Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning
Abstrakt
Context: The role of neuroinflammation in methanol- induced toxic brain damage has not been studied. Objective: We studied acute concentrations and the dynamics of leukotrienes (LT) in serum in hospitalized patients with acute methanol poisoning and in survivors.
Methods: Series of acute cysteinyl-LT and LTB4 concentration measurements were performed in 28/101 hospitalized patients (mean observation time: 88 +/- 20 h). In 36 survivors, control LT measurements were performed 2 years after discharge.
Results: The acute maximum (C-max) LT concentrations were higher than concentrations in survivors: C-max for LTC4 was 80.7 +/- 5.6 versus 47.9 +/- 4.5 pg/mL; for LTD4, 51.0 +/- 6.6 versus 23.1 +/- 2.1 pg/mL; for LTE4, 64.2 +/- 6.0 versus 26.2 +/- 3.9 pg/mL; for LTB4, 59.8 +/- 6.2 versus 27.2 +/- 1.4 pg/mL (all p 0.05). The mean decrease in LT concentration was 30.9 +/- 9.0 pg/mL for LTC4, 26.3 +/- 8.6 pg/ mL for LTD4, 37.3 +/- 6.4 pg/mL for LTE4, and 32.0 +/- 8.8 pg/mL for LTB4.
Conclusions: Our findings suggest that leukotriene- mediated neuroinflammation may play an important role in the mechanisms of toxic brain damage in acute methanol poisoning in humans. Acute elevation of LT concentrations was moderate, transitory, and was not followed by chronic neuroinflammation in survivors.