Abstract
Context: The role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning has not been studied. Objective: We measured the concentrations of lipid peroxidation markers in acutely intoxicated patients with known serum concentrations of methanol and leukotrienes.
Methods: Blood serum samples were collected from 28 patients hospitalized with acute intoxication and from 36 survivors 2 years after discharge. In these samples, concentrations of 4-hydroxy-trans-2hexenal (HHE), 4-hydroxynonenal (HNE), and malondialdehyde (MDA) were measured using the method of liquid chromatography-electrospray ionization-tandem mass spectrometry.
Results: The maximum acute serum concentrations of all three lipid oxidative damage markers were higher than the follow-up serum concentrations: HNE 71.7+-8.0ng/mL versus 35.4+-2.3ng/mL; p<.001; HHE 40.1+-6.7ng/mL versus 17.7+-4.1ng/mL; p<.001; MDA 80.0+-7.2ng/mL versus 40.9+-1.9ng/mL; p<.001. The survivors without methanol poisoning sequelae demonstrated higher acute serum concentrations of the markers than the patients with sequelae.
A correlation between measured markers and serum leukotrienes was present: HNE correlated with LTC4 (r1/40.663), LTD4 (r1/40.608), LTE4 (r1/40.771), LTB4 (r1/40.717), HHE correlated with LTC4 (r1/40.713), LTD4 (r1/40.676), LTE4 (r1/40.819), LTB4 (r1/40.746), MDA correlated with LTC4 (r1/40.785), LTD4 (r1/40.735), LTE4 (r1/40.814), LTB4 (r1/40.674); all p<.001. Lipid peroxidation markers correlated with anion gap (r1/40.428, 0.388, 0.334; p1/4.026, .045, .080 for HNE, HHE, MDA, respectively).
The follow-up serum concentrations of lipid oxidation markers measured in survivors with and without visual/neurological sequelae 2 years after discharge did not differ. Conclusion: Our results demonstrate that lipid peroxidation plays a significant role in the mechanisms of acute methanol poisoning.
The acute concentrations of three measured biomarkers were elevated in comparison with the follow-up concentrations. Neuronal membrane lipid peroxidation seems to activate leukotriene-mediated inflammation as a part of the neuroprotective mechanisms.
No cases of persistent elevation were registered among the survivors 2 years after discharge.