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Epigenetic: A missing paradigm in cellular and molecular pathways of sulfur mustard lung: a prospective and comparative study.

Authors
  • Imani, Saber
  • Panahi, Yunes
  • Salimian, Jafar
  • Fu, Junjiang
  • Ghanei, Mostafa
Type
Published Article
Journal
Iranian journal of basic medical sciences
Publication Date
Aug 01, 2015
Volume
18
Issue
8
Pages
723–736
Identifiers
PMID: 26557960
Source
Medline
Keywords
License
Unknown

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.

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