Sulfur mustard depletion

Among the most studied mechanisms of sulfur mustard toxicity are thiol depletion resulting in intracellular calcium... 

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. 

Martens, M.E., Smith, W.J. (2008). The role of NAD depletion in the mechanism of sulfur mustard-induced metabolic injury. J. Toxicol. Cutan. Ocul. Toxicol. 27 41-53. 

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. 

After sulfur and nitrogen mustards are absorbed and interact with body tissues, they are no longer intact molecules. Therefore, unlike nerve gas victims, the body fluids of decontaminated mustard-exposed patients pose no risk to health care providers or other responders (2). In contrast to the other vesicants, Lewisite does not require a cyclization reaction, so its effects are immediate. Through direct inhibition of thiol-containing enzymes. Lewisite disrupts energy pathways, causing ATP depletion, cell death, and clinical effects (15). 

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