Role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning
Language English Country England, Great Britain Media print-electronic
Document type Journal Article
- Keywords
- Methanol poisoning, lipid oxidative damage, lipid peroxidation, neuroinflammation,
- MeSH
- Aldehydes blood metabolism MeSH
- Alcoholism physiopathology MeSH
- Biomarkers blood MeSH
- Cysteine Proteinase Inhibitors blood metabolism MeSH
- Middle Aged MeSH
- Humans MeSH
- Activation, Metabolic physiology MeSH
- Methanol blood poisoning MeSH
- Follow-Up Studies MeSH
- Lipid Peroxidation physiology MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- 4-hydroxy-2-hexenal MeSH Browser
- 4-hydroxy-2-nonenal MeSH Browser
- Aldehydes MeSH
- Biomarkers MeSH
- Cysteine Proteinase Inhibitors MeSH
- Methanol MeSH
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-2-hexenal (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 ± 8.0 ng/mL versus 35.4 ± 2.3 ng/mL; p < .001; HHE 40.1 ± 6.7 ng/mL versus 17.7 ± 4.1 ng/mL; p < .001; MDA 80.0 ± 7.2 ng/mL versus 40.9 ± 1.9 ng/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 (r = 0.663), LTD4 (r = 0.608), LTE4 (r = 0.771), LTB4 (r = 0.717), HHE correlated with LTC4 (r = 0.713), LTD4 (r = 0.676), LTE4 (r = 0.819), LTB4 (r = 0.746), MDA correlated with LTC4 (r = 0.785), LTD4 (r = 0.735), LTE4 (r = 0.814), LTB4 (r = 0.674); all p < .001. Lipid peroxidation markers correlated with anion gap (r= -0.428, -0.388, -0.334; p = .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.
g J Heyrovsky Institute of Physical Chemistry Czech Academy of Sciences Prague Czech Republic
i Biocev 1st Faculty of Medicine Charles University Prague Czech Republic
Toxicological Information Centre General University Hospital Prague Prague Czech Republic
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