Past Issue

Volume 12, Supplement 1,Winter 2011 (Presented at The 1st International Student Congress) Pages: 44-45

P-11: Roles of Mn- and CuZn-superoxide Dismutase in Reducing Chronic Mustard Gas Inhalation Induced Lung Toxicity

Objective: Sulfur mustard (SM), is an alkylating agent and has been emerged as a chemical weapon in various battlefields. More recently, SM was employed in the Iraq conflict against Iranian military forces and civilians. Nowadays there are more than 40,000 people suffering from pulmonary lesions special chronic obstructive pulmonary disease (COPD) due to mustard gas in Iran. SM causes the endogenous production of reactive oxygen species (ROS). Superoxide dismutases (SODs) are known as protecting antioxidants against the harmful effects of ROS. They not only serve as the primary defense of human lung against free radicals produced as part of normal metabolism, but they are also critical in protecting against the progression of oxidant-related lung. Materials and Methods: The present study was undertaken to consider the regulation of Mn- and CuZn-superoxide dismutase the human airway wall, and to suggest a probable role that HOs may play in cellular defense against oxidative stress due to SM.In this research ten unexposed SM individuals and twenty SM exposed patients were included. Evaluation of CuZnSOD and MnSOD expressions in unexposed and SM exposed patients samples was performed by semiquantitative RT-PCR, real-time RT-PCR and Immunohistochemistry analysis. Results: While unexposed SM samples expressed same levels of SODs, expression level of CuZnSOD and MnSOD was upregulated in SM exposed patients in comparison with unexposed ones, we could not find any difference in expression of SODs in two groups. In contrast, immunohistochemistry results showed negative CuZnSOD protein expression in SM injured patients. Conclusion: Our results revealed that CuZnSOD may plays an important role in cellular protection against oxidative stress due to mustard gas toxicity in airway wall of SM exposed patients at mRNA level, but translational modifications might cause decrease in the amount of CuZnSOD protein