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Titlebook: Advances in DNA Damage and Repair; Oxygen Radical Effec Miral Dizdaroglu,Ali Esat Karakaya Book 1999 Springer Science+Business Media New Yo

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期刊全稱Advances in DNA Damage and Repair
期刊簡稱Oxygen Radical Effec
影響因子2023Miral Dizdaroglu,Ali Esat Karakaya
視頻videohttp://file.papertrans.cn/148/147647/147647.mp4
學(xué)科分類NATO Science Series A:
圖書封面Titlebook: Advances in DNA Damage and Repair; Oxygen Radical Effec Miral Dizdaroglu,Ali Esat Karakaya Book 1999 Springer Science+Business Media New Yo
影響因子Damage to DNA by both exogenous and endogenous sources isincreasingly regarded as highly important in the initiation andprogression of cancer and in the occurance of other pathologicalevents. DNA damage caused by reactive oxygen-derived species, alsocalled oxidative DNA damage, is most the frequent type encountered byaerobic cells. Mechanistic studies of carcinogenesis indicate animportant role of this type of damage to DNA. There is also strongevidence to support the role of oxidative DNA damage in the agingprocess. DNA damage is opposed .in vivo. by repair systems. If notrepaired, DNA damage may lead to detrimental biological consequences.Therefore, the repair of DNA damage is regarded as one of theessential events in all life forms. In recent years the field of DNArepair has flourished due to new findings on DNA repair mechanisms andthe molecular basis of cancer. A detailed knowledge of mechanisms ofDNA damage and repair, and how individual repair enzymes function maylead to manipulation of DNA repair in cells and ultimately to anincrease of the resistence of human cells to DNA-damaging agents. Thisvolume covers the most recent devlopments in this research field andcontains cont
Pindex Book 1999
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https://doi.org/10.1007/978-3-211-09422-8ietary antioxidant factors. In this article, assays for characterizing the potential prooxidant and antioxidant actions of food additives, antioxidant supplements, antioxidant drug molecules and nutrient components based on the assessment of products of DNA oxidation are reviewed.
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978-1-4613-7207-3Springer Science+Business Media New York 1999
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https://doi.org/10.1007/978-3-211-09422-8t ROS-modified bases with the Nth and Fpg proteins from . and then using the ligation-mediated PCR (LMPCR) technique to map induced break frequency. Damage was induced either . by exposing cultured human fibroblasts to H.O. or . by exposing purified genomic DNA to H.O. /ascorbate in the presence of
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https://doi.org/10.1007/978-3-211-09422-8ese sites are AP endonucleases, which can incise abasic residues or remove abasic deoxyribose fragments from oxidative strand breaks. We have examined the role of AP endonucleases in repair of oxidative damage caused by exogenous agents, and in limiting the spontaneous mutation rate that arises from
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