TY - JOUR ID - 241268 TI - Bcl-2 Protein Expression in Pulmonary Specimens of Sulfur Mustard Victims JO - TANAFFOS (Respiration) JA - RSPR LA - en SN - 1735-0344 AU - Roshanzamir, Turaj AU - Mirkheshti, Nooshin AU - Ghassami, Fatemeh AU - Moghadam, Nooshin Afshar AU - Alavi, Seyed Ali AD - Department of Internal Medicine, Isfahan University of Medical Sciences AD - Hakimane-Shargh Research Institute, Isfahan AD - Department of Pathology, Isfahan University of Medical Sciences, ISFAHAN-IRAN. Y1 - 2008 PY - 2008 VL - 7 IS - 1(winter) SP - 25 EP - 31 KW - Sulfur mustard KW - Pulmonary fibrosis KW - Bcl-2 KW - Apoptosis DO - N2 - Background: Considering the role of sulfur mustard gas in development of acute and chronic pulmonary complications and the role of some genes including Bcl-2 in pulmonary fibrosis, we decided to study Bcl-2 gene expression in lung biopsy specimens of victims in comparison with normal lung. Materials and Methods: Lung biopsy specimens were taken from 13 sulfur mustard (SM) victims with pulmonary complication and were stained by Hematoxylin and Eosin (H & E) and avidin-biotin methods. We used normal lung blocks from forensic medicine as the normal group. These blocks were treated and stained with the same procedure as the case group. Both groups’ blocks were studied by a pathologist simultaneously. Results: The percentage of macrophages in sulfur mustard victims’ specimens was significantly lower than that of the control group. There was also a significant increase in lymphocytes of victims in comparison with the normal group. Neutrophil percentage and Bcl-2 protein in these cells showed no significant difference between the two groups. Bcl-2 protein in fibroblasts and epithelial cells of sulfur mustard victims was significantly higher than the control group. Conclusion: According to the results of this study in comparison with the results of patients with idiopathic pulmonary fibrosis (IPF), pulmonary fibrosis can be confirmed as one of the late complications of SM victims. According to these results, upregulation of Bcl-2 protein and subsequent alveolar epithelial cell hyperplasia and proliferation of fibroblasts may be a mechanism for pulmonary fibrosis induced by mustard gas. It could be important for developing new strategies for the treatment of fatal complications of this chemical warfare. (Tanaffos 2008; 7(1): 25-31) UR - https://www.tanaffosjournal.ir/article_241268.html L1 - https://www.tanaffosjournal.ir/article_241268_3ecb7775e7b43752cd7d865bc7516bbe.pdf ER -