Enhanced pulmonary toxicity in copper-deficient rats exposed to hyperoxia

Stephen G. Jenkinson, Richard A. Lawrence, Warren D. Grafton, Paula E. Gregory, Mary A. Mckinney

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)170-177
Number of pages8
JournalToxicological Sciences
Volume4
Issue number2 PART1
DOIs
StatePublished - Apr 1984

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