Skip Navigation

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 Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by JENKINSON, S. G.
Right arrow Articles by MCKINNEY, M. A.
Right arrow Search for Related Content
PubMed
Right arrow Articles by JENKINSON, S. G.
Right arrow Articles by MCKINNEY, M. A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1984 Oxford University Press

research-article

Enhanced Pulmonary Toxicity in Copper-Deficient Rats Exposed to Hyperoxia1

STEPHEN G. JENKINSON2,3, RICHARD A. LAWRENCE2, WARREN D. GRAFTON, PAULA E. GREGORY and MARY A. MCKINNEY

Lung Unit, Department of Medicine, and the Department of Pathology, Louisiana State University School of Medicine Shreveport, Louisiana 71130

Enhanced Pulmonary Toxicity in Copper-Deficient Rats Exposed to Hyperoxia. JENKINSON, S. G., LAWRENCE, R. A., GRAFTON, W. D., GREGORY, P. E., AND MCKINNEY, M. A. (1984). Fundam. Appl. Toxicol. 4, 170–177. The antioxidant enzyme superoxide dismutase (SOD) found in the cytosol of eucaryotic cells and the plasma protein ceruloplasmin are copper containing proteins thought to be important in providing protection from oxygen toxicity. To investigate the hypothesis that copper deficiency in the rat could result in decreased lung SOD activity and plasma ceruloplasmin concentration resulting in increased susceptibility to O2 lung damage, we performed a series of experiments exposing copper-deficient and control rats to normobaric and hyperbaric hyperoxia. Lung SOD activity in the copper-deficient rats was found to be 56% of control and ceruloplasmin content was 6% of control. The copper-deficient rats exhibited increased mortality and enhanced pulmonary toxicity as evidenced by increased pathologic damage and lung edema during the normobaric exposure to 85% O2. Copper-deficient animals also showed increased susceptibility to a hyperbaric exposure of 4 ata of 100% O2 with a decreased time of survival. The copper-deficient rat represents a new model for the study of oxidant injury.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.