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10.1074/mcp.M115.052696 http://scihub22266oqcxt.onion/10.1074/mcp.M115.052696 C4813702!4813702 !26362317     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26362317 &cmd=llinks): Failed to open stream: HTTP request failed! 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Comprehensive Assessment of Oxidatively Induced Modifications of DNA in a Rat Model of Human Wilson s Disease |pdf=|usr=}}{{26362317 }} gab.com Text Comprehensive Assessment of Oxidatively Induced Modifications of DNA in a Rat Model of Human Wilson s Disease JO: Mol Cell Proteomics http://www.kidney.de/pget.php?&tw=1&pmid=26362317 #FOAvip Defective copper excretion from hepatocytes in Wilson's disease causes accumulation of copper ions with increased generation of reactive oxygen species via the Fenton-type reaction. Here we developed a nanoflow liquid chromatography-nanoelectrospray ionization-tandem mass spectrometry coupled with the isotope-dilution method for the simultaneous quantification of oxidatively induced DNA modifications. This method enabled measurement, in microgram quantities of DNA, of four oxidative stress-induced lesions, including direct ROS-induced purine cyclonucleosides (cPus) and two exocyclic adducts induced by byproducts of lipid peroxidation, i.e. 1,N(6)-etheno-2'-deoxyadenosine (?dA) and 1,N(2)-etheno-2'-deoxyguanosine (?dG). Analysis of liver tissues of Long-Evans Cinnamon rats, which constitute an animal model of human Wilson's disease, and their healthy counterparts [i.e. Long-Evans Agouti rats] showed significantly higher levels of all four DNA lesions in Long-Evans Cinnamon than Long-Evans Agouti rats. Moreover, cPus were present at much higher levels than ?dA and ?dG lesions. In contrast, the level of 5-hydroxymethyl-2'-deoxycytidine (5-HmdC), an oxidation product of 5-methyl-2'-deoxycytidine (5-mdC), was markedly lower in the liver tissues of Long-Evans Cinnamon than Long-Evans Agouti rats, though no differences were observed for the levels of 5-mdC. In vitro biochemical assay showed that Cu(2+) ions could directly inhibit the activity of Tet enzymes. Together, these results suggest that aberrant copper accumulation may perturb genomic stability by elevating oxidatively induced DNA lesions, and by altering epigenetic pathways of gene regulation. Twit Text FOAVip Comprehensive Assessment of Oxidatively Induced Modifications of DNA in a Rat Model of Human Wilson s Disease ????Mol Cell Proteomics http://www.kidney.de/pget.php?&tw=1&pmid=26362317 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26362317 #FOAvip English Wikipedia <ref>{{Cite pmid|26362317 }}</ref> Comprehensive Assessment of Oxidatively Induced Modifications of DNA in a Rat Model of Human Wilson s Disease #MMPMID26362317 Yu Y ; Guerrero CR ; Liu S ; Amato NJ ; Sharma Y ; Gupta S ; Wang Y Mol Cell Proteomics 2016[Mar]; 15 (3 ): 810-7 PMID26362317 show ga Defective copper excretion from hepatocytes in Wilson's disease causes accumulation of copper ions with increased generation of reactive oxygen species via the Fenton-type reaction. Here we developed a nanoflow liquid chromatography-nanoelectrospray ionization-tandem mass spectrometry coupled with the isotope-dilution method for the simultaneous quantification of oxidatively induced DNA modifications. This method enabled measurement, in microgram quantities of DNA, of four oxidative stress-induced lesions, including direct ROS-induced purine cyclonucleosides (cPus) and two exocyclic adducts induced by byproducts of lipid peroxidation, i.e. 1,N(6)-etheno-2'-deoxyadenosine (?dA) and 1,N(2)-etheno-2'-deoxyguanosine (?dG). Analysis of liver tissues of Long-Evans Cinnamon rats, which constitute an animal model of human Wilson's disease, and their healthy counterparts [i.e. Long-Evans Agouti rats] showed significantly higher levels of all four DNA lesions in Long-Evans Cinnamon than Long-Evans Agouti rats. Moreover, cPus were present at much higher levels than ?dA and ?dG lesions. In contrast, the level of 5-hydroxymethyl-2'-deoxycytidine (5-HmdC), an oxidation product of 5-methyl-2'-deoxycytidine (5-mdC), was markedly lower in the liver tissues of Long-Evans Cinnamon than Long-Evans Agouti rats, though no differences were observed for the levels of 5-mdC. In vitro biochemical assay showed that Cu(2+) ions could directly inhibit the activity of Tet enzymes. Together, these results suggest that aberrant copper accumulation may perturb genomic stability by elevating oxidatively induced DNA lesions, and by altering epigenetic pathways of gene regulation. |Animals [MESH] |Chromatography, Liquid/*methods [MESH] |Copper/*metabolism [MESH] |DNA/*metabolism [MESH] |Deoxycytidine/analogs & derivatives/metabolism [MESH] |Disease Models, Animal [MESH] |Epigenesis, Genetic [MESH] |Genomic Instability [MESH] |Hepatolenticular Degeneration/*genetics/metabolism [MESH] |Humans [MESH] |Lipid Peroxidation [MESH] |Liver/metabolism [MESH] |Nanotechnology [MESH] |Oxidation-Reduction [MESH] |Rats [MESH] |Rats, Long-Evans [MESH] |Reactive Oxygen Species/metabolism [MESH]Comprehensive Assessment of Oxidatively Induced Modifications of DNA i(epmc).pdf DeepDyve Pubget Overpricing