Sulfur Mustard-related Ocular Complications: A Review of Proteomic Alterations and Pathways Involved

Abstract

Sulphur mustard (SM; (2, 2'-dichloroethylsulfide)) was used for the first time in 1917, during the World War I. SM mainly induces DNA damage, oxidative stress, and inflammation. This compound injures the respiratory system, eyes, skin and the endocrine, gastrointestinal, and hematopoietic systems. However, due to the high lipophilicity of the SM and the lipophilic nature of the tear film, and also due to the direct contact of the eyes with the environment, the eyes are the most vulnerable part of the body to SM. SM causes several proteomic alterations in the eye. It increases the production and activity of inflammatory proteins, reduces the concentration of antioxidant proteins and activates the proteins involved in the onset of apoptosis. In this study, we reviewed SM-related proteomic alterations and the association of the found proteins with other eye disorders and diseases. Furthermore, using pathway enrichment analysis, we found the most central biological processes involved in the emergence of complications caused by SM. Our results revealed that deficient cellular homeostasis, especially in terms of iron-dependent regulations, as well as pathological changes in vascular endothelial growth factor (VEGF) expression, is the most central biological process involved in eye injuries caused by SM.