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Title: Effect of 2 ppm ozone exposure on rat lung lipid fatty acids

Abstract

Based on in vitro studies, the initial damage to lung cells by ozone exposure is believed to result in part from the breakdown of lipid polyunsaturated fatty acids to aldehydes, ozonides, and peroxides. The present study measured lipid breakdown products in lungs isolated from rats pretreated with (1-/sup 14/C)acetate 12 h before exposure for 4 h to either air or 2 ppm ozone. Lipid fatty acid breakdown was indicated by a 112% increase in thiobarbituric acid-reactive substances on ozone exposure and by changes in chemical and radioactive measurements of mono- and dicarboxylic acids formed by treatment of lipid fractions with hydrogen peroxide. Ozone exposure resulted in a 63% increase in recovery of short-chain fatty acids accounted for by increased recoveries of malonic acid by 37%, hexanoic acid by 47%, nonanoic acid by 118%, and azelaic acid by 107%. Recovery of glutaric acid was enhanced 15-fold by ozone exposure. Although decreases in tissue arachidonic acid could not be detected, oleic acid was significantly decreased by 36%. Recovery of radiolabel as short-chain fatty acids was increased by 65% on ozone exposure and was mainly accounted for by enhanced labeling of nonanoic and glutaric acid fractions. The failure to observe significant increases inmore » /sup 14/C recovery in the other fractions suggested ozone-induced breakdown of unlabeled fatty acids. These results demonstrate the cleavage of unsaturated fatty acid double bonds following in vivo exposure of lungs to ozone. Breakdown of arachidonic and oleic acids was specifically identified by increased recoveries of glutaric and nonanoic acids, respectively.« less

Authors:
;
Publication Date:
Research Org.:
Univ. of Pennsylvania, Philadelphia (USA)
OSTI Identifier:
6495789
Resource Type:
Journal Article
Resource Relation:
Journal Name: Exp. Lung Res.; (United States); Journal Volume: 14:4
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; METABOLISM; OZONE; TOXICITY; ACETATES; CARBON 14 COMPOUNDS; HYDROGEN PEROXIDE; LUNGS; RATS; TRACER TECHNIQUES; ANIMALS; BODY; CARBOXYLIC ACID SALTS; HYDROGEN COMPOUNDS; ISOTOPE APPLICATIONS; LABELLED COMPOUNDS; MAMMALS; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANS; OXYGEN COMPOUNDS; PEROXIDES; RESPIRATORY SYSTEM; RODENTS; VERTEBRATES; 560300* - Chemicals Metabolism & Toxicology; 550501 - Metabolism- Tracer Techniques

Citation Formats

Rabinowitz, J.L., and Bassett, D.J. Effect of 2 ppm ozone exposure on rat lung lipid fatty acids. United States: N. p., 1988. Web. doi:10.3109/01902148809087822.
Rabinowitz, J.L., & Bassett, D.J. Effect of 2 ppm ozone exposure on rat lung lipid fatty acids. United States. doi:10.3109/01902148809087822.
Rabinowitz, J.L., and Bassett, D.J. 1988. "Effect of 2 ppm ozone exposure on rat lung lipid fatty acids". United States. doi:10.3109/01902148809087822.
@article{osti_6495789,
title = {Effect of 2 ppm ozone exposure on rat lung lipid fatty acids},
author = {Rabinowitz, J.L. and Bassett, D.J.},
abstractNote = {Based on in vitro studies, the initial damage to lung cells by ozone exposure is believed to result in part from the breakdown of lipid polyunsaturated fatty acids to aldehydes, ozonides, and peroxides. The present study measured lipid breakdown products in lungs isolated from rats pretreated with (1-/sup 14/C)acetate 12 h before exposure for 4 h to either air or 2 ppm ozone. Lipid fatty acid breakdown was indicated by a 112% increase in thiobarbituric acid-reactive substances on ozone exposure and by changes in chemical and radioactive measurements of mono- and dicarboxylic acids formed by treatment of lipid fractions with hydrogen peroxide. Ozone exposure resulted in a 63% increase in recovery of short-chain fatty acids accounted for by increased recoveries of malonic acid by 37%, hexanoic acid by 47%, nonanoic acid by 118%, and azelaic acid by 107%. Recovery of glutaric acid was enhanced 15-fold by ozone exposure. Although decreases in tissue arachidonic acid could not be detected, oleic acid was significantly decreased by 36%. Recovery of radiolabel as short-chain fatty acids was increased by 65% on ozone exposure and was mainly accounted for by enhanced labeling of nonanoic and glutaric acid fractions. The failure to observe significant increases in /sup 14/C recovery in the other fractions suggested ozone-induced breakdown of unlabeled fatty acids. These results demonstrate the cleavage of unsaturated fatty acid double bonds following in vivo exposure of lungs to ozone. Breakdown of arachidonic and oleic acids was specifically identified by increased recoveries of glutaric and nonanoic acids, respectively.},
doi = {10.3109/01902148809087822},
journal = {Exp. Lung Res.; (United States)},
number = ,
volume = 14:4,
place = {United States},
year = 1988,
month = 1
}
  • Rats were fed basal diet that was either free of vitamin E or containing 100 mg/kg of the vitamin, and then exposed to 1.0 ppm O/sub 3/. Mean survival time (50%) was 8.2 days in depleted group and 18.5 days in supplemented group. Protective action was thus demonstrated. O/sub 3/ toxicity symptoms included respiratory difficulty, increased respiratory rate, massive pulmonary edema and hemorrhage, and death. Other rats were exposed to 0.5 ppm for 6 wk. O/sub 3/ caused slight increase in lung weight (% body wt.) of E-supplemented rats and pronounced increase in E-depleted rats, which also showed other signsmore » of O/sub 3/ toxicity. Lung-tissue fatty acid changes predicting edema included increase in arachidonic acid, but other unsaturated acids remained relatively constant. While mortality protection indicates peroxidation as O/sub 3/ toxicity mechanism, fatty acid analyses show quite the opposite. (i.e., surfactant lipids stable).« less
  • Rabbit articular chondrocytes were cultured for 8 h in the presence of various concentrations (5-500 microM) of {sup 14}C oleic, {sup 14}C linoleic, and {sup 3H} arachidonic acids. The radioactive unsaturated fatty acids were incorporated into triacylglycerol (TG) and phosphatidylcholine (PC) in a concentration-dependent manner; more fatty acids were incorporated into TG than into PC, at higher concentrations of extracellular fatty acids. Among these fatty acids, arachidonic acid was incorporated into TG much more than into PC, in spite of a very low concentration of arachidonic acid in TG. After transfer of the labeled cells to maintenance medium, the radioactivitymore » in TG declined rapidly and {sup 3}H arachidonic acid radioactivity in PC increased continuously during the chase time periods. Palmitoyl-unsaturated species were mainly formed in PC when cultured at a concentration of 5 microM of each fatty acid. However, when cultured at 500 microM, unsaturated-unsaturated species, specific for each unsaturated fatty acid were actively formed. These findings indicate that (1) fatty acid composition of TG and PC in articular chondrocytes is influenced by the degree of fatty acid supply, (2) formation and turnover of TG plays a role in fatty acid metabolism of cells, and (3) fatty acid pairing in PC is modulated by extracellular fatty acid concentrations.« less
  • Adult rats were exposed to 1 ppm (1.96 mg/m/sup 3/) ozone or air for 2 wk. Animals were sacrificed at 3, 5, 7, or 14 d after the onset of exposure, and samples of plasma and lung lavage were obtained. Heat-inactivated plasma, from animals exposed to ozone for 7 or 14 d, significantly increased DNA synthesis by lung fibroblasts compared with plasma from air-exposed animals. Fractionation of plasma and lavage samples indicated that the factor responsible had an isoelectric point of 6.45-6.75 and a molecular weight of 32 +/- 2 kDa. This factor has a dose-dependent effect on lung fibroblastmore » DNA synthesis in culture, but no significant effect on cultured pneumocyte DNA synthesis. The factor is detectable within 72 h of exposure, and may hold some promise as a marker of early oxidant lung injury.« less
  • Adult rats were exposed to 1 ppm (1.96 mg/m3) ozone or air for 2 wk. Animals were sacrificed at 3, 5, 7, or 14 d after the onset of exposure, and samples of plasma and lung lavage were obtained. Heat-inactivated plasma and lavage from animals exposed to ozone for 5 or 7 d significantly increased DNA synthesis by lung pneumocytes compared with plasma or lavage from air-exposed animals. Fractionation of plasma and lavage samples indicated that the factor responsible had an isoelectric point of 6.45-6.75, and a molecular weight of 38 +/- 3 kDa. This factor has a dose-dependent effectmore » on lung pneumocyte DNA synthesis in culture. It has no effect on cultured fibroblast DNA synthesis, and is distinct from a previously described factor in the plasma of these ozone-exposed animals that enhances fibroblast DNA synthesis. The factor is detectable within 5 d of exposure, and may hold some promise as a marker of early oxidant lung injury.« less
  • Neat samples of polyunsaturated fatty acids were exposed to ozone in air in a flow system, and the formation of peroxides, conjugated dienes and thiobarbituric acid (TBA)-reactive material was followed as a function of time. The effect of ozone is to shorten the induction period normally observed in autoxidation studies, but the ozone, at the concentrations used here (0-1.5 ppm), appears to have no effect on the rates of product formation after the induction period. During the induction period, increasing ozone concentrations gives rise to substantially increased rates of peroxide (or materials which titrate like peroxide) formation, a slightly increasedmore » rate of conjugated diene formation, and no significant increase in the rate of production of TBA-reactive material. Vitamin E lengthens the induction period but appears to have no other effect. Some of these data are in conflict with earlier reports of Menzel et al.« less