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Radical oxygen species and bile secretion

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dc.citation.titleSystems biology of free radicals and antioxidantses
dc.creatorBasiglio, Cecilia Lorena
dc.creatorToledo, Flavia D.
dc.creatorSánchez Pozzi, Enrique J.
dc.creatorRoma, Marcelo Gabriel
dc.date.accessioned2019-02-22T20:44:09Z
dc.date.available2019-02-22T20:44:09Z
dc.date.issued2014-05
dc.description.abstractOxidative stress is a common feature in most hepatopathies. Accumulating evidences indicate that reactive oxygen species (ROS) induce a number of functional changes either deleterious or adaptive in the capability of the hepatocytes to produce bile and to secrete exogenous and endogenous compounds. This review is aimed to describe the mechanisms involved in these changes. For this purpose, we will summarize: 1. The current evidence that acutely induced oxidative stress is cholestatic, by describing the mechanisms underlying the hepatocyte secretory failure, including the disorganization of the actin cytoskeleton and its most noticeable consequences, that is, the impairment of tight-junctional structures and the endocytic internalization of canalicular transporters relevant to bile formation. 2. The role for oxidative-stress-activated signalling pathways in the pathomechanisms described above, particularly those involving Ca2+ elevation and its consequent activation via Ca2+ of “classical” and “novel” PKC isoforms. 3. The mechanisms involved in the adaptive response against oxidative stress mediated by ROS-responsive transcription factors, such as upregulation of GSH synthesis pathway, antioxidant enzymes, and hepatocellular efflux pumps. 4. The consequences on hepatocellular secretory function when this adaptive response can be surpassed by the sustained/high production of ROS. This deleterious effects include transcriptional and posttranscriptional changes in the expression of transporters relevant to bile formation, as has been shown to occur, for example, after long-term administration of aluminum to rats, in the Long-Evans Cinnamon rat (a model of chronic hepatic copper accumulation mimicking Wilson’s disease), and in ischemia-reperfusion injury.es
dc.description.filFil: Basiglio, Cecilia Lorena. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.es
dc.description.filFil: Toledo, Flavia D. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.es
dc.description.filFil: Sánchez Pozzi, Enrique J. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.es
dc.description.filFil: Roma, Marcelo Gabriel. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.es
dc.formatapplication/pdf
dc.format.extent1787 - 1808es
dc.identifier.isbn978-3-642-30018-9es
dc.identifier.urihttp://hdl.handle.net/2133/14092
dc.language.isoenges
dc.publisherSpringeres
dc.relation.publisherversionhttp://dx.doi.org/10.1007/978-3-642-30018-9_140es
dc.relation.publisherversionhttps://link.springer.com/referenceworkentry/10.1007%2F978-3-642-30018-9_140es
dc.rightsopenAccesses
dc.rights.holderBasiglio, Cecilia Lorenaes
dc.rights.holderToledo, Flavia D.es
dc.rights.holderSánchez Pozzi, Enrique J.es
dc.rights.holderRoma, Marcelo Gabrieles
dc.rights.holderUniversidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticases
dc.rights.holderSpringeres
dc.rights.textAtribución-NoComercial-SinDerivadas 4.0 Internacional (CC BY-NC-ND 4.0)es
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es*
dc.subjectCanalicular transporterses
dc.subjectOxidative Stresses
dc.subjectBile Secretiones
dc.subjectSignallinges
dc.subjectCholestasises
dc.subjectProtein kinaseses
dc.subjectTight junctionses
dc.titleRadical oxygen species and bile secretiones
dc.typebookPart
dc.typeparte de libro
dc.typeacceptedVersion
dc.type.collectioncapitulo_libro
dc.type.versionacceptedVersiones

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(FBIOyF) Departamento de Bioquímica Clínica - Capítulo de Libro
CIUNR - Ciencias Naturales - Capítulos de Libro