Role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning

Kód výsledku v 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>

Nalezeny alternativní kódy

RIV/61388955:_____/18:00494639 RIV/61384399:31140/18:00051999 RIV/75010330:_____/18:00012308 RIV/00064165:_____/18:10381729

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

Role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning

Popis výsledku v původním jazyce

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&lt;.001; HHE 40.1+-6.7ng/mL versus 17.7+-4.1ng/mL; p&lt;.001; MDA 80.0+-7.2ng/mL versus 40.9+-1.9ng/mL; p&lt;.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&lt;.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.

Název v anglickém jazyce

Role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning

Popis výsledku anglicky

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&lt;.001; HHE 40.1+-6.7ng/mL versus 17.7+-4.1ng/mL; p&lt;.001; MDA 80.0+-7.2ng/mL versus 40.9+-1.9ng/mL; p&lt;.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&lt;.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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30108 - Toxicology

Projekt

<a href="/cs/project/NV16-27075A" target="_blank" >NV16-27075A: NEURODEGENERATIVNÍ PROCESY U PACIENTŮ EXPONOVANÝCH METANOLU: PROSPEKTIVNÍ STUDIE PO HROMADNÉ OTRAVĚ METANOLEM V ČESKÉ REPUBLICE V ROCE 2012</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2018

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Clinical Toxicology

ISSN

1556-3650

e-ISSN

—

Svazek periodika

56

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

893-903

Kód UT WoS článku

000449536500004

EID výsledku v databázi Scopus

2-s2.0-85044750203