Comparison of the Toxic Effects of Hydrogen Peroxide and Ozone on Cultured Human Bronchial Epithelial Cells

In this study, we compared the cytotoxic and genotoxic effects of hydrogen peroxide and ozone on cultured human airway epithelial cells in primary culture. Both agents caused a dose-dependent loss in the replicative ability of epithelial cells and at higher levels of exposure caused acute cytotoxici...

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Bibliographic Details
Published inEnvironmental health perspectives Vol. 102; no. 11; pp. 972 - 974
Main Authors Gabrielson, Edward W., Yu, Xiao-Ying, Spannhake, E. William
Format Journal Article
LanguageEnglish
Published United States National Institute of Environmental Health Sciences. National Institutes of Health. Department of Health, Education and Welfare 01.11.1994
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Summary:In this study, we compared the cytotoxic and genotoxic effects of hydrogen peroxide and ozone on cultured human airway epithelial cells in primary culture. Both agents caused a dose-dependent loss in the replicative ability of epithelial cells and at higher levels of exposure caused acute cytotoxicity as measured by release of lactate dehydrogenase. Differences were seen, however, between the agents' effects with regard to induction of DNA single-strand breaks as measured by alkaline elution: whereas single-strand breaks were detected in significant amounts at concentrations of hydrogen peroxide that caused acute cytotoxicity, none were detected at any of the levels of ozone exposure examined. A difference was also seen in the ability of the iron chelator deferoxamine to protect cells from the effects of the two oxidants. Preincubation of cultures with deferoxamine appreciably attenuated the toxicity of hydrogen peroxide but not of ozone. These data suggest that ozone has significant toxic effects on bronchial epithelial cells not mediated through the generation of hydrogen peroxide or hydroxyl radical. Furthermore, the data indicate that the inhibiting action of ozone on cell replicative ability is not mediated through a mechanism related to DNA single-strand breaks.
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ISSN:0091-6765
1552-9924
DOI:10.1289/ehp.94102972