DNA damage by filtered, tar- and aerosol-free cigarette smoke in rodent cells: a novel evaluation.
Nuclear accumulation of the tumorsuppressor protein p53 indicates the occurrence of chromatin injury (J. Cancer Res. Clin. Oncol. 1991, 117, 30; Oncogene 1993, 8, 307) and may be used as an analytical tool to detect genotoxic agents. This mechanism was used to evaluate the DNA-damaging potency (clastogenicity) of the tar- and aerosol-free, gaseous phase of cigarette smoke which is obtained by filtration through Cambridge glass fiber filters. This condensate-free gas phase was absorbed by phosphate-buffered saline and immediately thereafter poured onto monolayers of the murine cell line L929 for 10 min. Eighteen hours later the nuclear accumulation of p53, an indicator for DNA damage, was determined. The elicited level of p53 was similar to that obtained by direct incubation with the gas phase of filtered cigarette smoke for 2 min or with several micrograms of mitomycin C per ml. Previous exhaustive filtration obviously does not inhibit the clastogenic property of tobacco smoke to exert severe DNA damage.
Hess
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Abteilung Virologie, Universität, Hermann-Herder-Str, Freiburg, Germany.
Brandner
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D000818:Animals; D002460:Cell Line; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects*; D005347:Fibroblasts / Q000187:drug effects; D019084:Fluorescent Antibody Technique, Indirect; D051379:Mice; D008809:Mice, Inbred C3H; D016685:Mitomycin / Q000494:pharmacology; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*
D014028:Tobacco Smoke Pollution; D016159:Tumor Suppressor Protein p53; D016685:Mitomycin