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Accumulation of the Oxidative Base Lesion 8-Hydroxyguanine in DNA of Tumor-Prone Mice Defective in Both the Myh and Ogg1 DNA Glycosylases

¹ Department of Environment and Primary Prevention, Istituto Superiore di Sanita’, Rome, Italy; ² Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy; ³ Cancer Research UK, London Research Institute, Clare Hall Laboratories, Herts, United Kingdom; and ⁴ Department of Microbiology, Immunology and Molecular Genetics and the Molecular Biology Institute, University of California, Los Angeles, California

The OGG1 and MYH DNA glycosylases prevent the accumulation of DNA 8-hydroxyguanine. In Myh^–/– mice, there was no time-dependent accumulation of DNA 8-hydroxyguanine in brain, small intestine, lung, spleen, or kidney. Liver was an exception to this general pattern. Inactivation of both MYH and OGG1 caused an age-associated accumulation of DNA 8-hydroxyguanine in lung and small intestine. The effects of abrogated OGG1 and MYH on hepatic DNA 8-hydroxyguanine levels were additive. Because there is an increased incidence of lung and small intestine cancer in Myh^–/–/Ogg1^–/– mice, these findings support a causal role for unrepaired oxidized DNA bases in cancer development.

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