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Published ahead of print on April 21, 2005, doi:10.1165/rcmb.2003-0341OC

Am. J. Respir. Cell Mol. Biol., Volume 33, Number 2, August 2005, 121-129

A more recent version of this article appeared on August 1, 2005
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Submitted on September 16, 2003
Revised on April 20, 2005

Cigarette Smoke Extract Induces DNA Damage but not Apoptosis in Human Bronchial Epithelial Cells

Xiangde Liu1*, Heather Conner1, Tetsu Kobayashi1, Huijung Kim2, Fuqiang Wen1, Shinji Abe1, Qiuhong Fang1, Xingqi Wang1, Mitsuyoshi Hashimoto1, Peter Bitterman3, and Stephen I Rennard1

1 Pulmonary, Critical Care and Sleep Medicine Section, Department of Internal Medicine, University of Nebraska, Omaha, NE, USA, 2 Department of Pulmonary Medicine, Seoul Adventist Hospital and WonKwang University Kunpo Medical Center, Seoul, Korea, Republic of, 3 University of Minnesota, Minneapolis, Minnesota, USA

* To whom correspondence should be addressed. E-mail: xdliu{at}unmc.edu.

Whether DNA damage caused by cigarette smoke leads to repair or apoptosis has not been fully elucidated. The current study demonstrates that cigarette smoke induces single strand DNA damage in human bronchial epithelial cells. Cigarette smoke also stimulated caspase 3 precursors as well as intact PARP production, but did not activate caspase 3 or cleave PARP, while the alkaloid camptothecin did so. Neither apoptosis nor necrosis was induced by cigarette smoke when the insult was removed within a designated time period. In contrast, DNA damage following cigarette smoke exposure was repaired as evidenced by decreasing TUNEL positivity. The PARP inhibitor, 3-aminobenzamide blocked this repair. Furthermore, cells subjected to DNA damage were able to survive and proliferate clonogenically when changed to smoke-free conditions. These results suggest that cigarette smoke-induced DNA damage in bronchial epithelial cells is not necessarily lethal, and that PARP functions in the repair process. Our data also suggest that the potency of cigarettes as a carcinogenic may result from its ability to induce DNA damage while failing to trigger the apoptotic progression permitting survival of cells harboring potentially oncogenic mutations.




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