CHARACTERISTICS OF BRONCHOALVEOLAR LEUKOCYTES FROM THE LUNGS OF RATS INHALING 0.2-0.8 PPM OF OZONE

被引:6
作者
DONALDSON, K
BROWN, GM
BROWN, DM
SLIGHT, J
MACLAREN, W
DAVIS, JMG
机构
[1] Institute of Occupational Medicine Ltd., Edinburgh, Scotland, Roxburgh Place
关键词
D O I
10.3109/08958379309034499
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
The study was aimed at investigating the likely role of the bronchoalveolar leukocytes in the epithelial injury arising from exposure to ozone at low concentrations. Rats were exposed to 0.2-0.8 ppm of ozone for 7 hr/day for up to 4 days. At the selected time points the lungs were lavaged and the bronchoalveolar lavage cell profile was assessed by differential counting. Selected activities of the bronchoalveolar leukocytes, which could contribute to epithelial injury in vivo, were assessed in vitro, including (1) spontaneous and phorbol-stimulated release of superoxide anion, (2) proteolysis of fibronectin, and (3) ability to damage epithelial cells. Exposure to ozone at the highest concentrations caused inflammation in the bronchoalveolar region as shown by an increase in the proportion of neutrophils in the lavage. There was adaptation to the ozone-induced injury as shown by the fact that this inflammation was reduced as the time of exposure increased No increases in any of the indicators of ability to injure epithelial cells in vivo were seen. There was evidence of decreased ability to mount an oxidative burst in the bronchoalveolar leukocytes from rats inhaling 0.6 ppm of ozone but this was not present in those rats that were inhaling 0.8 ppm. The macrophages from the lungs of rats inhaling the highest concentrations of ozone showed blebbing and this was reflected in an increase in the size compared to controls. We conclude that ozone, at the time points and concentration utilized here, causes inflammation but that the inflammatory cells are unlikely to mediate injury to the epithelial cells.
引用
收藏
页码:149 / 164
页数:16
相关论文
共 30 条
[11]   AN IMPROVED MACROPHAGE SPREADING ASSAY - A SIMPLE AND EFFECTIVE MEASURE OF ACTIVATION [J].
DONALDSON, K ;
BOLTON, RE ;
BROWN, D ;
DOUGLAS, A .
IMMUNOLOGICAL COMMUNICATIONS, 1984, 13 (03) :229-244
[12]   ALVEOLAR MACROPHAGE-STIMULATED NEUTROPHIL AND MONOCYTE MIGRATION - EFFECTS OF INVITRO OZONE EXPOSURE [J].
DRISCOLL, KE ;
SCHLESINGER, RB .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1988, 93 (02) :312-318
[13]   CHARACTERIZATION OF THE OXIDANT GENERATION BY INFLAMMATORY CELLS LAVAGED FROM RAT LUNGS FOLLOWING ACUTE EXPOSURE TO OZONE [J].
ESTERLINE, RL ;
BASSETT, DJP ;
TRUSH, MA .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1989, 99 (02) :229-239
[14]  
HASSETT C, 1985, J NATL CANCER I, V75, P771
[15]  
HOLTZMAN MJ, 1983, AM REV RESPIR DIS, V127, P686
[16]   COMPARISON OF ACUTE OZONE-INDUCED NASAL AND PULMONARY INFLAMMATORY RESPONSES IN RATS [J].
HOTCHKISS, JA ;
HARKEMA, JR ;
SUN, JD ;
HENDERSON, RF .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1989, 98 (02) :289-302
[17]   RESPONSE OF RAT ALVEOLAR MACROPHAGES TO OZONE - QUANTITATIVE ASSESSMENT OF POPULATION-SIZE, MORPHOLOGY, AND PROLIFERATION FOLLOWING ACUTE EXPOSURE [J].
HOTCHKISS, JA ;
HARKEMA, JR ;
KIRKPATRICK, DT ;
HENDERSON, RF .
EXPERIMENTAL LUNG RESEARCH, 1989, 15 (01) :1-16
[18]   PROTEIN ACCUMULATION IN LUNG LAVAGE FLUID FOLLOWING OZONE EXPOSURE [J].
HU, PC ;
MILLER, FJ ;
DANIELS, MJ ;
HATCH, GE ;
GRAHAM, JA ;
GARDNER, DE ;
SELGRADE, MK .
ENVIRONMENTAL RESEARCH, 1982, 29 (02) :377-388
[19]  
JOHNSTON RB, 1981, METHODS STUDYING MON, P489
[20]   OZONE-INDUCED INFLAMMATION IN THE LOWER AIRWAYS OF HUMAN-SUBJECTS [J].
KOREN, HS ;
DEVLIN, RB ;
GRAHAM, DE ;
MANN, R ;
MCGEE, MP ;
HORSTMAN, DH ;
KOZUMBO, WJ ;
BECKER, S ;
HOUSE, DE ;
MCDONNELL, WF ;
BROMBERG, PA .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1989, 139 (02) :407-415