Lipid peroxidation sulfur mustard-induced

Sulfur mustard-induced lipid peroxidation is a function of glutathione (GSH) depletion. For this mechanism, depletion of GSH results in an accumulation of reactive oxygen species via hydrogen peroxide-dependent processes (Miccadei et al., 1988). The oxygen radicals react with membrane phospholipids forming lipid peroxides that alter membrane structure resulting in membrane breakdown. 

Among the most studied mechanisms of sulfur mustard toxicity are thiol depletion, resulting in intracellular calcium imbalance and subsequent cell death alkylation of DNA and other cellular macromolecules lipid peroxidation resulting from sulfur mustard-induced gluthathione depletion and induction of an inflammatory response. The overall mechanism of sulfur mustard toxicity likely involves an interlinking of the aforementioned processes which are briefly described below. 

As previously mentioned, studies51 have shown changes in membrane fluidity following sulfur mustard exposure. In addition, in 1989, Elsayed and colleagues54 demonstrated the presence of lipid peroxidation indicators in the tissue of mice exposed to subcutaneous butyl mustard. However, as with the thiol-calcium hypothesis, no studies have directly linked lipid peroxidation with the mustard-induced injury. 

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