Interfacial phospholipids inhibit ozone-reactive absorption-mediated cytotoxicity in vitro.

@article{Connor2004InterfacialPI,
  title={Interfacial phospholipids inhibit ozone-reactive absorption-mediated cytotoxicity in vitro.},
  author={Lydia M Connor and Carol A. Ballinger and Thomas Albrecht and Edward M. Postlethwait},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2004},
  volume={286 6},
  pages={
          L1169-78
        }
}
The intrapulmonary distribution of inhaled ozone (O(3)) and induction of site-specific cell injury are related to complex interactions among airflow patterns, local gas-phase concentrations, and the rates of O(3) flux into, and reaction and diffusion within, the epithelial lining fluid (ELF). Recent studies demonstrated that interfacial phospholipid films appreciably inhibited NO(2) absorption. Because surface-active phospholipids are present on alveolar and airway interfaces, we investigated… Expand
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References

SHOWING 1-10 OF 43 REFERENCES
Ozone-reactive absorption by pulmonary epithelial lining fluid constituents.
TLDR
The pH, aqueous substrate, and temperature-dependence and the Ea and Q10 are consistent with reaction-dependent O3 uptake by ELF, which suggests that the ELF represents the primary site for O3-reactive absorption. Expand
O3-induced formation of bioactive lipids: estimated surface concentrations and lining layer effects.
TLDR
Estimations of bioactive ozonation and autoxidation product accumulation within the ELF suggested possible nanomolar to low micromolar concentrations and the use of reaction products as metrics of O3 exposure may have intrinsic sensitivity and specificity limitations. Expand
Influence of epithelial lining fluid lipids on NO(2)-induced membrane oxidation and nitration.
TLDR
The data suggest that reaction/diffusion limitations govern (*)NO(2) distribution, that the induction of secondary oxidative processes is dependent on nonlinear relationships among (*) NO( 2) flux rates, antioxidant concentrations, and diffusivity of secondary reactive species. Expand
NO2 interfacial transfer is reduced by phospholipid monolayers.
TLDR
It is proposed that pulmonary surfactant may influence the intrapulmonary gas phase distribution of inhaled NO2, and monolayer-induced resistance to NO2 flux is related to physicochemical properties of the film itself rather than alterations within the aqueous and gas phases. Expand
Ozone injury to alveolar epithelium in vitro does not reflect loss of antioxidant defenses.
TLDR
The sensitivity of alveolar epithelial monolayers to ozone injury in vitro reflects a disproportionate degree of oxidant stress on cell membranes relative to intracellular antioxidant defenses, i.e., cellular susceptibility to oxidant injury may depend on the ratio of the surface area of the cell to its cytoplasmic volume. Expand
Airspace Surface Chemistry Mediates O3-Induced Lung Injury
Ozone (O3) produces diverse pulmonary pathophysiologies but with marked heterogeneities relative to species, age, anatomic site, disease, and exposure history. These pronounced susceptibilityExpand
Determinants of inhaled ozone absorption in isolated rat lungs.
TLDR
The data suggest that O3 uptake may be principally localized to the conducting airways and at concentrations above 1 ppm other contributory factors such as O3/substrate reaction kinetics, epithelial damage, and solute O3 backpressure may affect the overall net absorption rate. Expand
Three-dimensional mapping of ozone-induced acute cytotoxicity in tracheobronchial airways of isolated perfused rat lung.
TLDR
For the model used, identification of injured epithelial cells by differential permeability and laser confocal microscopy appeared to be highly sensitive and permitted mapping of acute cytotoxicity throughout the airway tree and quantitative comparisons of sites with different branching histories and potential dosimetry rates. Expand
The cascade mechanism to explain ozone toxicity: the role of lipid ozonation products.
TLDR
Preliminary data show that individual LOP cause the activation of specific lipases, which trigger the release of endogenous mediators of inflammation, and lipid ozonation products are suggested to be the most likely species to act as signal transduction molecules. Expand
Ozone exposure increases aldehydes in epithelial lining fluid in human lung.
TLDR
It is confirmed that exposure to ozone with exercise, at concentrations relevant to urban outdoor air, results in ozonation of lipids in the airway epithelial lining fluid of humans. Expand
...
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4
5
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