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Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning
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SYSNO ASEP 0471295 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning Author(s) Zakharov, S. (CZ)
Kotíková, K. (CZ)
Nurieva, O. (CZ)
Hlušička, J. (CZ)
Kačer, P. (CZ)
Urban, P. (CZ)
Vaněčková, M. (CZ)
Seidl, Z. (CZ)
Diblík, P. (CZ)
Kuthan, P. (CZ)
Navrátil, Tomáš (UFCH-W) RID, ORCID
Pelclová, D. (CZ)Source Title Clinical Toxicology. - : Taylor & Francis - ISSN 1556-3650
Roč. 55, č. 4 (2017), s. 249-259Number of pages 11 s. Language eng - English Country US - United States Keywords brain damage ; leukotrienes ; methanol poisoning ; Neuroinflammation ; nontraumatic brain injury ; sequelae of poisoning Subject RIV CG - Electrochemistry OECD category Electrochemistry (dry cells, batteries, fuel cells, corrosion metals, electrolysis) Institutional support UFCH-W - RVO:61388955 UT WOS 000394936500003 EID SCOPUS 85011685025 DOI 10.1080/15563650.2017.1284332 Annotation 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< 0.001). The patients who survived had higher LT concentrations than those who died (all p< 0.01). Among survivors, patients with CNS sequelae had lower LTE4 and LTB4 than did those without sequelae ( both p< 0.05). The LT concentrations increased at a rate of 0.4-0.5 pg/mL/h and peaked 4-5 days after admission. The patients with better outcomes had higher cys-LTs (all p< 0.01) and LTB4 (p< 0.05). More severely poisoned patients had lower acute LT concentrations than those with minor acidemia. The follow-up LT concentrations in survivors with and without CNS sequelae did not differ (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.Workplace J. Heyrovsky Institute of Physical Chemistry Contact Michaela Knapová, michaela.knapova@jh-inst.cas.cz, Tel.: 266 053 196 Year of Publishing 2018
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