@phdthesis{Schniertshauer2020Influ-51425,
  year={2020},
  title={Influence of ubiquinol/ubiquinone on energy metabolism and DNA repair enzyme hOGG1 in mitochondria of human skin fibroblasts},
  author={Schniertshauer, Daniel},
  address={Konstanz},
  school={Universität Konstanz}
}

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    <dcterms:issued>2020</dcterms:issued>
    <dc:contributor>Schniertshauer, Daniel</dc:contributor>
    <dcterms:title>Influence of ubiquinol/ubiquinone on energy metabolism and DNA repair enzyme hOGG1 in mitochondria of human skin fibroblasts</dcterms:title>
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    <dcterms:abstract xml:lang="eng">Human skin is continuously exposed to a number of harmful substances, of which the ultraviolet portion of solar radiation is the most significant. UV-induced damage includes direct DNA lesions and oxidative damage to DNA, proteins and lipids caused by reactive oxygen species. Approximately 1.000 - 1.0x105 oxidative lesions occur daily in the cell, with one of the most common defects in this category being 7,8-dihydro-8-oxoguanine. Because of their role in oxidative phosphorylation and because mitochondria are the main site of production of reactive oxygen species in the cell, these organelles are particularly affected. Here, the above-mentioned exogenous influences can lead to an accumulation of reactive oxygen species as well as 7,8-dihydro-8-oxoguanine, which can ultimately lead to functional disorders within the electron transport chain and finally to mitochondrial dysfunctions. To counteract the accumulation of oxidative damage and the formation of reactive oxygen species, coenzyme Q10 has been used for some time. Its redox-reactive character and its central role in the electron transport chain is the reason why this coenzyme is used in mitochondrial medicine for the treatment of age-related diseases. However, since the exact mechanisms of action are still unclear in many aspects, this work deals with the influence of coenzyme Q10 on the energy metabolism after short-term induced damage via UV irradiation, long-term induced damage (age-related) as well as on DNA repair in human fibroblasts. For this purpose, we analysed several mitochondrial parameters, including respiration, membrane potential and ATP levels in skin fibroblasts after UV irradiation. After treatment of the cells with coenzyme Q10, an accelerated regeneration of the ATP level, a preservation of the membrane potential and thus a decrease in mitochondrial dysfunction was observed. In addition to short-term induced damage such as that caused by UV radiation, the effect of coenzyme Q10 on age- and long-term induced damage was also investigated. Thus, for the first time ex vivo in the human epidermis, a decrease in mitochondrial respiration as well as ATP production could be shown with the age of the donor, which corresponds to the "mitochondrial theory of ageing". This decrease could be mitigated by coenzyme Q10. Finally, attention was focused on human 8-oxoguanine DNA glycosylase 1, the repair enzyme for 7,8-dihydro-8-oxoguanine, under the influence of coenzyme Q10. For the first time, a concentration-dependent increase in activity, a change in bifunctionality in XIV favor of increased N-glycosylase activity by coenzyme Q10 and a direct interaction between 8-oxoguanine DNA glycosylase 1 and this coenzyme could be shown. The results of this work suggest that the achieved effects of coenzyme Q10 on mitochondrial function are mediated primarily by its antioxidant function and by increased activity of the electron transport chain. In particular, the preservation of the mitochondrial membrane potential seems to be of great importance. An increase in the activity of 8-oxoguanine DNA glycosylase 1 is probably due to the fact that coenzyme Q10 contributes to the dissolution of an end product complex which is formed between the repair enzyme and the resulting unsaturated hydroxyl aldehyde at the 3' end and thus inhibits further enzymatic steps. Based on this work, further interesting starting points for the use of coenzyme Q10 as a drug for both preventive and acute treatment of numerous age-related diseases in the field of mitochondrial medicine have been identified.</dcterms:abstract>
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    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-10-20T13:44:49Z</dc:date>
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