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Mutagenesis and Carcinogenesis Caused by the Oxidation of Nucleic Acids by Yusaku Nakabeppu; Kunihiko Sakumi; Katsumi Sakamoto; Daisuke Tsuchimoto; Teruhisa Tsuzuki; Yoshimichi Nakatsu is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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Genomes and their precursor nucleotides are highly exposed to reactive oxygen species, which are generated both as byproducts of oxygen respiration or molecular executors in the host defense, and by environmental exposure to ionizing radiation and chemicals. To counteract such oxidative damage in nucleic acids, mammalian cells are equipped with three distinct enzymes. MTH1 protein hydrolyzes oxidized purine nucleoside triphosphates, such as 8-oxo-29-deoxyguanosine triphosphate and 2-hydroxy-29-deoxyadenosine triphosphate (2-OH-dATP), to the corresponding monophosphates. We observed increased susceptibility to spontaneous carcinogenesis in MTH1-null mice, which exhibit an increased occurrence of A:TTMC:G and G:CTMT:A transversion mutations. 8-Oxoguanine (8-oxoG) DNA glycosylase, encoded by the OGG1 gene, and adenine DNA glycosylase, encoded by the MUTYH gene, are responsible for the suppression of G:C to T:A transversions caused by the accumulation of 8-oxoG in the genome. Deficiency of these enzymes leads to increased tumorigenesis in the lung and intestinal tract in mice, respectively. MUTYH deficiency may also increase G:C to T:A transversions through the misincorporation of 2-OH

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Author

Yusaku Nakabeppu; Kunihiko Sakumi; Katsumi Sakamoto; Daisuke Tsuchimoto; Teruhisa Tsuzuki; Yoshimichi Nakatsu

Publisher

Walter de Gruyter GmbH

Published

2006

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)