Effects of NQO1 deficiency on levels of cyclopurines and other oxidative DNA lesions in liver and kidney of young mice

International Journal of Cancer. Journal International Du Cancer
Guo-Dong ZhouAnil K Jaiswal

Abstract

I-compounds are bulky indigenous DNA adducts that can be detected by (32)P-postlabeling. A subgroup, termed type II I-compounds, represents DNA lesions induced by oxidative stress. Several major type II I-compounds have been identified as dinucleotides containing 3'-terminal 8,5'-cyclo-2'-deoxyadenosine (cA). Levels of type II I-compounds depend on the pro-oxidant status of the cell. For example, enhanced formation of such oxidative DNA lesions in newborn rodents appears to be a consequence of incomplete development of neonatal antioxidant defense systems. We tested the hypothesis that young mice deficient in NAD(P)H:quinone oxidoreductase 1 (NQO1), an antioxidant enzyme catalyzing the detoxification of quinones and their derivatives, show increased formation of these oxidative DNA lesions. Type II I-compound levels were determined by (32)P-postlabeling in liver and kidney DNA of untreated male wild-type or NQO1-null C57BL/6 mice of different ages. NQO1 catalytic activities and contents were measured by spectrophotometric and Western blotting techniques, respectively. Elevated oxidative adduct levels including those containing cA were detected in NQO1-null compared to wild-type mice at 10, 30 and 90 days in liver and at 30 and ...Continue Reading

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Citations

Feb 8, 2011·American Journal of Physiology. Lung Cellular and Molecular Physiology·Brian J LindemerMarilyn P Merker
Jul 15, 2015·DNA Repair·Irfan KhanRobert M Brosh
Mar 11, 2008·Organic & Biomolecular Chemistry·Liliana B JimenezMiguel A Miranda
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