. J. H. HOFSTEDE, A. H. PETERSEN, H. P. HAAGSMAN, S. B. OETOMO, and J. PROP
Effects of Early Surfactant Treatment Persisting for One Week after Lung Transplantation in Rats
Am. J. Respir. Crit. Care Med., July 1, 1997; 156(2): 567 - 572.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online