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Role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning
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SYSNO ASEP 0494639 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning Author(s) Hlušička, J. (CZ)
Löster, T. (CZ)
Lischková, L. (CZ)
Vaněčková, M. (CZ)
Seidl, Z. (CZ)
Diblík, P. (CZ)
Kuthan, P. (CZ)
Urban, P. (CZ)
Navrátil, Tomáš (UFCH-W) RID, ORCID
Kačer, P. (CZ)
Zakharov, S. (CZ)Source Title Clinical Toxicology. - : Taylor & Francis - ISSN 1556-3650
Roč. 56, č. 10 (2018), s. 893-903Number of pages 11 s. Language eng - English Country US - United States Keywords methanol poisoning ; lipid peroxidation ; neuroinflammation Subject RIV CF - Physical ; Theoretical Chemistry OECD category Physical chemistry Institutional support UFCH-W - RVO:61388955 UT WOS 000449536500004 EID SCOPUS 85044750203 DOI 10.1080/15563650.2018.1455980 Annotation 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.Workplace J. Heyrovsky Institute of Physical Chemistry Contact Michaela Knapová, michaela.knapova@jh-inst.cas.cz, Tel.: 266 053 196 Year of Publishing 2019
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