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Am J Physiol Lung Cell Mol Physiol 262: L63-L68, 1992;
1040-0605/92 $5.00
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AJP - Lung Cellular and Molecular Physiology, Vol 262, Issue 1 63-L68, Copyright © 1992 by American Physiological Society

ARTICLES

Exposure of surfactant protein A to ozone in vitro and in vivo impairs its interactions with alveolar cells

R. S. Oosting, J. F. Van Iwaarden, L. Van Bree, J. Verhoef, L. M. Van Golde and H. P. Haagsman
Laboratory of Veterinary Biochemistry, Utrecht University, The Netherlands.

This study focused on the question of whether exposure of surfactant protein A (SP-A) to ozone affected properties of this protein that may be involved in regulating alveolar type II cell and alveolar macrophage functions. In vitro exposure of human or canine SP-A to ozone reduced the ability of this protein to inhibit phorbol-ester induced secretion of [3H]phosphatidylcholine by alveolar type II cells in culture. Ozone-exposed human SP-A showed a decreased ability to enhance phagocytosis of herpes simplex virus and to stimulate superoxide anion production by alveolar macrophages. Experiments with elastase showed that ozone-exposed canine SP-A was more susceptible to proteolysis. A conformational change of the protein could underlie this phenomenon. Surfactant isolated from ozone-exposed rats (0.4 ppm ozone for 12 h) was also less able to stimulate superoxide anion production by alveolar macrophages than surfactant from control rats, which suggested that SP-A in vivo was also susceptible to ozone. The results of this study suggest that SP-A-alveolar cell interactions can be inhibited by ozone exposure, which may contribute to the toxicity of ozone in the lungs.


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