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Published ahead of print on February 21, 2003, doi:10.1165/rcmb.2002-0269OC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 2, August 2003, 180-187

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Submitted on December 3, 2002
Revised on February 20, 2003

PM INDUCES AEC DNA DAMAGE AND APOPTOSIS: ROLE OF FREE RADICALS AND THE MITOCHONDRIA

Daya Upadhyay1, Vijayalakshmi Panduri1, Andrew Ghio2, and David W. Kamp3*

1 Pulmonary and Critical Care Medicine, Northwestern University Medical School, Chicago, Illinois, USA, 2 Pulmonary and Critical Care Medicine, NHEERL, EPA, Research Triangle Park, NC, USA, 3 Pulmonary and Critical Care Medicine, Northwestern University Medical School, Chicago, Illinois, USA; Department of Medicine, Veterans Administration Chicago Health Care System: Lakeside Division, Chicago, Illinois, USA

* To whom correspondence should be addressed. E-mail: d-kamp{at}northwestern.edu.

Airborne particulate matter (PM) increases morbidity and mortality resulting from cardiopulmonary diseases including cancer. We hypothesized that PM is genotoxic to AEC by causing DNA damage and apoptosis. PM caused dose-dependent AEC DNA strand break formation, reductions in mitochondrial membrane potential ({Delta}{psi}m), caspase 9 activation and apoptosis. An iron chelator and a free radical scavenger prevented these effects. Finally, overexpression of Bcl-xl, a mitochondrial anti-apoptotic protein, blocked PM-induced {Delta}{psi}m and DNA fragmentation. We conclude that PM causes AEC DNA damage and apoptosis by mechanisms that involve the mitochondria-regulated death pathway and the generation of iron-derived free radicals.




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