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Epigenetic alterations can accompany DNA repair of oxidative damage or double-strand breaks. In human cells, oxidative DNA damage occurs about 10,000 times a day and DNA double-strand breaks occur about 10 to 50 times a cell cycle in somatic replicating cells (see DNA damage (naturally occurring)). The selective advantage of DNA repair is to ...
DNA oxidation is the process of oxidative damage of deoxyribonucleic acid.As described in detail by Burrows et al., [1] 8-oxo-2'-deoxyguanosine (8-oxo-dG) is the most common oxidative lesion observed in duplex DNA because guanine has a lower one-electron reduction potential than the other nucleosides in DNA.
More than 100 types of oxidative DNA damage have been characterized, and 8-oxodG constitutes about 5% of the steady state oxidative damages in DNA. [18] Helbock et al. [ 14 ] estimated that there were 24,000 steady state oxidative DNA adducts per cell in young rats and 66,000 adducts per cell in old rats.
RAD51 plays a major role in homologous recombinational repair of DNA during double strand break repair. In this process, an ATP dependent DNA strand exchange takes place in which a template strand invades base-paired strands of homologous DNA molecules. RAD51 is involved in the search for homology and strand pairing stages of the process.
Oxidative stress mechanisms in tissue injury. Free radical toxicity induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).. Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. [1]
XthA (exonuclease III, a DNA repair enzyme) and KatE (catalase) are known to play important roles in the defense against oxidative stress but KatF regulon genes are not induced by oxidative stress. [2] There is an overlap between oxidative stress response and other regulatory networks like heat shock response, SOS response.
Other DNA damaging, cancer-causing agents include asbestos, which can cause damage through physical interaction with DNA or by indirectly setting off a reactive oxygen species, [10] excessive nickel exposure, which can repress the DNA damage-repair pathways, [11] aflatoxins, which are found in food, [9] and many more.
Steady-state levels of DNA damages represent the balance between formation and repair. Swenberg et al. [3] measured average frequencies of steady state endogenous DNA damages in mammalian cells. The most frequent oxidative DNA damage normally present in DNA is 8-oxo-dG, occurring at an average frequency of 2,400 per cell.