5 SUMMARY Context: Acute methanol poisoning is a life-threatening condition. Methanol is metabolized in the organism to formaldehyde and than to formic acid, which inhibits cytochrome c oxidase in mitochondria and thus contributes to the development of oxidative stress. Aim: To study the role of oxidative stress in the pathogenesis of acute neuronal damage to the central nervous system (CNS), in the development of long-term sequelae of methanol poisoning and chronic neurodegenerative processes in the years following acute methanol exposure. Material and Methods: Methanol intoxication was confirmed analytically in 55 patients included in he d ; hei age a he ime f i ning a 46.7 3.6 ea (9 female and 46 male ). All a ien , together with 41 control subjects, were examined in a prospective longitudinal cohort study. At admission, during hospitalisation, and at regular intervals after discharge during the follow-up, the patients were sampled for serum concentrations of lipid oxidative damage markers 4-hydroxy-trans-2- hexenal (HHE), 4-hydroxynonenal (HNE), malondialdehyde (MDA), and 8-isoprostane, for nucleic acids oxidative damage markers 8-hydroxy-2 -deoxyguanosine (8-OHdG), 8-hydroxyguanosine (8- OHG), 5- (hydroxymethyl) uracil (5-OHMU), for proteins oxidative damage markers ortho-tyrosine (o- Tyr),...
| Identifer | oai:union.ndltd.org:nusl.cz/oai:invenio.nusl.cz:434165 |
| Date | January 2020 |
| Creators | Hlušička, Jiří |
| Contributors | Zacharov, Sergej, Lambert, Lukáš, Pohanka, Miroslav |
| Source Sets | Czech ETDs |
| Language | Czech |
| Detected Language | English |
| Type | info:eu-repo/semantics/doctoralThesis |
| Rights | info:eu-repo/semantics/restrictedAccess |
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