Oxidative DNA damage and repair in thyroid gland
Journal Title: Postępy Nauk Medycznych - Year 2011, Vol 24, Issue 11
Abstract
Reactive oxygen species (ROS) are formed as a consequence of cell metabolism but can also get into cells from external sources. Hydrogen peroxide (H2O2), singlet oxygen (1O2) and hydroxyl radical (•OH) are produced in many physiological processes such as respiration in the mitochondria and oxidation in the peroxisomes. In thyroid H2O2 participate in hormone synthesis. ROS induce DNA damages that are implied in mutagenesis, tumorigenesis and other human diseases. Among these DNA lesions 8-oxoG is one of the most mutagenic. The main pathway to repair 8-oxoG and other oxidized bases is base excision repair (BER). The efficiency of BER when it comes to eliminating oxidative DNA lesions may be a risk factor for thyroid cancer and other diseases development. Molecular mechanisms responsible for impaired DNA repair have been widely studied and include polymorphisms of repair genes, their transcriptional activation/down-regulation, post-translational modifications and possibly other factors. The data presented here and literature reports demonstrate that increased oxidative stress, DNA damage and somatic mutation rates are contributing factors to the development of thyroid cancers. Moreover, alterations in DNA repair mechanisms, including polymorphisms of repair genes (OGG1, APE1 and XRCC1) may be linked to the risk of thyroid malignant transformation.
Authors and Affiliations
Justyna Janik, Barbara Czarnocka
Keywords
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