Effects of in vitro ozone exposure on peroxidative damage, membrane leakage, and taurine content of rat alveolar macrophages

Banks, Melanie A.; Porter, Dale W.; Martin, William G.; Castranova, Vincent

doi:10.1016/0041-008x(90)90358-2

Cited by 34 publications

(13 citation statements)

References 47 publications

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“…This result is confirmed by the study by Higgins et al (1995) but not by Brunekreef et al (1994), although the irritant effect linked to ozone, but more specifically, to peroxyacyl nitrates (PAN components), has already been described (WHO, Regional Office for Europe, 1987;Banks et al, 1990;Becker et al, 1991).…”

Section: Figsupporting

confidence: 87%

Air Pollution and Doctors' House Calls: Results from the ERPURS System for Monitoring the Effects of Air Pollution on Public Health in Greater Paris, France, 1991–1995

Médina

Tertre

Quénel

et al. 1997

Environmental Research

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Section: Figsupporting

confidence: 87%

Air Pollution and Doctors' House Calls: Results from the ERPURS System for Monitoring the Effects of Air Pollution on Public Health in Greater Paris, France, 1991–1995

Médina

Tertre

Quénel

et al. 1997

Environmental Research

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“…Increase of phagocytic activity and of cytotoxicity toward mammary adenocarcinoma cells have been reported both in alveolar macrophages exposed to 10 ppm NO 2 in vitro and in cells obtained from animals exposed in vivo to 40 ppm [167]. By contrast, after longer in vitro or in vivo exposures to oxidant gases, alveolar macrophage superoxide anion production, mobility, phagocytosis, and bacterial killing decreases [92,154,158,159,168].…”

Section: Cell Culture and Mediator Releasementioning

confidence: 98%

“…Reduced viability after in vitro exposure to O 3 has been observed on cultured cells [159][160][161]. Exposure to O 3 induces cytoplasmic vacuolization, cell necrosis and lipid peroxidation in monolayer cultures of tracheal epithelium [161].…”

Section: Cell Culture and Mediator Releasementioning

confidence: 99%

“…Exposure to O 3 induces cytoplasmic vacuolization, cell necrosis and lipid peroxidation in monolayer cultures of tracheal epithelium [161]. Lipid peroxidation and an alteration of membrane fluidity and properties after exposure to O 3 and NO 2 have been reported in epithelial and endothelial cells [161][162][163], fibroblasts [164], and macrophages [159,165]. Impaired membrane function seems, therefore, an important aspect of oxidant-induced injury, as it may be the primary event of the development of pulmonary oedema.…”

Section: Cell Culture and Mediator Releasementioning

confidence: 99%

See 1 more Smart Citation

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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“…The clinical and histopathologic changes of lung injury produced by these agents are indistinguishable from the changes seen in hyperoxic lung injury. Excessive pulmonary exposure to these oxidant gases results in peroxidative damage to pulmonary membranes with biochemical and metabolic changes in lung tissue (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). In humans, the histologic features of these injuries are described as diffuse alveolar damage, and the resultant clinical presentation of hypoxemia, increased physiologic shunt, and diminished pulmonary compliance are associated with such injuries and are known as adult respiratory distress syndrome.…”

Section: Introductionmentioning

confidence: 99%

Pulmonary Response to Hyperoxia: Effects of Magnesium

Dedhia¹,

Banks²

1994

Environmental Health Perspectives

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Animals and humans rapidly develop respiratory failure and die within a few days when exposed to 100% oxygen. Postmortem examination of the lungs shows histopathologic features characteristic of diffuse alveolar damage, clinically recognized as adult respiratory distress syndrome (ARDS). At the present time, there is no effective therapy available to alter outcomes in ARDS. Importantly, hypomagnesemia also is frequently observed in critically ill patients at risk of developing ARDS. In a model of hyperoxic lung injury, rats were exposed to 100% oxygen for 48, 64, and 96 hr and several experiments were performed. First, changes in the features of bronchoalveolar lavage and in alveolar macrophage function were compared in rats exposed to room air and those exposed to hyperoxia. Second, we studied the effect of hypomagnesemia on the severity of hyperoxic lung injury. Third, we evaluated the pulmonary responses to high-dose and normal-dose Mg therapy in rats exposed to hyperoxia. In all groups, hyperoxia induced significant changes in the total and differential cell counts with increased lipid peroxidation of lavaged cells, enhanced chemiluminescence from alveolar macrophages, and protein leakage into the alveolar spaces. After 48 hr of hyperoxia, oxygen-free radical formation and hydrogen peroxide production by the alveolar macrophage were diminished compared to baseline, implying a toxic effect of hyperoxia on the alveolar macrophages. Overall, hypomagnesemia tended to magnify the degree of hyperoxic lung injury, while high-dose Mg therapy tended to attenuate the effects of hyperoxia. In conclusion, in this animal model of diffuse alveolar damage, alterations in host serum magnesium levels may modulate the degree of lung damage. -Environ Health Perspect 102(Suppl 10): 101-105 (1994)

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Effects of in vitro ozone exposure on peroxidative damage, membrane leakage, and taurine content of rat alveolar macrophages

Cited by 34 publications

References 47 publications

Air Pollution and Doctors' House Calls: Results from the ERPURS System for Monitoring the Effects of Air Pollution on Public Health in Greater Paris, France, 1991–1995

Air Pollution and Doctors' House Calls: Results from the ERPURS System for Monitoring the Effects of Air Pollution on Public Health in Greater Paris, France, 1991–1995

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

Pulmonary Response to Hyperoxia: Effects of Magnesium

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