Formation of chlorinated lipids post-chlorine gas exposure

Myeloperoxidase-derived 2-chlorofatty acids contribute to human sepsis mortality via acute respiratory distress syndrome

“…2-ClFA has been shown to be present as a relatively stable chlorinated lipid produced as a result of inflammation, including endotoxemia and Sendai virus exposure (35,36). Additionally, lung 2-ClFA is elevated in mice exposed to chlorine gas, and intranasal administration of 2-ClFA resulted in increased protein and macrophage levels in bronchoalveolar fluid (47). The reported results demonstrate for the first time to our knowledge that systemic levels of 2-ClFA in sequential septic patients are associated with risk for ARDS and 30-day mortality.…”

Bromofatty aldehyde derived from bromine exposure and myeloperoxidase and eosinophil peroxidase modify GSH and protein

“…MPO-derived α-ClFALD has also been implicated in endothelial dysfunction (7), neuronal apoptosis (8), activating the nuclear factor κB pathway, eNOS inhibition (9), neutrophil chemotaxis (3), and myocardial contractile dysfunction (6). Recently, α-ClFALD was also found in the lungs of mice and rats exposed to chlorine gas (Cl 2 ) along with its GSH adduct (FALD-GSH) and it was found to contribute to increased lung inflammation and permeability as well as systemic loss of eNOS-dependent vasodilation (10).…”

“…Inhalation of chlorine and bromine gas has been shown to elicit severe systemic physiological effects including cardiac dysfunction and vasoregulatory dysfunction (10,27,28). Bromine gas has many industrial applications, and is collapse (29,30).…”

“…Lung and plasma of Br 2 exposed mice were analyzed for FALD-GSH as previously described (19 Extraction and Quantification of α-BrFALD: α-BrFALD was extracted from Br 2 exposed mice as was previously described for α-ClFALD extraction from Cl 2 exposed mice (19). Briefly, 10 mg of frozen, GC-MS as previously described (11).…”

Peroxisome proliferator-activated receptor-α accelerates α-chlorofatty acid catabolism

“…In endotoxemia models of inflammation, systemic plasma levels of -ClFA rise from 1 nM (naïve rats) to 3 nM (LPS treated) (18). Systemic plasma levels of -ClFA were recently shown to reach levels above 100 nM in mice subjected to a sublethal exposure of chlorine gas (38). It is likely that plasma levels of -ClFA may be even higher in mice subjected to higher exposure levels of chlorine gas.…”