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Journal of Toxicology
Volume 2010, Article ID 373612, 7 pages
http://dx.doi.org/10.1155/2010/373612
Research Article

The Role of Fas-FasL Signaling Pathway in Induction of Apoptosis in Patients with Sulfur Mustard-Induced Chronic Bronchiolitis

1Chemical Injury Research Center, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran 1956837173, Iran
2Department of Biochemistry, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran 1956837173, Iran
3Clinical Research and Development Center, Shahid Modarres Hospital, Shahid Beheshti University, Tehran 1991733981, Iran
4Department of Anatomy, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran 14359151371, Iran
5National Training Program in Allergy and Asthma, University of Manitoba, Winnipeg, MB, Canada R3T 2N2
6Biotechnology Center, Faculty of Allied Medicine, Iran University of Medical Sciences, Tehran 1956837173, Iran

Received 11 October 2010; Accepted 16 December 2010

Academic Editor: Robert H. Rice

Copyright © 2010 Gila Pirzad et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Sulfur mustard (SM) is an alkylating agent that induces apoptosis and necrosis in cells. Fas-Fas ligand (FasL) interaction could induce apoptosis as well. In this study, it was hypothesized that apoptosis might play an important role in the pathogenesis of SM-induced lung injury via Fas-FasL signaling pathway. In a case-control study, Fas and FasL levels, caspase-3 activity and percent of apoptotic cells were measured in bronchoalveolar lavage (BAL) fluid of patients 20 years after exposure to sulfur mustard and compared with the control group. Results show that Fas and FasL levels were significantly higher in BAL fluid cells in patients group compared with the control ( 𝑃 = . 0 0 1 ). No significant differences were observed between mild and moderate-severe groups. BAL fluid cells caspase-3 activity was not significantly different among the mild, moderate-severe, and control groups. The data suggest that Fas-FasL-induced apoptosis was impaired in BAL fluid cells of SM-exposed patients which might be one of the initiators of pathogenesis in SM-induced lung injury in these patients.