Effects of NO2 on the lungs of aging rats

Cabral‐Anderson, Linda J.; Evans, Michael J.; Freeman, Gustave

doi:10.1016/0014-4800(77)90006-5

Cited by 56 publications

(31 citation statements)

References 19 publications

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“…In the experimental group exposed to a high concentration (20 ppm) for 20 hr, slight degeneration was observed in a small number of type I alveolar epithelial cells after the discontinuation of exposure; swelling and hyperplasia of type II alveolar epithelial cells followed, and the reparation of the epithelium terminated with the transformation of type II cells to type I. The morphological and numerical changes in both types of cells are consistent with the reports of Evans et al (3)(4)(5)(6)(7)(8)(9) and Sherwin et al (10,11). The fact that type II cells transform to type I has confirmed the results Evans et al (4) found with the use of autoradiography.…”

Section: Discussionsupporting

confidence: 88%

Morphological effects of nitrogen dioxide on the rat lung.

Hayashi

Kohno

Ohwada

1987

Environ Health Perspect

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Morphological studies of the rat lung exposed to 20 ppm NO2 for 20 hr (experiment 1), to 0.5 ppm for 19 months (experiment 2), and to 10 ppm for 14 days (experiment 3) were conducted. Changes in the mast cells of the tracheas and main bronchi of rats exposed to 0.5 ppm (experiment 4) were also observed.In the alveolus, cytoplasmic blebbing occurred in a small number of type I cells immediately after exposure to 20 ppm NO2 for 20 hr, and remarkable vacuolar change was observed 3 days after 10 ppm exposure. Exposure to 0.5 ppm did not cause degeneration.Swelling In each experiment, pinocytotic vesicles of endothelial cells in capillaries, followed by interstitial edema in the alveolar walls, were observed. In addition to these changes, desquamation of endothelium and widening of the endothelial junction of endothelial cells occurred in experiment 3.The early changes observed in the animals exposed to 0.5 ppm NO2 were the numerical and histochemical changes of mast cells in the trachea and main bronchus.

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Section: Discussionsupporting

confidence: 88%

Morphological effects of nitrogen dioxide on the rat lung.

Hayashi

Kohno

Ohwada

1987

Environ Health Perspect

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“…Structural damage is induced both by acute and chronic exposure to NO 2 or O 3 , mainly affecting cells at the junctions of the terminal airways and the proximal alveolar regions. It includes loss of cilia and secretory granules, necrosis and sloughing of epithelium [12,13,41,[64][65][66][67][68][69][70][71][72][73][74][75][76][77][78][79][80].…”

Section: Histopathologymentioning

confidence: 99%

“…Necrosis of airway epithelial ciliated cells in terminal airways and of type I alveolar epithelial cells in centriacinar regions constitutes the main cellular alteration [65,[69][70][71][72][73][74][75][76]. Other morphological changes frequently reported are damage to tight junctions and to Clara cells and goblet cells, with loss of secretory granules [66,71,72,79], as well as thickening of the epithelium and of the alveolar wall with hypertrophy and hyperplasia of epithelial cells, particularly Clara cells and alveolar type II cells [65][66][67][68][69][70][71][72][73][74][75][76][77][78][79][80]. After either subchronic or chronic exposure, hypertrophy of smooth muscle and endothelial cells, hyperplasia of goblet cells and accumulation of mucus are also found in respiratory bronchioles [65,[76][77][78].…”

Section: Histopathologymentioning

confidence: 99%

Effect of oxidant air pollutants on the respiratory system: insights from experimental animal research

Chitano¹,

Hosselet²,

Mapp³

et al. 1995

Eur Respir J

100

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In the present paper, we have reviewed experimental animal studies on the effects of the two most important oxidant airborne pollutants, nitrogen dioxide and ozone, on the respiratory system.The toxic effects depend on concentration and length of exposure, and are generally similar for both oxidants, with ozone operative at lower concentrations. High doses of both oxidants cause death due to lung oedema Exposure to sublethal levels causes functional alterations such as airflow limitation and airway hyperresponsiveness to bronchoconstrictor stimuli. These effects, which are generally reversible, are associated with epithelial injury, oedema and airway and parenchymal infiltration by inflammatory cells. Loss of cilia of airway epithelium and necrosis of type I alveolar epithelial cells are the most prominent consequences at the epithelial level. Inmation is characterized by early neutrophilic infiltration, followed by an increased number of mononuclear cells, predominantly alveolar macrophages.After long-term exposure, whilst nitrogen dioxide causes predominantly emphysema, ozone produces mainly pulmonary fibrosis. Biochemical effects include lipid peroxidation, increased antioxidant metabolism, and alteration of enzyme activity. Nitrogen dioxide and ozone may also alter the immunological response and reduce the defence against infections, increasing the susceptibility of exposed animals to infections.

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“…Many investigations on the repair of bronchioles injured by 03 or N02 have been reported (4,6,22,32,43,45,46). The common features are an early loss or shortening of cilia, variable sloughing of necrotic ciliated cells, subsequent appearance of nonciliated cells with proliferation or a high labeling index, and final regeneration of ciliated and Clara cells.…”

Section: Discussionmentioning

confidence: 99%

“…In N02-or 03-exposed animals, ciliated cells which are more easily altered than Clara cells (2,4,31,45) have been observed to regenerate from Clara cells (11,12). Stephens et al (45) observed a loss of cilia and subsequent sloughing of ciliated cells after exposure of terminal bronchioles to 0.5 and 0.9 ppm 03.…”

mentioning

confidence: 99%

Contribution of ciliated cells to Clara cell regeneration following complete loss of bronchiolar Clara cells in bromobenzene-injected mice.

Ueda

Hirai

Ogawa

1991

Acta Histochem. Cytochem

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The paper investigates, by electron microscopy, the mechanism of regeneration of Clara cells killed selectively and completely by bromobenzene (BB) in mouse terminal bronchioles. Male specific pathogen free mice received an intraperitoneal injection of 0.76 g/kg BB. Within 24 hr, Clara cells showed vacuolization of the massive smooth endoplasmic reticulum (SER) followed by severe cell damage, and all Clara cells then exfoliated into the airway. Only ciliated cells remained intact; 99.9% of the lining cells were ciliated cells, which flattened and covered all of the terminal bronchioles. Many ciliated cells then lost the cilia and basal bodies; concurrently, nonciliated cells occurred although cell proliferation was negligible. Between 3 and 5 days, these nonciliated cells divided and increased in number, but some of them still maintained a few basal bodies, strongly suggesting that they are "post-ciliated" cells. At the same time, some cells showed ciliogenesis to replenish the decreased ciliated cell population, and at day 5 some formed a cluster of SER. After eight days, granules were formed in the SER-containing cells, and resulted in Clara cell development. Cycloheximide did not affect the reservation of ciliated cells but spoiled the reappearance of Clara cells during the bronchiolar regeneration after BB injection. At day 2 when Clara cells were thoroughly destroyed, [3H]-thymidine was incorporated into some ciliated cells, which transformed into nonciliated cells at days 3 and 4. Therefore, the present results may prove that a bronchiolar regeneration mechanism involves dedifferentiation of ciliated cells to form nonciliated cells, from which columnar epithelium regenerates.

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Effects of NO2 on the lungs of aging rats

Cited by 56 publications

References 19 publications

Morphological effects of nitrogen dioxide on the rat lung.

Morphological effects of nitrogen dioxide on the rat lung.

Effect of oxidant air pollutants on the respiratory system: insights from experimental animal research

Contribution of ciliated cells to Clara cell regeneration following complete loss of bronchiolar Clara cells in bromobenzene-injected mice.

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