Plasma proteomic profile of sulfur mustard exposed lung diseases patients using 2-dimensional gel electrophoresis

Prior to analysis, plasma was fractionated using ethanol precipitation. Using two dimensional SDS-PAGE; fractionated protein profiles of 20 healthy and 20 exposed patients with lung diseases were established. Selected protein spots were successfully identified with MALDI TOF MS/MS.The results show that α1 haptoglobin isoforms were detected in plasma of the all lung disease patients but none of the healthy controls. Amyloid A1 isoforms was also detected in plasma of the lung disease patients but none of the healthy controls. Moreover, low molecular weight proteins were enriched in ethanol supernatant compared to ethanol precipitate.Our present results and previous studies suggest that ongoing tissue remodeling is involved in SM exposed lung damage patients. These finding might improve patient care and suitable therapies.Sulfur mustard is a chemical warfare agent that remains a threat to human health.. More than lethality, SM causes debilitating effects that can leave an exposed individual incapacitated for days, months, or years. Lung injury is a common health problem after inhalation, which leads to chronic bronchitis and interstitial lung diseases [1]. The clinical picture of the poisoning is well known from the thousands of victims during World War I and the recent Iran-Iraq conflict. In the latter, sulfur mustard was heavily used and at the present time about 30,000 victims still suffer from late effects of the agent, such as chronic obstructive lung disease, lung fibrosis, recurrent corneal ulcer disease, and chronic conjunctivitis [2]. Late complications of mustard gas exposure and main clinical findings include; chronic bronchitis, bronchiectasis and bronchiolitis obliterans (BO) [3-5]. However, Clinical manifestation in lung disorders due to sulfur mustard is different from other lung diseases, due to the fact that mustard lung is not responsive to corticosteroids. There is no common consensus about the pathophysiological basis of chronic pulmonary disease ca