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Cigarette smoke augments asbestos-induced alveolar epithelial cell injury: role of free radicals

Kamp, David W., Greenberger, Marc J., Sbalchierro, Jane S., Preusen, Scott E., Weitzman, Sigmund A.·1998·Free Radical Biology and Medicine
DOI 10.1016/s0891-5849(98)00158-0
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Abstract

Cigarette smoke augments asbestos-induced bronchogenic carcinoma by mechanisms that are not established. Alveolar epithelial cell (AEC) injury due to oxidant-induced DNA damage and depletion of glutathione (GSH) and adenosine triphosphate (ATP) may be one important mechanism. We previously showed that amosite asbestos-induces hydroxyl radical production and DNA damage to cultured AEC and that phytic acid, an iron chelator, is protective. We hypothesized that whole cigarette smoke extracts (CSE) augment amosite asbestos-induced AEC injury by generating iron-induced free radicals that damage DNA and reduce cellular GSH and ATP levels. Asbestos or CSE each caused dose-dependent toxicity to AEC (WI-26 and rat alveolar type I-like cells) as assessed by 51chromium release. The combination of asbestos (5 microg/cm2) and CSE (0.O1-0.1%) caused synergistic injury whereas higher doses of each agent primarily had an additive toxic effect. Asbestos (5 microg/cm2) augmented CSE-induced (0.01-1.0%) AEC DNA damage over a 4 h exposure period as assessed by an alkaline unwinding, ethidium bromide fluorometric technique. These effects were synergistic in A549 cells and additive in WI-26 cells. Asbestos (5 microg/cm2) and CSE (0.5-1.0%) reduced A549 and WI-26 cell GSH levels as assessed spectrophotometrically and ATP levels as assessed by luciferin/luciferase chemiluminescence but a synergistic interaction was not detected. Phytic acid (500 microM) and catalase (100 microg/ml) each attenuated A…

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Citations

Cites

Research works printed but not linked: 37

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Metadata

Authors
Kamp, D. W., Greenberger, M. J., Sbalchierro, J. S., Preusen, S. E., & Weitzman, S. A.
Venue
Free Radical Biology and Medicine
Publisher
Elsevier BV
Published
1998-10
Volume
25
Issue
6
Pages
728-739
ISSN
0891-5849
DOI
10.1016/s0891-5849(98)00158-0
Cited by
44
References
2
Language
en
Licence

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