Skip Navigation



Mutagenesis Advance Access published online on July 26, 2006

Mutagenesis, doi:10.1093/mutage/gel032
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
21/4/225    most recent
gel032v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Knaapen, A. M.
Right arrow Articles by Van Schooten, F. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Knaapen, A. M.
Right arrow Articles by Van Schooten, F. J.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received May 30, 2006
Revised June 26, 2006
Accepted June 26, 2006

Review

Neutrophils and respiratory tract DNA damage and mutagenesis: a review

Ad M. Knaapen 1 *, Nejla Güngör 1, Roel P. F. Schins 2, Paul J. A. Borm 3, and Frederik J. Van Schooten 1

1 Nutrition and Toxicology Research Institute, Department of Health Risk Analysis and Toxicology, Maastricht University, Maastricht, The Netherlands
2 Institut für umweltmedizinische Forschung (IUF), Heinrich-Heine University, Düsseldorf, Germany
3 Centre of Expertise in Life Sciences, Zuyd University, Heerlen, The Netherlands

* To whom correspondence should be addressed.
Ad M. Knaapen, E-mail: a.knaapen{at}GRAT.unimaas.nl


   Abstract

Inflammation has been recognized as an important factor in cancer development. For the lung, experimental studies with rats, as well as molecular epidemiological studies in humans, have provided evidence that the influx of neutrophils into the airways may be an important process linking inflammation with carcinogenesis. Currently it is believed that the genotoxic capacity of neutrophils is a crucial aetiological factor in this carcinogenic response. In the present review we discuss two major pathways of neutrophil-induced genotoxicity: (i) induction of oxidative DNA damage through release of reactive oxygen species (ROS) and (ii) myeloperoxidase (MPO)-related metabolic activation of chemical carcinogens. So far, direct evidence for a role of neutrophils in pulmonary genotoxicity has largely been derived from in vitro studies using co-cultures of activated neutrophils and target cells. Current evidence from in vivo studies is primarily indirect and additional animal studies are needed to substantiate causality. A further challenge will be to extrapolate results from such studies to humans. Taken together, this will provide a better insight into the role of neutrophils in pulmonary carcinogenicity and may, hence, lead to novel approaches for cancer prevention strategies.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
N. J. Serkova, Z. Van Rheen, M. Tobias, J. E. Pitzer, J. E. Wilkinson, and K. A. Stringer
Utility of magnetic resonance imaging and nuclear magnetic resonance-based metabolomics for quantification of inflammatory lung injury
Am J Physiol Lung Cell Mol Physiol, July 1, 2008; 295(1): L152 - L161.
[Abstract] [Full Text] [PDF]


Home page
FASEB J.Home page
N. Gungor, R. W.L. Godschalk, D. M. Pachen, F. J. Van Schooten, and A. M. Knaapen
Activated neutrophils inhibit nucleotide excision repair in human pulmonary epithelial cells: role of myeloperoxidase
FASEB J, August 1, 2007; 21(10): 2359 - 2367.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.