Ozonolysis products of membrane fatty acids activate eicosanoid metabolism in human airway epithelial cells

Leikauf, G D; Zhao, Q; Zhou, S; Santrock, J

doi:10.1165/ajrcmb/9.6.594

Title: Ozonolysis products of membrane fatty acids activate eicosanoid metabolism in human airway epithelial cells

Full Record
Other Related Research

Abstract

When inhaled, ozone reacts at the airway luminal surface with unsaturated fatty acids contained in the extracellular fluid and plasma membrane to form an aldehyde and hydroxyhydroperoxide. The resulting hydroxyhydroperoxide degrades in aqueous systems to yield a second aldehyde and hydrogen peroxide (H2O2). Previously, we demonstrated that ozone can augment eicosanoid metabolism in bovine airway epithelial cells. To examine structure-activity relationships of ozone-fatty acid degradation products on eicosanoid metabolism in human airway epithelial cells, 3-, 6-, and 9-carbon saturated aldehydes and hydroxyhydroperoxides were synthesized and purified. Eicosanoid metabolism was evaluated by determination of total 3H-activity release from confluent cells previously incubated with [3H]arachidonic acid and by identification of specific metabolites with high performance liquid chromatography and radioimmunoassay. The major metabolites detected were prostaglandin E2, prostaglandin F2 alpha, and 15-hydroxyeicosatetraenoic acid. The 9-carbon aldehyde, nonanal, in contrast to 3- or 6-carbon aldehydes, stimulated release at concentrations > or = 100 microM, suggesting that the stimulatory effect increases with increasing chain length. When tested under identical conditions, the 3-, 6-, and 9-carbon hydroxyhydroperoxides were more potent than the corresponding aldehydes. Again, a greater effect was noted when the chain length was increased. One possible explanation for the increased potency of the hydroxyhydroperoxidesmore »« less

Authors:

Leikauf, G D; Zhao, Q; Zhou, S; Santrock, J ^[1]

Univ. of Cincinnati Medical Center, OH (United States)

Publication Date:: Wed Dec 01 00:00:00 EST 1993

OSTI Identifier:: 5475178

Resource Type:: Journal Article

Journal Name:: American Journal of Respiratory Cell and Molecular Biology; (United States)

Additional Journal Information:: Journal Volume: 9:6; Journal ID: ISSN 1044-1549

Country of Publication:: United States

Language:: English

Subject:: 63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; 59 BASIC BIOLOGICAL SCIENCES; CARBOXYLIC ACIDS; STRUCTURE-ACTIVITY RELATIONSHIPS; EICOSANOIC ACID; METABOLISM; LUNGS; EPITHELIUM; OZONE; BIOLOGICAL EFFECTS; TRITIUM; ANIMAL TISSUES; BETA DECAY RADIOISOTOPES; BETA-MINUS DECAY RADIOISOTOPES; BODY; HYDROGEN ISOTOPES; ISOTOPES; LIGHT NUCLEI; MONOCARBOXYLIC ACIDS; NUCLEI; ODD-EVEN NUCLEI; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANS; RADIOISOTOPES; RESPIRATORY SYSTEM; TISSUES; YEARS LIVING RADIOISOTOPES; 560300* - Chemicals Metabolism & Toxicology; 550200 - Biochemistry

Citation Formats


                    Leikauf, G D, Zhao, Q, Zhou, S, and Santrock, J. Ozonolysis products of membrane fatty acids activate eicosanoid metabolism in human airway epithelial cells.  United States: N. p., 1993. 
        Web.  doi:10.1165/ajrcmb/9.6.594.

Copy to clipboard


                    Leikauf, G D, Zhao, Q, Zhou, S, & Santrock, J. Ozonolysis products of membrane fatty acids activate eicosanoid metabolism in human airway epithelial cells.  United States.  https://doi.org/10.1165/ajrcmb/9.6.594

Copy to clipboard


                    Leikauf, G D, Zhao, Q, Zhou, S, and Santrock, J. 1993.  
        "Ozonolysis products of membrane fatty acids activate eicosanoid metabolism in human airway epithelial cells".  United States.  https://doi.org/10.1165/ajrcmb/9.6.594.

Copy to clipboard


                    
@article{osti_5475178,

  title        = {Ozonolysis products of membrane fatty acids activate eicosanoid metabolism in human airway epithelial cells},

  author       = {Leikauf, G D and Zhao, Q and Zhou, S and Santrock, J},

  abstractNote = {When inhaled, ozone reacts at the airway luminal surface with unsaturated fatty acids contained in the extracellular fluid and plasma membrane to form an aldehyde and hydroxyhydroperoxide. The resulting hydroxyhydroperoxide degrades in aqueous systems to yield a second aldehyde and hydrogen peroxide (H2O2). Previously, we demonstrated that ozone can augment eicosanoid metabolism in bovine airway epithelial cells. To examine structure-activity relationships of ozone-fatty acid degradation products on eicosanoid metabolism in human airway epithelial cells, 3-, 6-, and 9-carbon saturated aldehydes and hydroxyhydroperoxides were synthesized and purified. Eicosanoid metabolism was evaluated by determination of total 3H-activity release from confluent cells previously incubated with [3H]arachidonic acid and by identification of specific metabolites with high performance liquid chromatography and radioimmunoassay. The major metabolites detected were prostaglandin E2, prostaglandin F2 alpha, and 15-hydroxyeicosatetraenoic acid. The 9-carbon aldehyde, nonanal, in contrast to 3- or 6-carbon aldehydes, stimulated release at concentrations > or = 100 microM, suggesting that the stimulatory effect increases with increasing chain length. When tested under identical conditions, the 3-, 6-, and 9-carbon hydroxyhydroperoxides were more potent than the corresponding aldehydes. Again, a greater effect was noted when the chain length was increased. One possible explanation for the increased potency of the hydroxyhydroperoxides over the aldehydes could be due to degradation of the hydroxyhydroperoxide into H2O2 and aldehyde. We consider this an unlikely explanation because responses varied with chain length (although each hydroxyhydroperoxide would produce an equivalent amount of H2O2) and because exposure to H2O2 alone or H2O2 plus hexanal produced a response dissimilar to 1-hydroxy-1-hexanehydroperoxide.},

  doi          = {10.1165/ajrcmb/9.6.594},

  url          = {https://www.osti.gov/biblio/5475178},
  journal      = {American Journal of Respiratory Cell and Molecular Biology; (United States)},

  issn         = {1044-1549},

  number       = ,

  volume       = 9:6,

  place        = {United States},

  year         = {Wed Dec 01 00:00:00 EST 1993},

  month        = {Wed Dec 01 00:00:00 EST 1993}

}

Copy to clipboard

Journal Article:

https://doi.org/10.1165/ajrcmb/9.6.594

Other availability

Find in Google Scholar

Search WorldCat to find libraries that may hold this journal

Save / Share:

Export Metadata

Save to My Library

Similar records in OSTI.GOV collections:

Acrolein stimulates eicosanoid release from bovine airway epithelial cells

Journal Article Doupnik, C; Leikauf, G - American Journal of Physiology; (USA)

Injury to the airway mucosa after exposure to environmental irritants is associated with pulmonary inflammation and bronchial hyperresponsiveness. To better understand the relationships between mediator release and airway epithelial cell injury during irritant exposures, we studied the effects of acrolein, a low-molecular-weight aldehyde found in cigarette smoke, on arachidonic acid metabolism in cultured bovine tracheal epithelial cells. Confluent airway epithelial cell monolayers, prelabeled with (3H)arachidonic acid, released significant levels of 3H activity when exposed (20 min) to 100 microM acrolein. (3H)arachidonic acid products were resolved using reverse-phase high-performance liquid chromatography. Under control conditions the released 3H activity coeluted predominantly withmore »« less
Ozone-induced augmentation of eicosanoid metabolism in epithelial cells from bovine trachea

Journal Article Leikauf, G; Driscoll, K; Wey, H - Am. Rev. Respir. Dis.; (United States)

Epithelial injury and inflammation have been implicated in ozone-induced airway hyperresponsiveness. Because ozone is relatively insoluble and highly reactive, toxicologic effects of this compound may be limited to the plasma membranes of airway epithelium. We hypothesize that oxidant damage to epithelium may result in elaboration of various eicosanoids, which are known to alter airway smooth muscle responsiveness and epithelial cell functions (including ion transport). To examine eicosanoid metabolism after exposure to 0.1 to 10.0 ppm ozone, epithelial cells derived from bovine trachea were isolated and grown to confluency. Bovine tracheal cells in culture expressed differentiated features characteristic of epithelial cells,more »« less
https://doi.org/10.1164/ajrccm/137.2.435
Ozone (O/sub 3/)-induced augmentation of eicosanoid metabolism in cultured epithelial cells derived from bovine trachea

Conference Leikauf, G; Driscoll, K; Weideman, P; ... - Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)

Epithelial damage and inflammation have been implicated in ozone-induced airway hyperresponsiveness. Because O/sub 3/ is relatively insoluble and highly reactive, initiating effects of this compound are likely limited to the epithelium. To examine eicosanoid metabolism following exposure to 0.1-10.0 ppm O/sub 3/, epithelial cell monolayers derived from bovine trachea were alternately exposed to O/sub 3/ and culture medium for 2h by rotating on inclined platforms. After control exposures, basal release rates determined by RIA were: PG(Prostaglandin) E/sub 2/ = 93.0(19.6), PGF/sub 2..cap alpha../=4.0(1.3), 6kPGF/sub 1..cap alpha../=4.9(0.9), Tx (Thromboxane) B/sub 2/=3.9(0.9), LT(Leukotriene)B/sub 4/=0.6(0.4)pg/cm/sup 2/ x h (mean (SE), n=6 to 22).more »« less
Age-dependent effect of ozone on pulmonary eicosanoid metabolism in rabbits and rats

Journal Article Gunnison, A; Finkelstein, I; Weideman, P; ... - Fundamental and Applied Toxicology; (USA)

Acute exposures to ozone have previously been shown to cause quantitative changes in the spectrum of arachidonic acid (AA) metabolites in lung lavage fluid. Since age appears to be an important variable in the toxicity of inhaled ozone, we investigated its effect on ozone-induced changes in pulmonary eicosanoid metabolism. Rats and rabbits ranging in age from neonates to young adults were exposed either to air or to 1 ppm ozone for 2 hr. Lung lavage fluid was collected within 1 hr following exposure and analyzed for its content of selected eicosanoids. In both species, there was a pronounced effect ofmore »« less
https://doi.org/10.1016/0272-0590(90)90194-O
In vitro ozone exposure increases release of arachidonic acid products from a human bronchial epithelial cell line

Journal Article McKinnon, K; Madden, M; Noah, T; ... - Toxicology and Applied Pharmacology; (United States)

Eicosanoids released after ozone exposure of a human bronchial epithelial cell line, BEAS-S6, were analyzed by high-pressure liquid chromatography (HPLC) of supernatants from exposed cells prelabeled with [3H]arachidonic acid. BEAS cells released thromboxane B2 (TxB2), prostaglandin E2 (PGE2), leukotriene C4 (LTC4), LTD4, LTE4, and 12-hydroxyheptadecatrienoic acid (HHT) after exposure to ozone at concentrations of 0.1, 0.25, 0.5, and 1.0 ppm. The eicosanoids were identified by coelution with authentic standards. The largest product from ozone-exposed BEAS cells was the most polar peak, designated Peak 1. Release of cyclooxygenase products such as TxB2, PGE2, and HHT was inhibited by acetylsalicylic acid. Peaksmore »« less
https://doi.org/10.1006/taap.1993.1027

Similar Records