Non-alcoholic fatty liver disease is the most common chronic liver disease in the developed world, which, together with the obesity epidemic, has become increasingly common in the adolescent population and is becoming the leading cause of liver failure in children and adolescents in the Western world. The onset and progression of the disease is influenced by numerous factors, the most important of which are metabolic disorders, unhealthy lifestyle, oxidative stress and genetic predisposition. Most of the research to date has been conducted on adults, therefore data on the adolescent population is limited. The polymorphism rs4880 in the SOD2 gene has been associated in literature with altered antioxidant capacity of cells, while the polymorphism rs641738 in the MBOAT7 gene has been associated with disorders in lipid metabolism and is an increased factor for the development of liver diseases. The purpose of the Master's thesis was to investigate its association with markers of oxidative status and the incidence of the disease in adolescents. Genomic DNA was isolated from the whole blood of 200 adolescents and genotyping was performed by real-time polymerase chain reaction using hydrolyzing probes. In addition to genetic data, we also analyzed markers of oxidative status, including markers of oxidative defense, overall redox balance, and oxidative damage to biomolecules, and took into account important demographic data. When calculated, the values of total antioxidant capacity (p=0,001), total oxidative capacity (p<0,001), advanced protein oxidation products (p<0,001), paraoxonase 1 (p=0,003) and sulfhydryl groups (p<0,001) were significantly higher compared to the control group, while the values of the ratio between total antioxidant and oxidative capacity (p<0,001) and prooxidant-antioxidant balance (p=0,015) were significantly reduced. Genetic analysis of SOD2 rs4880 did not show statistically significant associations with markers of oxidative status. In MBOAT7 rs641738, however, differences were mostly absent, with the exception of sulfhydryl group values in the additive model (p=0,048) and dominant model (p=0,025), with T allele carriers having lower values compared to other genotypes. In the control group, statistically significant lower values of ischemically modified albumin were found in individuals with the T/T genotype (p=0,043) compared to other genotypes in the recessive model, but this difference was not repeated in the patient group. Logistic regression did not confirm the independent predictive value of oxidative status markers for the disease. The findings indicate an altered oxidative status in adolescents with the disease, while the studied polymorphisms do not show a significant independent effect on the studied markers. The research contributes to a better understanding of the role of oxidative stress and genetic influences in disease in a population of adolescents aged 16 to 19 years, and highlights the need for further research in larger and age-specific populations due to the limited comparable literature in adolescents.
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