| Comparison of the Toxic Effects of Hydrogen Peroxide and Ozone on Cultured Human Bronchial Epithelial Cells Edward W. Gabrielson,
1
Xiao-Ying Yu,
2
and E. William Spannhake
2
1
Department of Pathology, Johns Hopkins University School of Medicine
2
Department of Environmental Health Sciences, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD 21205 USA Abstract
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. Key words : cell replication, cytotoxicity, deferoxamine, hydrogen peroxide, ozone, single-strand breaks. Environ Health Perspect 102:972-974 (1994) http://ehpnet1.niehs.nih.gov/docs/1994/102-11/gabrielson.html
Address correspondence to E.W. Gabrielson, Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224 USA. This work was supported by grants ES03505 and ES03819 from the National Institute of Environmental Health Sciences. Received 19 May 1994 ; accepted 15 August 1994.
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