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dc.rights.licensehttp://creativecommons.org/licenses/by/4.0es_MX
dc.creatorGLORIA CRISTINA ENRIQUEZ CORTINAes_MX
dc.creatorOSCAR BELLO MONROYes_MX
dc.creatorDIANA PATRICIA ROSALES CRUZes_MX
dc.creatorVERONICA SOUZA ARROYOes_MX
dc.creatorROXANA URI MIRANDA LABRAes_MX
dc.creatorRAFAEL TOLEDO PEREZes_MX
dc.creatorARMANDO LUNA LOPEZes_MX
dc.creatorARTURO SIMONI NIEVESes_MX
dc.creatorROGELIO ENRIQUE HERNANDEZ PANDOes_MX
dc.creatorMARIA CONCEPCION GUTIERREZ RUIZes_MX
dc.creatorDiego Francesco CALVISIes_MX
dc.creatorJens Marquardtes_MX
dc.creatorLETICIA BUCIO ORTIZes_MX
dc.creatorLUIS ENRIQUE GOMEZ QUIROZes_MX
dc.date2017-
dc.date.accessioned2021-09-20T17:57:48Z-
dc.date.available2021-09-20T17:57:48Z-
dc.identifier.urihttp://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17247-
dc.descriptionPrimary liver cancers represent the second leading cause of cancer-related deaths worldwide. Diverse etiological factors include chronic viral hepatitis, aflatoxin and alcohol exposure as well as aberrant liver lipid overload. Cholesterol has been identified as a key inducer of metabolic impairment, oxidative stress and promoter of cellular dysfunction. The aim of this work was to address the oxidative stress-mediated DNA damage induced by cholesterol overload, and its role in the development of hepatocellular carcinoma. C57BL/6 male mice were fed with a high cholesterol diet, followed by a single dose of N-diethylnitrosamine (DEN, 10 μg/g, ip). Reactive oxygen species generation, DNA oxidation, antioxidant and DNA repair proteins were analyzed at different time points. Diet-induced cholesterol overload caused enhanced oxidative DNA damage in the liver and was associated with a decrease in key DNA repair genes as early as 7 days. Interestingly, we found a cell survival response, induced by cholesterol, judged by a decrement in Bax to Bcl2 ratio. Importantly, N-acetyl-cysteine supplementation significantly prevented DNA oxidation damage. Furthermore, at 8 months after DEN administration, tumor growth was significantly enhanced in mice under cholesterol diet in comparison to control animals. Together, these results suggest that cholesterol overload exerts an oxidative stress-mediated effects and promotes the development of liver cancer.es_MX
dc.formatAdobe PDFes_MX
dc.languageenges_MX
dc.publisherImpact Journalses_MX
dc.relationhttps://www.oncotarget.com/article/22024/#R10es_MX
dc.relation.requiresSies_MX
dc.rightsAcceso Abiertoes_MX
dc.sourceOncotarget (1949-2553) vol. 8 (2017)es_MX
dc.subjectMEDICINA Y CIENCIAS DE LA SALUDes_MX
dc.subjectCiencias médicases_MX
dc.subjectCiencias clínicases_MX
dc.subjectColesteroles_MX
dc.subjectCholesteroles_MX
dc.subjectEstrés oxidativoes_MX
dc.subjectOxidative Stresses_MX
dc.subjectDaño de ADNes_MX
dc.subjectDNA Damagees_MX
dc.subjectCarcinogenesises_MX
dc.subjectCáncer de hígadoes_MX
dc.subjectLiver Neoplasmses_MX
dc.titleCholesterol overload in the liver aggravates oxidative stress-mediated DNA damage and accelerates hepatocarcinogenesises_MX
dc.typeArtículoes_MX
dc.audienceResearcherses_MX
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