Susceptibility to amiodarone-induced pulmonary toxicity: Relationship to the uptake of amiodarone by isolated lung cells

Lung ◽  
2004 ◽  
Vol 174 (1) ◽  
Author(s):  
B.D. Wilson ◽  
M.L. Lippmann
Keyword(s):  
Pulmonary Toxicity ◽  
Lung Cells ◽  
Isolated Lung ◽  
Toxicity Relationship

Use of isolated lung cells in pulmonary toxicology

1993 ◽  
Vol 7 (4) ◽  
pp. 359-364 ◽  
Author(s):  
B. Nemery ◽  
P.H.M. Hoet
Keyword(s):  
Lung Cells ◽  
Isolated Lung

Volcanic ash: Toxicity to isolated lung cells

1982 ◽  
Vol 9 (2) ◽  
pp. 317-325 ◽  
Author(s):  
V. Castranova ◽  
L. Bowman ◽  
J. M. Shreve ◽  
G. S. Jones ◽  
P. R. Miles
Keyword(s):  
Volcanic Ash ◽  
Lung Cells ◽  
Isolated Lung

scholarly journals In vitrotoxicity of indoor fungi from dwellings in Slovakia: testing on the isolated lung cells

2008 ◽  
Author(s):  
Z. Kováčiková ◽  
E. Tátrai ◽  
E. Piecková ◽  
Z. Kolláriková ◽  
V. Jančinová ◽  
...  
Keyword(s):  
Lung Cells ◽  
Isolated Lung ◽  
Indoor Fungi

Membrane permeability of isolated lung cells to nonelectrolytes at different temperatures

1982 ◽  
Vol 243 (5) ◽  
pp. C285-C292 ◽  
Author(s):  
R. A. Garrick ◽  
F. P. Chinard
Keyword(s):  
Membrane Permeability ◽  
Tritiated Water ◽  
Cellular Systems ◽  
Lung Cells ◽  
Cell Preparation ◽  
Rabbit Lung ◽  
Novikoff Hepatoma ◽  
Permeability Coefficients ◽  
Diffusional Permeability ◽  
Isolated Lung

Membrane permeability coefficients (P0) of rabbit lung cells consisting primarily of alveolar epithelial and endothelial cells and of alveolar macrophages from dog lungs were determined for tritiated water, n-[14C]alcohols, and [14C]antipyrine over the temperature range 10 to 37 degrees C with the series-parallel pathway model. In the mixed cell preparation both the diffusional permeability to water (755 X 10(-5) cm.s-1 at 37 degrees C) and the response to temperature change (apparent activation energy, Ea, 10 kcal.mol-1) are greater than the corresponding values in the macrophages (110 X 10(-5) cm.s-1 and 4.8 kcal.mol-1, respectively). The permeability coefficients for the small alcohols (C1-C3) are similar and considerably higher than for water in both cellular preparations. The values of the permeability coefficients and the temperature dependence for antipyrine and the larger alcohols in the mixed lung cells differ from the values obtained in the macrophages. Comparison of our results with those obtained in erythrocytes and Novikoff hepatoma cells demonstrates the differences in water permeability in each cell preparation and the similarity in permeation for the more lipophilic solutes in the cell preparations. These differences may be important in the comparison of results obtained in isolated cellular systems and in intact tissues and organs.

Glucocorticoid Binding by Isolated Lung Cells*

Endocrinology ◽  
1978 ◽  
Vol 102 (5) ◽  
pp. 1570-1575 ◽  
Author(s):  
PHILIP L. BALLARD ◽  
ROBERT J. MASON ◽  
WILLIAM H. J. DOUGLAS
Keyword(s):  
Lung Cells ◽  
Isolated Lung

Biochemical and morphological changes in lung tissue and isolated lung cells of rats induced by short-term nitrogen dioxide exposure

2000 ◽  
Vol 19 (7) ◽  
pp. 392-401 ◽  
Author(s):  
L van Bree ◽  
I MCM Rietjens ◽  
G M Alink ◽  
J AMA Dormans ◽  
M Marra ◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Nitrogen Dioxide ◽  
Lung Tissue ◽  
Lung Cells ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lamellar Bodies ◽  
Morphometric Analyses ◽  
Isolated Lung

To investigate the effects of repeated exposure to nitrogen dioxide (NO2) on antioxidant enzymes in lung tissue and isolated lung cells, rats were continuously exposed to 20 mg/m3 NO2 (10.6 ppm) for 4 days. The activities of glucose-6-phosphate dehydrogenase (G6PDH), glutathione reductase (GR), and glutathione peroxidase (GSHPx) were measured in the cytosolic fraction of lung tissue of both control and NO2-exposed rats as well as in isolated alveolar macrophages (AMs) and type II cells. Qualitative and quantitative changes in AM and type II cells were studied by electron microscopy and by morphometric analyses using enzyme and immunohistochemistry. NO2 exposure resulted in significantly increased pulmonary activities of G6PDH, GR, and GSHPx, both expressed per lung and per gram of lung weight. Morphometric data show that NO2 exposure significantly increased the number of type II cells, predominantly in the centriacinar region, indicating proliferation of epithelium following cellular injury. Type II cells in lungs of NO2-exposed rats had a squamous, less cuboidal appearance with more lamellar bodies compared to type II cells in lungs of control rats. Compared to control lungs, a higher number of macrophages could be isolated from NO2-exposed lungs, while numbers of type II cells isolated from lungs of control and NO2-exposed rats were the same. Isolated type II cells from control and NO2-exposed rats were polymorphic, with a small number of lamellar bodies and without polarity. Isolated macro-phages were rounded and contained many filopodia. NO2 exposure caused increases in the activities of G6PDH and GSHPx in isolated type II cells and of GSHPx in isolated macrophages, when expressed per number of cells. Macrophages and type II cells isolated from control and NO2-exposed rats and re-exposed in vitro to NO2, showed no differences in phagocytosis and viability features. Our results indicate that NO2-induced increases in pulmonary antioxidant enzymes are also reflected in isolated AM and type II cells. Since these lung cells do not display a decreased sensitivities toward an in vitro NO2 exposure, overall increase in antioxidant enzyme activities do not seem to play the most pivotal role in controlling cellular NO2 sensitivity and oxidant defence. Combined data from biochemical, morphological, and morphometric analyses of lungs and lung cells suggest that lung cell and tissue oxidant sensitivity and defence largely depends on the cell and tissue organisation, i.e., cell numbers and morphology as well as the ratio of surface area to cytoplasmic volume.

Synthesis and binding of lactose-specific lectin by isolated lung cells

1985 ◽  
Vol 248 (3) ◽  
pp. C258-C264 ◽  
Author(s):  
P. Whitney ◽  
S. Maxwell ◽  
U. Ryan ◽  
D. Massaro
Keyword(s):  
Cell Types ◽  
Lung Fibroblasts ◽  
Lung Cells ◽  
Type Ii Cells ◽  
Type Ii ◽  
Rat Lung ◽  
Peak Activity ◽  
Alveolar Epithelial ◽  
Isolated Lung ◽  
Pulmonary Macrophages

Neonatal maturation of alveolar structure in rat lung temporally coincides with the peak activity of a beta-galactoside-specific endogenous lung lectin of the type that has been linked to developmental processes in other tissues. To learn more about the lung lectin we examined four cell types for their ability to synthesize and bind the lectin. Cultured lung fibroblasts and pulmonary artery endothelial cells synthesized and bound the lectin, alveolar macrophages bound but did not synthesize it, and alveolar epithelial type II cells neither bound nor synthesized it. Pulmonary macrophages made a different lactose-binding protein that did not agglutinate or bind trypsin-treated red blood cells, a property of lung lectin that is the means of its assay.

scholarly journals Lung Oxidative Damage by Hypoxia

2012 ◽  
Vol 2012 ◽  
pp. 1-18 ◽  
Author(s):  
O. F. Araneda ◽  
M. Tuesta
Keyword(s):  
Oxidative Damage ◽  
Vascular Remodeling ◽  
Redox State ◽  
Lung Cells ◽  
Hypoxic Vasoconstriction ◽  
Isolated Lung ◽  
Chronic Pulmonary Hypertension ◽  
Oxide Synthase ◽  
Adequate Oxygenation

One of the most important functions of lungs is to maintain an adequate oxygenation in the organism. This organ can be affected by hypoxia facing both physiological and pathological situations. Exposure to this condition favors the increase of reactive oxygen species from mitochondria, as from NADPH oxidase, xanthine oxidase/reductase, and nitric oxide synthase enzymes, as well as establishing an inflammatory process. In lungs, hypoxia also modifies the levels of antioxidant substances causing pulmonary oxidative damage. Imbalance of redox state in lungs induced by hypoxia has been suggested as a participant in the changes observed in lung function in the hypoxic context, such as hypoxic vasoconstriction and pulmonary edema, in addition to vascular remodeling and chronic pulmonary hypertension. In this work, experimental evidence that shows the implied mechanisms in pulmonary redox state by hypoxia is reviewed. Herein, studies of cultures of different lung cells and complete isolated lung and tests conductedin vivoin the different forms of hypoxia, conducted in both animal models and humans, are described.

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