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Toxic Effects of Oxygen on Cultured Alveolar Epithelial Cells, Lung Fibroblasts and Alveolar Macrophages

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Toxic Effects of Oxygen on Cultured Alveolar Epithelial Cells, Lung Fibroblasts and Alveolar Macrophages Eur Reaplr J 1991' 4, 1068-1075 Toxic effects of oxygen on cultured alveolar epithelial cells, lung fibroblasts and alveolar macrophages B. Housset, I. Hurbain, J. Masliah*, A. Laghsal*, M.T. Chaumette-Demaugre**, H. Karam, J.Ph. Oerenne Toxic effects of oxygen on cultured alveolar epithelial cells, lung fibroblasts Service de Pneumologie. HOpital Saint-Antoine, 184 and alveolar macrophages, B. Housset, I. Hurbain, J. Masliah, A. Laghsa~ rue du Fg Saint Antoioe 75012, Paris. M.T. Chaumette-Demaugre, H. Karam, J.Ph. Derenne. ABSTRACf: Exposure to hyperoxia results in endothelial necrosis followed • Service de Biochimie B, CHU Saiot-Antoine, 12 by type ll cell proliferation. This suggests that type ll cells are resistant rue de Chaligny, F-75571 Paris, Cedex 12. to hyperoxla. Oxygen-Induced lung Injury may result from an overpro­ •• Laboratoire d'histophysiologie des processus de duction of oxygen metabolltes normally scavenged by antioxidants such as dUense, CHU Henri Mondor, 8 rue du G~n~ral superoxide dismutase (SOD), glutathione peroxidase, catalase and reduced Sarrai!, F-94000 Cr~teil, France. glutathione (GSH). Therefore, resistance of type 11 cells to hyperoxia may be linked to high antioxidant activities. To test this hypothesis we com­ Correspondence: B. Housset, Service de Pneumologie, H6pital Saint-Antoine, 184 rue du Fg Saint Antoioe pared in vitro the efTects of a 24 h exposure period to 95% 0 2 on cultured type 11 cells, lung ftbroblasts and alveolar macrophages isolated from rats. 75012, Paris. We show that type 11 cells, when compared with other cell types, are Keywords: Catalase; culture; fibroblasts; glutathione highly sensitive to hyperoxla as shown by Increased lactate dehydrogenase peroxidase; lung; oxygen; poeumocytes; superoxide (LDH) release, decreased deoxyribose nucleic acid (DNA) and protein con· dismutase. tent of Petri dishes and decreased thymidine Incorporation Into DNA. Synthesis of dlpalmltoylphosphatldylcboline was also signlflcantly reduced. Received: March 6, 1989; accepted after revision Antioxidant enzyme activities as well as glutathione content were not higher April 22, 1991. In type 11 cells than In other cell types. However, hyperoxla results In a decreased SOD activity and glutathione content In type II cells which was Supported by grant No. 86 MR/13 and 87 D/4 from not observed In ftbroblasts. We conclude that adaptatlve changes In SOD "Foods s~cial des Comit~s d~partementaux contre les and a:lutathlone metabolism could be Important defence mechanisms In Maladies Respiratoires et la Tuberculose", grant No. 855014 from INSERM and by a grant from "le Conseil cells exposed to hyperoxla. Scientifique de l'UBR St. Antoioe". Eur Respir J., 1991, 4, 1066-1075. In most species, exposure to normobaric hyperoxia sensitivity of specific cell types to oxygen injury could results in lung injury. Morphometric studies show in be related in part to activities of endogenous cellular rats an early necrosis of endothelial cells followed by a antioxidant enzymes. proliferation of alveolar type II cells and fibroblasts For a better understanding of the factors affecting cell [1, 2]. These data suggest that type II cells and fibroblasts injury, we used an in vitro model as a critical approach are resistant to oxygen toxicity. A substantial number of of the direct mechanisms of cell damage induced by studies have shown in various species that alveolar oxidant stress. This contrasts with in vivo studies where macrophages are altered early in the course of in vivo the toxic effects also result from complex cellular or in vitro hyperoxic exposure [3-5]. Antioxidant interactions. defences such as superoxide dismutase, glutathione In this study we compared the activities of antioxidant peroxidase, catalase and glutathione may protect, enzymes, superoxide dismutase, catalase and glutathione at least partly, the cells against oxidant stress. This is in peroxidase, and total glutathione content in cultured keeping with the biochemical mechanisms leading to alveolar type II cells, alveolar macrophages and oxygen-induced lung injury. Cell damage may result fibroblasts isolated from rat lung. We also investigated from intracellular oxygen-derived free radicals in these three cultured cell types, the effects of a 24 h overproduction [6] or from toxic products release by exposure period to 95% 0 2 on these antioxidant phagocytes such as polymorphonuclear neutrophils [7]. substances, on some indexes of cytotoxicity as well as Under these circumstances, oxygen metabolites on the incorporation of 3H-palmitate into production exceeds the capacity of the cellular antioxi­ dipalmitoylphosphatidylcholine, an index of function of dant defence mechanisms [8]. It follows that the cultured type II cells. OXYGEN TOXICITY IN CULTURED LUNG CELLS ltX>7 Materials and methods was monitored using a Toptronic oxymeter (Bioblock, France) and was consistently found to be over 90% Cell isolation and culture until the end of the exposure period. The other group was maintained under control conditions (5% - Type 11 epithelial cells (PI/). Male Wistar rats C02 air). (200-250 g) were anaesthetized with ether. Then 500 U·kg·1 of heparin was injected i.p. The trachea was cannulated, the vena cava was cut and the lungs were Thymidine incorporation into DNA perfused via the pulmonary artery with 20 ml of sterile saline and then excised. To remove some of the Cells were incubated for 24 h with 1 ~-tCi·mi- 1 of macrophages, the lungs were lavaged four times via the tritiated thymidine (45 Ci·mmol·t, CEA, Saclay). At the trachea with a solution containing 140 mM NaCI, 5 mM end of the exposure period, cells were washed twice, KCl, 2.5 mM sodium phosphate, 10 mM HEPES scraped in saline and sonicated. One volume of cell (N-2-hydroxyeth ylpiperazine-N-2-ethane sulfonic acid), homogenate was diluted with two volumes of 15% 6 mM glucose, 0.2 mM EGTA (ethylene glycobis(B­ trichloracetic acid (TCA). After centrifugation (4°C , 5000 amino ethyl ether), N-tetraacetic acid), pH 7.4. Then 10 x g for 10 min) the pellet was suspended in 10% TCA m1 of a 0.25% trypsin solution (Worthington Biochemical and sonicated. Radioactivity was counted in a scintillation Corp., Freehold, New Jersey) was injected for a 30 min counter (Delta 300, Searle). As the efficiency was incubation period at 37°C. Reaction was stopped by constant, results were expressed in cpm. Incorporation adding 10 ml DMEM (Dulbecco's Modified Eagle of labelled thymidine into DNA was expressed as the 1 Medium containing 4500 mg glucose·l- ; Gibco Limited, ratio of the radioactivity found in TCA insoluble extract Paisley, Scotland) and 20% FBS (Foetal Bovine Serum; to the total radioactivity added to the Petri dish. Gibco). The lungs were minced in the presence of 2 This ratio was reported to the cell mass and therefore l-l&·ml·1 DNAase I (Sigma, St Louis, MO) and then shaken expressed per 1-lg DNA. In some type II cells cultures for 5 min. Lung minces and cell suspension were filtered autoradiography was performed with a pulse of 10 through a nylon gauze (100 ~-t). Cells were centrifuged !!Ci·ml·1 3H-thymidine for 4 h in order to identify, after at 200 x g for 5 min. The resulting pellet was resuspended a tannic acid coloration, the cell types taking up in DMEM supplemented with penicillin (50 U·ml·1) and radioactivity [9]. For each experiment, 400 cells were streptomycin (50 ~-ts·ml·1) and cells were incubated for counted to obtain the percentage of cells with a labelled one hour in 100 mm diameter Petri dishes. Then nucleus (labelling index). supernatant was collected and centrifuged at 200 >< g for 5 min. Cells were resuspended in DMEM 10% FBS and added at a density of 2 x 106 cells per 2 ml medium in Incorporation of palmitic acid and identification of 35 mm diameter Petri dishes. Plates were incubated for labelled lipids : 24 h at 37°C in a 5% C02 air atmosphere. Type li cells were identified on their morphological appearance under Alveolar type II cells were incubated with DMEM 10% optic and electron microscopy. FBS containing 2 ~-tCi·mi· 1 tritiated palmitic acid (27.5 Ci·mmol·1, New England Nuclear, Boston, MA). Cells Macrophages. Cells were obtained by bronchoalveolar were exposed to hyperoxic conditions or maintained under lavage as described above. The pooled lavage fluid was control conditions for 24 h. Cells were scraped and centrifuged at 200 x g for 5 min and the pellet was sonicated. Lactate dehydrogenase (LDH), protein and resuspended in DMEM. The cells were plated in 35 mm DNA were measured in cell homogenate. Radioactivity culture dishes at a density of 106 cells per dish and was counted in cells and media. Lipids were extracted incubated for one hour at 37°C to allow macrophages to according to the method of BuoH and DYER [10). The adhere. After removal of medium and of non adhering lipid extract from cell homogenate was evaporated to cells, alveolar macrophages were incubated in DMEM dryness and separated in two aliquots before resolution containing 10% FBS. by thin layer chromatography following the method described by Gu.FILIAN et al. (11 ]. A lipid extract from Fibroblasts. Lung fibroblasts were isolated from minced whole rat lung was added as a standard to these aliquots lung which was incubated in 0.25% trypsin. After before migration. The lipids were visualized by exposure digestion for one hour at 3rc, minces were incubated to iodine vapour. In the first aliquot, the spots corre­ in DMEM 10% FBS. Fibroblasts were passed at least 3 sponding to the different lipid classes were scraped into times before use and were cultured till the twentieth scintillation vials and counted. In the second aliquot passage. only phosphatidylcholine (PC) was scraped and extracted by the method of BLIGH and DYER (10).
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