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

Abstract

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.

Authors:
; ; ; ; ;  [1]
  1. (Laboratory of Veterinary Biochemistry, Utrecht University (Netherlands))
Publication Date:
OSTI Identifier:
5905622
Resource Type:
Journal Article
Resource Relation:
Journal Name: American Journal of Physiology; (United States); Journal Volume: 262:1 Pt 1
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; LUNGS; SENSITIVITY; OZONE; TOXICITY; PHORBOL ESTERS; BIOLOGICAL EFFECTS; PROTEINS; CHEMICAL PROPERTIES; DOGS; IN VITRO; IN VIVO; LAVAGE; MACROPHAGES; MAN; PHAGOCYTOSIS; PHOSPHOLIPIDS; RATS; TRYPAN BLUE; AMINES; ANIMAL CELLS; ANIMALS; AROMATICS; AZO COMPOUNDS; AZO DYES; BODY; CARCINOGENS; CONNECTIVE TISSUE CELLS; DYES; ESTERS; HYDROXY COMPOUNDS; LIPIDS; MAMMALS; NAPHTHOLS; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANIC NITROGEN COMPOUNDS; ORGANIC PHOSPHORUS COMPOUNDS; ORGANIC SULFUR COMPOUNDS; ORGANS; PHAGOCYTES; PHENOLS; PRIMATES; RESPIRATORY SYSTEM; RODENTS; SOMATIC CELLS; SULFONIC ACIDS; VERTEBRATES 560300* -- Chemicals Metabolism & Toxicology

Citation Formats

Oosting, R.S., Van Iwaarden, J.F., Van Bree, L., Verhoef, J., Van Golde, L.M., and Haagsman, H.P. Exposure of surfactant protein A to ozone in vitro and in vivo impairs its interactions with alveolar cells. United States: N. p., 1992. Web.
Oosting, R.S., Van Iwaarden, J.F., Van Bree, L., Verhoef, J., Van Golde, L.M., & Haagsman, H.P. Exposure of surfactant protein A to ozone in vitro and in vivo impairs its interactions with alveolar cells. United States.
Oosting, R.S., Van Iwaarden, J.F., Van Bree, L., Verhoef, J., Van Golde, L.M., and Haagsman, H.P. 1992. "Exposure of surfactant protein A to ozone in vitro and in vivo impairs its interactions with alveolar cells". United States. doi:.
@article{osti_5905622,
title = {Exposure of surfactant protein A to ozone in vitro and in vivo impairs its interactions with alveolar cells},
author = {Oosting, R.S. and Van Iwaarden, J.F. and Van Bree, L. and Verhoef, J. and Van Golde, L.M. and Haagsman, H.P.},
abstractNote = {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.},
doi = {},
journal = {American Journal of Physiology; (United States)},
number = ,
volume = 262:1 Pt 1,
place = {United States},
year = 1992,
month = 1
}
  • The effect of in vivo O/sub 3/ exposure on the mobility of pulmonary alveolar macrophages (PAM) in vitro was investigated. Eight randomly selected rats were exposed for 4 h. Four rats were exposed to a clean air (sham) atmosphere, and four to an atmosphere containing 1 ppM O/sub 3/. PAM were obtained by lung lavage and placed on gold-colloid coated coverslips. The area cleared of gold particles by migrating PAM after 24, 48, and 72 h was used as an indicator of cell mobility. The number of PAM recoverable by lavage was similar for both groups (2 x 10/sup 5/),more » but the percentage of macrophages that made tracks was significantly smaller with 95% certainty in the O/sub 3/ group. For sham-exposed and O/sub 3/-exposed groups, the area cleared by the sham-exposed group being about 50% greater during each time period. It was concluded that the in vitro migrational potential of PAM was most likely decreased by in vivo exposure to O/sub 3/.« less
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