Abstract

Sulfur mustard (SM) is a potent alkylating agent that targets several organs, especially lung tissue. Although pathological effects of SM have been widely considered, molecular and cellular mechanisms for these pathologies are not well understood, yet. General cellular and molecular events such as inflammation, DNA damage, cell membrane disintegrity, apoptosis and cell death were observed either in in vitro or in vivo models exposed to SM. However, it is not obvious that which specific molecules and signaling pathways are relevant to the pathogenesis of mustard lung. Oxidative stress (OS) and antioxidants depletion induced by SM seem to be one of these factors. SM can trigger several molecular and cellular pathways linked to oxidative stress and inflammation that can cause cell necrosis and apoptosis as well as loss of tissue structure and function. Identification of these signaling pathways and molecules gives us valuable information regarding the toxic mechanisms of SM on injured tissues and the way for developing a better clinical approach. In this review we aimed to discuss the proposed cellular and molecular mechanisms of SM on pulmonary damage, the importance of oxidative stress and the mechanisms by which SM induces OS and antioxidants depletion along with research on antioxidant therapy as a suitable antidote.