Effects of chronic exposure to ozone on pulmonary lipids in rats

Wright, Elaine S.; White, David M.; Smiler, Kathleen L.

doi:10.1016/0300-483x(90)90123-x

Cited by 10 publications

(9 citation statements)

References 22 publications

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“…Statistically significantly decreased incorporation of [1-~4C]acetate into both unsaturated and saturated PC, PE, and total phospholipid of lung tissue was observed after 3-and 12-month exposure. Decreased concentration-related incorporation rates of [1-~4C]acetate into alveolar phospholipids were observed after 6-month of exposure to 0.13, 0.25, and 0.50 ppm 03 [154]. These studies suggest that surfactant synthesis is impaired after chronic 03 exposure.…”

Section: Stratospheric Generation Of 0 3 (Ozone Layer)mentioning

confidence: 57%

“…They reported changes in fatty acid and lipid composition of the lung lavage of these animals. Chronic exposure of rats to low (0.12, 0.25, or 0.50 ppm) concentrations of 03 did not affect phospholipid content of lavage fluid, although it did change lung tissue phospholipid synthesis [154]. Statistically significantly decreased incorporation of [1-~4C]acetate into both unsaturated and saturated PC, PE, and total phospholipid of lung tissue was observed after 3-and 12-month exposure.…”

Section: Stratospheric Generation Of 0 3 (Ozone Layer)mentioning

confidence: 84%

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Toxic oxidant species and their impact on the pulmonary surfactant system

Putman

Golde

Haagsman

1997

Lung

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In this review the effects of oxidant inhalation on the pulmonary surfactant system of laboratory animals are discussed. Oxidant lung injury is a complex phenomenon with many aspects. Inhaled oxidants interact primarily with the epithelial lining fluid (ELF), a thin layer covering the epithelial cells of the lung which contains surfactant and antioxidants. In the upper airways this layer is thick and contains high levels of antioxidants. Therefore oxidant injury in this area is rare and is more common in the lower airways where the ELF is thin and contains fewer antioxidants. In the ELF oxidants can react with antioxidants or biomolecules, resulting in inactivation of the biomolecules or in the formation of even more reactive agents. Oxidation of extracellular surfactant constituents may impair its function and affect breathing. Oxidized ELF constituents may promote inflammation and edema, which will impair the surfactant system further. Animal species differences in respiratory tract anatomy, ventilatory rate, and antioxidant levels influence susceptibility to oxidants. The oxidant exposure dose dictates injury, subsequent repair processes, and tolerance induction.

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Section: Stratospheric Generation Of 0 3 (Ozone Layer)mentioning

confidence: 57%

Section: Stratospheric Generation Of 0 3 (Ozone Layer)mentioning

confidence: 84%

Toxic oxidant species and their impact on the pulmonary surfactant system

Putman

Golde

Haagsman

1997

Lung

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“…Owing to its high chemical reactivity, it has also the potency to cause oxidative damage to extracellular secretory lung products. However, the content of surfactant phospholipids found in lavages after chronic exposure to a low concentration of O 3 (0.1–0.5 ppm) was not affected [ 78], but lavage phospholipid composition showed a slight increase in the PC species. Although after acute exposure to 0.8 ppm (for 2 and 12 h) neither quantity nor quality of phospholipids in the BAL was changed, the structure of surfactant subtypes was altered [ 79, 80].…”

Section: Toxicitymentioning

confidence: 99%

Effect of air pollutants on the pulmonary surfactant system

Müller

Seifart

Barth

1998

Eur J Clin Investigation

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Air pollutants have been recognized to influence the structure and function of the surfactant system. Agents that have received the most attention include ozone, nitrogen dioxide, hyperoxia, diesel exhaust, tobacco smoke, silica and fibrous materials such as asbestos. The deleterious effects of air pollutants on the surfactant system depend on the size of the agent, on its solubility in aqueous solutions and chemical reactivity and on its concentration and the duration of exposure. Hereby the following general rules apply: the smaller the agent's size and the less water soluble the pollutant is, the greater the tendency to reach the alveoli during breathing. In addition, the reactivity also determines the depth of penetration into alveoli. Compounds with high reactivity such as O 3 , which also fulfil the earlier rules, will react with the upper respiratory tract compared with compounds with slightly reduced reactivity, such as NO 2 , which will penetrate the alveoli. The common consequence of exposure to air pollutants is an accumulation of surfactant phospholipids and surfactant-specific proteins in the bronchoalveolar lavage fluid. These components also are structurally altered, mainly by oxidant gases, resulting in impairment of their biological activity. Thus, for surfactant phospholipids, there is impaired adsorption to the air-liquid interface due to oxidation of their fatty acids. Also, surfactant protein A, regarded as a modulator of the surfactant system, shows impaired functions after exposure to oxidants. It is likely that in addition to the effects described in this review not all effects are known because the molecular effects of several key components (e.g SP-B and C) have not been well studied.

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“…Several different binary surfactant phospholipid mixtures are known to resist inhibition like serum albumin to different extents [13,14]. This study evaluated the relative resistance offered by the binary surfactant mixtures to mycolicacid-induced inhibition.…”

Section: Binary Surfactant Lipid Mixturesmentioning

confidence: 99%

“…Several substances such as serum, red cell membrane, pollutants, and bacterial toxins cause inhibition of lung surfactant by different mechanisms [12][13][14]. Different binary surfactant lipid mixtures have different packing and squeeze-out in response to high compression.…”

Section: Introductionmentioning

confidence: 99%