Role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F18%3A10381729" target="_blank" >RIV/00216208:11110/18:10381729 - isvavai.cz</a>
Alternative codes found
RIV/61388955:_____/18:00494639 RIV/61384399:31140/18:00051999 RIV/75010330:_____/18:00012308 RIV/00064165:_____/18:10381729
Result on the web
<a href="https://doi.org/10.1080/15563650.2018.1455980" target="_blank" >https://doi.org/10.1080/15563650.2018.1455980</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1080/15563650.2018.1455980" target="_blank" >10.1080/15563650.2018.1455980</a>
Alternative languages
Result language
angličtina
Original language name
Role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning
Original language description
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.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30108 - Toxicology
Result continuities
Project
<a href="/en/project/NV16-27075A" target="_blank" >NV16-27075A: NEURODEGENERATIVE PROCESSES IN PATIENTS EXPOSED TO METHANOL: PROSPECTIVE STUDY AFTER CZECH MASS METHANOL POISONING OUTBREAK IN 2012</a><br>
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2018
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Clinical Toxicology
ISSN
1556-3650
e-ISSN
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Volume of the periodical
56
Issue of the periodical within the volume
10
Country of publishing house
US - UNITED STATES
Number of pages
11
Pages from-to
893-903
UT code for WoS article
000449536500004
EID of the result in the Scopus database
2-s2.0-85044750203