New insights in the removal of the Hydantoins, oxidation product of pyrimidines, via the base excision and Nucleotide incision repair pathways

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Abstract

Oxidative damage to DNA, if not repaired, can be both miscoding and blocking. These genetic alterations can lead to mutations and/or cell death, which in turn cause cancer and aging. Oxidized DNA bases are substrates for two overlapping repair pathways: base excision (BER) and nucleotide incision repair (NIR). Hydantoin derivatives such as 5-hydroxyhydantoin (5OH-Hyd) and 5-methyl-5-hydroxyhydantoin (5OH-5Me-Hyd), major products of cytosine and thymine oxidative degradation pathways, respectively, have been detected in cancer cells and ancient DNA. Hydantoins are blocking lesions for DNA polymerases and excised by bacterial and yeast DNA glycosylases in the BER pathway. However little is known about repair of pyrimidine-derived hydantoins in human cells.

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Redrejo-Rodríguez, M., Saint-Pierre, C., Couve, S., Mazouzi, A., Ishchenko, A. A., Gasparutto, D., & Saparbaev, M. (2011). New insights in the removal of the Hydantoins, oxidation product of pyrimidines, via the base excision and Nucleotide incision repair pathways. PLoS ONE, 6(7). https://doi.org/10.1371/journal.pone.0021039

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