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© 1991 Oxford University Press

research-article

Effects of Inhaled Phosgene on Rat Lung Antioxidant Systems

RICHARD H. JASKOT*, ELAINE C. GROSE{dagger}, JUDY H. RICHARDS* and DONALD L. DOERFLER*

*ManTech Environmental Technologies Inc. Research Triangle Park, North Carolina, 27709 {dagger}U. S. Environmental Protection Agency, Health Effects Research Laboratory Research Triangle Park, North Carolina 27711

Received March 4, 1991; accepted June 14, 1991

Effects of Inhaled Phosgene on Rat Lung Antioxidant Systems. JASKOT, R. H., GROSE, E. C, RICHARDS, J. H., AND DOERFLER, D. L. (1991). Fundam. Appl. Toxicol 17, 666–674. A concentration-response and CxT study were undertaken to determine the effect of phosgene (COCl2) inhalation on pulmonary antioxidant processes as determined by changes in endogenous glutathione (GSH) and antioxidant-associated enzymes (GSH peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase, and superoxide dismutase). Rats were exposed to 0.0,0.1,0.25,0.5, and 1.0 ppm phosgene for 4 hr and 0.25 ppm phosgene for 8 hr. The endpoints were assayed at 0, 1, 2, 3 and 7 days after exposure cessation. The lowest effective concentration was 0.1 ppm phosgene (increases in measured variables from 8 to 35% above control values). At all concentrations, major effects were observed 1 to 2 days after exposure (12 to 159% above control), peaking at 2 to 3 days postexposure (11 to 253% above control), and in some cases were still evident 7 days (10 to 65% above control) after exposure. The CxT study using the same dose (120 ppm-min), but different times and concentration (0.25 ppm for 8 hr and 0.5 ppm for 4 hr), showed a concentration dependence. The peak antioxidant enzyme changes observed for the higher concentration (0.5 ppm) were at least double those observed for the lower concentration (0.25 ppm). These enzyme changes were similar to those reported for the oxidants O3 and NO2. Although the suspected mechanism of initial damage between phosgene and these oxidants is different (acylation vs oxidation) the biological result is similar (i.e., damage, repair, and influx of cells), thus eliciting similar biochemical changes in response to pulmonary injury. These changes, observed as increases in the pulmonary antioxidant enzymes, appear to play a role in the lung's ability to recover from significant toxic injury to near normal preinjury homeostasis.


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