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Ozone injury to alveolar epithelium in vitro does not reflect loss of antioxidant defenses.
Toxicol Appl Pharmacol 1994; 125(1):59-69TA

Abstract

The objective of this study was to characterize an in vitro model of oxidant gas toxicity, using primary cultures of alveolar type II cells maintained in serum-free medium, by evaluating (1) epithelial barrier function, (2) the stability of cellular antioxidant defenses, and (3) the response of alveolar epithelial barrier properties to ozone exposure. Antioxidant enzyme activities and glutathione levels were measured in rat type II cells that were freshly isolated, cultured for 1 day in serum-supplemented medium, and subsequently grown in serum-free nutrient medium. After measurement of peak bioelectric properties on Day 4 in primary culture, alveolar epithelial monolayers were exposed to ozone at various concentrations and lengths of exposure. Ozone-induced alterations in monolayer bioelectric properties and impairment of cellular organization were used to evaluate oxidant injury. The primary effect of ozone exposure was a dose-dependent increase in monolayer permeability, which resulted from damage to intercellular junctions and/or loss of epithelial integrity. Extensive and persistent permeability increases correlated with focal areas of epithelial degradation. The focal nature of ozone injury to alveolar epithelium in vitro suggests that individual cell susceptibility to oxidant stress may account for the overall decrement in barrier function. However, this sensitivity does not result from overall loss of antioxidant defenses associated with cell culture, as these monolayers (when cultured in serum-free medium) maintained their antioxidant enzyme activities and glutathione content at levels found in freshly isolated cells. We conclude that the sensitivity of these 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.

Authors+Show Affiliations

Department of Veterinary Anatomy, University of California, Davis 95616.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8128496

Citation

Cheek, J M., et al. "Ozone Injury to Alveolar Epithelium in Vitro Does Not Reflect Loss of Antioxidant Defenses." Toxicology and Applied Pharmacology, vol. 125, no. 1, 1994, pp. 59-69.
Cheek JM, Buckpitt AR, Li C, et al. Ozone injury to alveolar epithelium in vitro does not reflect loss of antioxidant defenses. Toxicol Appl Pharmacol. 1994;125(1):59-69.
Cheek, J. M., Buckpitt, A. R., Li, C., Tarkington, B. K., & Plopper, C. G. (1994). Ozone injury to alveolar epithelium in vitro does not reflect loss of antioxidant defenses. Toxicology and Applied Pharmacology, 125(1), pp. 59-69.
Cheek JM, et al. Ozone Injury to Alveolar Epithelium in Vitro Does Not Reflect Loss of Antioxidant Defenses. Toxicol Appl Pharmacol. 1994;125(1):59-69. PubMed PMID: 8128496.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ozone injury to alveolar epithelium in vitro does not reflect loss of antioxidant defenses. AU - Cheek,J M, AU - Buckpitt,A R, AU - Li,C, AU - Tarkington,B K, AU - Plopper,C G, PY - 1994/3/1/pubmed PY - 1994/3/1/medline PY - 1994/3/1/entrez SP - 59 EP - 69 JF - Toxicology and applied pharmacology JO - Toxicol. Appl. Pharmacol. VL - 125 IS - 1 N2 - The objective of this study was to characterize an in vitro model of oxidant gas toxicity, using primary cultures of alveolar type II cells maintained in serum-free medium, by evaluating (1) epithelial barrier function, (2) the stability of cellular antioxidant defenses, and (3) the response of alveolar epithelial barrier properties to ozone exposure. Antioxidant enzyme activities and glutathione levels were measured in rat type II cells that were freshly isolated, cultured for 1 day in serum-supplemented medium, and subsequently grown in serum-free nutrient medium. After measurement of peak bioelectric properties on Day 4 in primary culture, alveolar epithelial monolayers were exposed to ozone at various concentrations and lengths of exposure. Ozone-induced alterations in monolayer bioelectric properties and impairment of cellular organization were used to evaluate oxidant injury. The primary effect of ozone exposure was a dose-dependent increase in monolayer permeability, which resulted from damage to intercellular junctions and/or loss of epithelial integrity. Extensive and persistent permeability increases correlated with focal areas of epithelial degradation. The focal nature of ozone injury to alveolar epithelium in vitro suggests that individual cell susceptibility to oxidant stress may account for the overall decrement in barrier function. However, this sensitivity does not result from overall loss of antioxidant defenses associated with cell culture, as these monolayers (when cultured in serum-free medium) maintained their antioxidant enzyme activities and glutathione content at levels found in freshly isolated cells. We conclude that the sensitivity of these 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. SN - 0041-008X UR - https://www.unboundmedicine.com/medline/citation/8128496/Ozone_injury_to_alveolar_epithelium_in_vitro_does_not_reflect_loss_of_antioxidant_defenses_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0041008X84710490 DB - PRIME DP - Unbound Medicine ER -