Mucus protection and airway peroxidation following nitrogen dioxide exposure in the rat

Cavanagh, David G.; Morris, John B.

doi:10.1080/15287398709531074

Cited by 15 publications

(10 citation statements)

References 30 publications

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“…Both after short-and long-term exposure to NO 2 or O 3 at concentrations varying from 0.04 to 10 ppm, fatty acid peroxidation, which is considered an integral part of cell damage, has been demonstrated by the use of several markers of this reaction. Ethane exhalation in the breath has been measured in living animals, whilst in tissue homogenate the determination of the amount of tissue which reacts with thiobarbituric acid and of the content of conjugated dienes have been employed [116][117][118][119][120][121].…”

Section: Biochemical Alterationsmentioning

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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Section: Biochemical Alterationsmentioning

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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show abstract

“…The epithelium lining the lung airways, which possesses a significant content of PUFA (8), represents one of the first major targets of NO2 and receives a large burden of the exposure (9)(10)(11). The mucin layer overlying airway epithelial cells also possesses a significant content of PUFA, as well as other compounds such as sugars, which may potentially interact with this gas (12). Lipid radicals, generated by hydrogen abstraction, in the presence of molecular oxygen initiate free radical chain autoxidation of membrane PUFA (5)(6)(7).…”

mentioning

confidence: 99%

Generation of glycolaldehyde from guinea pig airway epithelial monolayers exposed to nitrogen dioxide and its effects on sodium pump activity.

Robison

Zhou

Kim

1996

Environ Health Perspect

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Pulmonary injury from nitrogen dioxide (NO2) may in part be related to the generation of aldehydic compounds, which bind with cellular proteins and subsequently impair or inhibit cell function. We examined the generation of aldehydes from guinea pig tracheobronchial epithelial (GPTE) cell monolayers exposed to NO2. With the use of dinitrophenylhydrazine (DNP) to derivatize aldehydic compounds, glycolaldehyde, a two carbon alpha-hydroxyaldehyde, was identified in elevated levels in the basolateral fluid from monolayers exposed to NO2. DNP-glycolaldehyde levels were 81.2 +/- 2.7 and 234.0 +/- 42.6 nM in response to a 1-hr exposure to 1 and 5 ppm NO2, respectively, as compared to an air-control value of 20.3 +/- 6.8 nM. Taking into account dilution and reactivity, cellular glycolaldehyde levels could have reached as high as 3 mM for the 60-min exposure period (i.e., 0.05 mM/min). The effects of exogenous glycolaldehyde on GPTE ouabain-sensitive basolateral 86Rb uptake (an index of Na+,K(+)-ATPase activity) were examined and compared with the actions of NO2 exposure. Bolus addition of glycolaldehyde to the basolateral fluid at concentrations > or = 5 mM led to an inhibition of ouabain-sensitive 86Rb uptake, while lower concentrations had no effect. the effects of exogenous glycolaldehyde differ from NO2 exposure, which led to a sustained elevation of ouabain-sensitive 86Rb uptake with presumed generation of glycolaldehyde at a continuous low level. Glycolaldehyde does not appear to play a significant role in the acute alterations of sodium pump activity, suggesting that the NO2-induced changes in Na+,K(+)-ATPase activity of GPTE monolayers probably are further mediated by other lipid peroxidation products/oxidation processes yet to be identified. Images Figure 1. Figure 2. Figure 3. Figure 4.

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“…For example, the bronchioles, alveolar ducts and alveoli are known to be more susceptible to NO 2 injury, at least when examined histologically. However, in one study where rats were exposed to NO 2 (40 ppm x I h) via a whole-body inhalation chamber, lipid peroxidation, as measured by thiobarbituric acid-reactive material, was significant only in the trachea, rather than in the lung parenchyma (Cavanagh and Morris, 1987). This disparity could be explained by the reduction in antioxidant capacity of the trachea.…”

Section: Experimental Models and Research Issuesmentioning

confidence: 98%

“…Most studies in the civilian literature have investigated the effects of relatively low level NO, exposure whereas the US Army studies have concentrated on acute high-level NO 2 exposure (Januszkiewicz et al, 1992). Some studies have investigated the differences in distribution of histological damage as well as biochemical alterations (Kubota et al, 1987;Cavanagh and Morris, 1987). Correlation between histological and biochemical alterations may not necessarily be present.…”

Section: Experimental Models and Research Issuesmentioning

confidence: 99%

“…Though the exact mechanism of NO 2 toxicity is unknown, a direct effect through lipid peroxidation of cellular membranes and the oxidation of reducing equivalents and proteins has been hypothesized (Cavanagh and Morris, 1987;Menzel). Whole lung or lung segments have been analyzed for i, evidence of lipid or protein oxidation, oxidative enzymes or antioxidant compounds and enzymes.…”

Section: Mechanisms Of No 2 Injurymentioning

confidence: 99%

See 1 more Smart Citation

Overview of nitrogen dioxide effects on the lung with emphasis on military relevance

Mayorga¹

1994

Toxicology

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Mucus protection and airway peroxidation following nitrogen dioxide exposure in the rat

Cited by 15 publications

References 30 publications

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

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

Generation of glycolaldehyde from guinea pig airway epithelial monolayers exposed to nitrogen dioxide and its effects on sodium pump activity.

Overview of nitrogen dioxide effects on the lung with emphasis on military relevance

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