Author/Authors :
-، - نويسنده Systems Biology Institute, Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran Imani, Saber , -، - نويسنده Systems Biology Institute, Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran Panahi, Yunes , -، - نويسنده Systems Biology Institute, Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran Salimian, Jafar , -، - نويسنده Key Laboratory of Epigenetics and Oncology, the Research Center for Preclinical Medicine, Sichuan Medical University, Luzhou, Sichuan, China Fu, Junjiang , -، - نويسنده Systems Biology Institute, Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran Ghanei, Mostafa
Abstract :
Sulfur mustard (SM, bis- (2-chloroethyl) sulphide) is a chemical warfare agent that causes DNA alkylation, protein modification and membrane damage. SM can trigger several molecular pathways involved in inflammation and oxidative stress, which cause cell necrosis and apoptosis, and loss of cells integrity and function. Epigenetic regulation of gene expression is a growing research topic and is addressed by DNA methylation, histone modification, chromatin remodeling, and noncoding RNAs expression. It seems SM can induce the epigenetic modifications that are translated into change in gene expression. Classification of epigenetic modifications long after exposure to SM would clarify its mechanism and paves a better strategy for the treatment of SM-affected patients. In this study, we review the key aberrant epigenetic modifications that have important roles in chronic obstructive pulmonary disease (COPD) and compared with mustard lung.
