Radical oxygen species and bile secretion

Autores
Basiglio, Cecilia Lorena; Toledo, Flavia D.; Sánchez Pozzi, Enrique J.; Roma, Marcelo Gabriel
Año de publicación
2014
Idioma
inglés
Tipo de recurso
parte de libro
Estado
versión aceptada
Descripción
Oxidative 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.
Fil: Fil: Basiglio, Cecilia Lorena. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.
Fil: Fil: Toledo, Flavia D. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.
Fil: Fil: Sánchez Pozzi, Enrique J. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.
Fil: Fil: Roma, Marcelo Gabriel. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.
Materia
Canalicular transporters
Oxidative Stress
Bile Secretion
Signalling
Cholestasis
Protein kinases
Tight junctions
Nivel de accesibilidad
acceso abierto
Condiciones de uso
Atribución-NoComercial-SinDerivadas 4.0 Internacional (CC BY-NC-ND 4.0)
Repositorio
RepHipUNR (UNR)
Institución
Universidad Nacional de Rosario
OAI Identificador
oai:rephip.unr.edu.ar:2133/14092

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spelling Radical oxygen species and bile secretionBasiglio, Cecilia LorenaToledo, Flavia D.Sánchez Pozzi, Enrique J.Roma, Marcelo GabrielCanalicular transportersOxidative StressBile SecretionSignallingCholestasisProtein kinasesTight junctionsOxidative 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.Fil: Fil: Basiglio, Cecilia Lorena. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.Fil: Fil: Toledo, Flavia D. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.Fil: Fil: Sánchez Pozzi, Enrique J. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.Fil: Fil: Roma, Marcelo Gabriel. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.Springer2014-05info:eu-repo/semantics/bookPartinfo:eu-repo/semantics/acceptedVersionhttp://purl.org/coar/resource_type/c_3248info:ar-repo/semantics/parteDeLibroapplication/pdfhttp://hdl.handle.net/2133/14092urn:isbn: 978-3-642-30018-9enghttp://dx.doi.org/10.1007/978-3-642-30018-9_140https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-30018-9_140info:eu-repo/semantics/openAccessAtribución-NoComercial-SinDerivadas 4.0 Internacional (CC BY-NC-ND 4.0)https://creativecommons.org/licenses/by-nc-nd/4.0/deed.esLicencia RepHipreponame:RepHipUNR (UNR)instname:Universidad Nacional de Rosario2025-09-29T13:41:07Zoai:rephip.unr.edu.ar:2133/14092instacron:UNRInstitucionalhttps://rephip.unr.edu.ar/Universidad públicaNo correspondehttps://rephip.unr.edu.ar/oai/requestrephip@unr.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:15502025-09-29 13:41:08.027RepHipUNR (UNR) - Universidad Nacional de Rosariofalse
dc.title.none.fl_str_mv Radical oxygen species and bile secretion
title Radical oxygen species and bile secretion
spellingShingle Radical oxygen species and bile secretion
Basiglio, Cecilia Lorena
Canalicular transporters
Oxidative Stress
Bile Secretion
Signalling
Cholestasis
Protein kinases
Tight junctions
title_short Radical oxygen species and bile secretion
title_full Radical oxygen species and bile secretion
title_fullStr Radical oxygen species and bile secretion
title_full_unstemmed Radical oxygen species and bile secretion
title_sort Radical oxygen species and bile secretion
dc.creator.none.fl_str_mv Basiglio, Cecilia Lorena
Toledo, Flavia D.
Sánchez Pozzi, Enrique J.
Roma, Marcelo Gabriel
author Basiglio, Cecilia Lorena
author_facet Basiglio, Cecilia Lorena
Toledo, Flavia D.
Sánchez Pozzi, Enrique J.
Roma, Marcelo Gabriel
author_role author
author2 Toledo, Flavia D.
Sánchez Pozzi, Enrique J.
Roma, Marcelo Gabriel
author2_role author
author
author
dc.subject.none.fl_str_mv Canalicular transporters
Oxidative Stress
Bile Secretion
Signalling
Cholestasis
Protein kinases
Tight junctions
topic Canalicular transporters
Oxidative Stress
Bile Secretion
Signalling
Cholestasis
Protein kinases
Tight junctions
dc.description.none.fl_txt_mv Oxidative 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.
Fil: Fil: Basiglio, Cecilia Lorena. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.
Fil: Fil: Toledo, Flavia D. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.
Fil: Fil: Sánchez Pozzi, Enrique J. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.
Fil: Fil: Roma, Marcelo Gabriel. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental (IFISE‑CONICET); Argentina.
description Oxidative 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.
publishDate 2014
dc.date.none.fl_str_mv 2014-05
dc.type.none.fl_str_mv info:eu-repo/semantics/bookPart


info:eu-repo/semantics/acceptedVersion
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urn:isbn: 978-3-642-30018-9
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dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv http://dx.doi.org/10.1007/978-3-642-30018-9_140
https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-30018-9_140
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
Atribución-NoComercial-SinDerivadas 4.0 Internacional (CC BY-NC-ND 4.0)
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
Licencia RepHip
eu_rights_str_mv openAccess
rights_invalid_str_mv Atribución-NoComercial-SinDerivadas 4.0 Internacional (CC BY-NC-ND 4.0)
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Licencia RepHip
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Springer
publisher.none.fl_str_mv Springer
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instname:Universidad Nacional de Rosario
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