Markers of nucleic acids and proteins oxidative damage in acute methanol poisoning
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The aim of the study is to measure serum concentrations of markers of nucleic acids and proteins oxidative damage in humans to study the dynamics and clinical determinants of oxidative stress caused by acute methanol poisoning. Acute blood serum samples for this study were collected from 28 patients with methanol poisoning and the follow-up samples from 36 survivors of poisoning were collected 2 years after discharge. Serum concentrations of 8-hydroxy-2′-deoxyguanosine (8-OHdG), 8-hydroxyguanosine (8-OHG), 5-(hydroxymethyl)uracil (5-OHMU), ortho-tyrosine (o-Tyr), nitrotyrosine (NO-Tyr), and chlorotyrosine (Cl-Tyr) were measured by liquid chromatography-electrospray ionisation-tandem mass spectrometry. Acute concentrations of 8-OHdG and o-Tyr were significantly higher than the follow-up concentrations (94.4 ± 6.2 versus 78.0 ± 10.0 pg cm−3; p = 0.009 and 163.0 ± 11.0 versus 124.0 ± 17.0 pg cm−3; p < 0.001, correspondingly). Survivors of methanol poisoning had higher acute 8-OHdG and 8-OHG concentrations than those who died (97.3 ± 7.4 versus 50.0 ± 23.0 pg cm−3; p < 0.001 and 97.9 ± 7.2 versus 83.7 ± 6.7 pg cm−3; p = 0.047). Acute concentrations of 8-OHdG, 8-OHG, 5-OHMU, and o-Tyr were higher in the patients who survived without health sequelae than in those who survived with visual and CNS sequelae (all p < 0.05). Acute concentrations of markers of proteins and nucleic acids damage correlated with laboratory parameters of acidemia (anion gap) and serum ethanol concentration on admission (both p < 0.05). Acute elevation of the concentration of markers of nucleic acids and proteins oxidative damage in the patients with methanol poisoning suggest that mild-to-moderate oxidative stress may play an important role in the non-specific mechanisms of brain protection against direct neurotoxic effects of formic acid.
KeywordsOxidative stress Oxidation Alcohols Biomarkers Nucleic acids Proteins
Supported in part by: (1) Ministry of Health of the Czech Republic, Czech Health Research Council (AZV), Grant no. 16-27075A; (2) Ministry of the Health of the Czech Republic, the Project 44/18/D; (3) First Faculty of Medicine, Charles University, Projects PROGRES Q25 and Q29. No funding organizations had a role in the design or conduct of this research.
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