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Aberrant repair of etheno-DNA adducts in leukocytes and colon tissue of colon cancer patients.

Obtułowicz, Tomasz and Winczura, Alicja and Speina, Elzbieta and Swoboda, Maja and Janik, Justyna and Janowska, Beata and Cieśla, Jarosław M. and Kowalczyk, Paweł and Jawien, Arkadiusz and Gackowski, Daniel and Banaszkiewicz, Zbigniew and Krasnodebski, Ireneusz and Chaber, Andrzej and Oliński, Ryszard and Nair, Jagadesaan and Bartsch, Helmut and Douki, Thierry and Cadet, Jean and Tudek, Barbara (2010) Aberrant repair of etheno-DNA adducts in leukocytes and colon tissue of colon cancer patients. Free radical biology & medicine, 49 (6). pp. 1064-71. ISSN 1873-4596

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To assess the role of lipid peroxidation-induced DNA damage and repair in colon carcinogenesis, the excision rates and levels of 1,N(6)-etheno-2'-deoxyadenosine (epsilondA), 3,N(4)-etheno-2'-deoxycytidine (epsilondC), and 1,N(2)-etheno-2'-deoxyguanosine (1,N(2)-epsilondG) were analyzed in polymorphic blood leukocytes (PBL) and resected colon tissues of 54 colorectal carcinoma (CRC) patients and PBL of 56 healthy individuals. In PBL the excision rates of 1,N(6)-ethenoadenine (epsilonAde) and 3,N(4)-ethenocytosine (epsilonCyt), measured by the nicking of oligodeoxynucleotide duplexes with single lesions, and unexpectedly also the levels of epsilondA and 1,N(2)-epsilondG, measured by LC/MS/MS, were lower in CRC patients than in controls. In contrast the mRNA levels of repair enzymes, alkylpurine- and thymine-DNA glycosylases and abasic site endonuclease (APE1), were higher in PBL of CRC patients than in those of controls, as measured by QPCR. In the target colon tissues epsilonAde and epsilonCyt excision rates were higher, whereas the epsilondA and epsilondC levels in DNA, measured by (32)P-postlabeling, were lower in tumor than in adjacent colon tissue, although a higher mRNA level was observed only for APE1. This suggests that during the onset of carcinogenesis, etheno adduct repair in the colon seems to be under a complex transcriptional and posttranscriptional control, whereby deregulation may act as a driving force for malignancy.

Item Type:Article
Subjects:Q Science > Q Science (General)
Divisions:Department of Molecular Biology
ID Code:90
Deposited By: Dr Elżbieta Speina
Deposited On:22 Mar 2011 06:56
Last Modified:29 Sep 2015 14:58

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