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
- Institución
- Universidad Nacional de Rosario
- OAI Identificador
- oai:rephip.unr.edu.ar:2133/14092
Ver los metadatos del registro completo
id |
RepHipUNR_5db918bc25e4b24d519633ebd7075c4f |
---|---|
oai_identifier_str |
oai:rephip.unr.edu.ar:2133/14092 |
network_acronym_str |
RepHipUNR |
repository_id_str |
1550 |
network_name_str |
RepHipUNR (UNR) |
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 http://purl.org/coar/resource_type/c_3248 info:ar-repo/semantics/parteDeLibro |
format |
bookPart |
status_str |
acceptedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/2133/14092 urn:isbn: 978-3-642-30018-9 |
url |
http://hdl.handle.net/2133/14092 |
identifier_str_mv |
urn:isbn: 978-3-642-30018-9 |
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) https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es Licencia RepHip |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Springer |
publisher.none.fl_str_mv |
Springer |
dc.source.none.fl_str_mv |
reponame:RepHipUNR (UNR) instname:Universidad Nacional de Rosario |
reponame_str |
RepHipUNR (UNR) |
collection |
RepHipUNR (UNR) |
instname_str |
Universidad Nacional de Rosario |
repository.name.fl_str_mv |
RepHipUNR (UNR) - Universidad Nacional de Rosario |
repository.mail.fl_str_mv |
rephip@unr.edu.ar |
_version_ |
1844618779889238016 |
score |
13.070432 |