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Reactive carbonyl compounds, carbonyl stress, and neuroinflammation in methyl alcohol intoxication
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SYSNO ASEP 0537139 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Reactive carbonyl compounds, carbonyl stress, and neuroinflammation in methyl alcohol intoxication Author(s) Hlušička, J. (CZ)
Löster, T. (CZ)
Lischková, L. (CZ)
Vaněčková, M. (CZ)
Diblík, P. (CZ)
Urban, P. (CZ)
Navrátil, Tomáš (UFCH-W) RID, ORCID
Kačer, P. (CZ)
Kačerová, T. (GB)
Zakharov, S. (CZ)Source Title Monatshefte fur Chemie. - : Springer - ISSN 0026-9247
Roč. 150, č. 9 (2019), s. 1723-1730Number of pages 8 s. Language eng - English Country AT - Austria Keywords acute optic neuropathy ; oxidative stress ; neurodegenerative diseases ; methanol intoxication ; traumatic injury ; damage ; brain ; outbreak ; epidemiology ; dysfunction ; Methanol ; Poisoning ; Carbonyl stress ; Markers ; Neuroinflammation Subject RIV CF - Physical ; Theoretical Chemistry OECD category Physical chemistry Method of publishing Limited access Institutional support UFCH-W - RVO:61388955 UT WOS 000482907600024 EID SCOPUS 85068894277 DOI 10.1007/s00706-019-02429-z Annotation Methyl alcohol intoxications are characterized by high lethality and high prevalence of serious visual and brain damage in survivors. The mechanisms of toxic brain damage are complex and the role of carbonyl stress has not been studied yet. We measured the acute and follow-up concentrations of reactive carbonyl compounds in patients with acute methyl alcohol intoxication. Blood samples were collected from 28 subjects hospitalized with confirmed methyl alcohol intoxication and from 36 subjects who survived poisoning 2 years after discharge. Serum concentrations of C6-12 reactive aldehydes were measured by liquid chromatography-electrospray ionization-tandem mass spectrometry. The acute concentrations of all measured reactive aldehydes were higher than the follow-up concentrations: 36.4 +/- 4.8 vs. 21.6 +/- 5.2 ng cm(-3) for C-6, 38.9 +/- 5 vs. 17.0 +/- 2.0 ng cm(-3) for C-7, 18.8 +/- 3.9 vs. 4 +/- 0 cm(-3) for C-8, 36.5 +/- 3.9 vs. 19.0 +/- 3.0 ng cm(-3) for C-9, 6.1 +/- 0.4 vs. 4.0 +/- 0.5 ng cm(-3) for C-10, 13.6 +/- 3.0 vs. 3.7 +/- 0.6 ng cm(-3) for C-11, and 7.8 +/- 0.4 vs. 4.7 +/- 0.4 ng cm(-3) for C-12 (all p < 0.001). The patients who survived the intoxication had higher concentration of reactive carbonyl compounds than those who died: 38.6 +/- 5.9 vs. 28.3 +/- 1.7 ng cm(-3) for C-6 (p = 0.002), 20.7 +/- 4.7 vs. 11.8 +/- 1.2 ng cm(-3) for C-8 (p = 0.001), 37.7 +/- 4.8 vs. 31.8 +/- 3.8 ng cm(-3) for C-9 (p = 0.042), and 7.9 +/- 0.6 vs. 7.3 +/- 0.5 ng cm(-3) for C-12 (p = 0.022). A significant association was present between severity of metabolic acidosis, anion gap, and the acute concentration of measured biomarkers: r = 0.39, p = 0.046 for C-6, r = 0.42, p = 0.035 for C-7, r = 0.48, p = 0.012 for C-8, r = 0.39, p = 0.046 for C-9, and r = 0.47, p = 0.015 for C-11. The acute concentration of C-6-C-12 reactive aldehydes positively correlated with the acute serum concentration of leukotrienes (all p < 0.05). Acute elevation of serum concentration of reactive carbonyl compounds suggests that carbonyl stress is involved in the mechanisms of leukotriene-mediated neuroinflammatory response to methyl alcohol-induced toxic brain damage. Workplace J. Heyrovsky Institute of Physical Chemistry Contact Michaela Knapová, michaela.knapova@jh-inst.cas.cz, Tel.: 266 053 196 Year of Publishing 2021 Electronic address http://hdl.handle.net/11104/0314888
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