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Oxidative damage occurs in all living organisms from reactive oxygen species (ROS), which are a consequence of normal body processes such as metabolism. ROS react with proteins, resulting in protein modification, such as introduction of carbonyl groups into the protein. The modified proteins are dysfunctional and can be removed through degradation. Both mitochondrial DNA and nuclear DNA are constantly exposed to oxygen radicals, causing extensive oxidative damage. DNA damage by ROS has significant consequences since it causes mutations and genomic instability. Studies have shown that oxidative DNA damage accumulates with aging. Oxidative DNA damage has been implicated to be important in many diseases, including cancer.1 Assessment of this damage in various biological matrices is essential for understanding the mechanisms of oxidative damage and its biological effects. Over the past decades, many analytical techniques, such as LC- |
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1
Cooke, M.S., Evans, M.D., Dizdaroglu, M., et al. Oxidative DNA damage: Mechanisms, mutation, and disease. FASEB J 17 1195-
2
Nakamura, J., Walker, V.E., Upton, P.B., et al. Highly sensitive apurinic/apyrimidinic site assay can detect spontaneous and chemically induced depurination under physiological conditions. Cancer Res 58 222-
3
Poulsen, H.E., Weimann, A., Loft, S. Methods to detect DNA damage by free radicals: Relation to excercise. Proc Nutr Soc 58 1007-
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Elbling, L., Weiss, R., Teufelhofer, O., et al. Green tea extract and (−)-
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Tachibana, H. Molecular basis for cancer chemoprevention by green tea polyphenol EGCG. Forum Nutr 61 156-
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![]() | Download Kit Booklet 798 Kb PDF |
![]() | Download Material Safety Data Sheet (MSDS) 86 Kb PDF |
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