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Reestablishment of Ischemia-Reperfusion Liver Injury by N-Acetylcysteine Administration prior to a Preconditioning Iron Protocol

The role of iron (Fe)-induced prooxidant status in Fe preconditioning against ischemia (1 h)-reperfusion (20 h) induced liver injury was assessed using N-acetylcysteine (NAC) (1 g/kg) before Fe (50 mg/kg), given to male Sprague Dawley rats on alternate days during 10 days. IR significantly increased...

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Autores principales: Fernández, Virginia, Vargas, Romina, Castillo, Valentina, Cádiz, Nicolás, Bastías, Daniela, Román, Sebastián, Tapia, Gladys, Videla, Luis A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826321/
https://www.ncbi.nlm.nih.gov/pubmed/24288495
http://dx.doi.org/10.1155/2013/607285
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author Fernández, Virginia
Vargas, Romina
Castillo, Valentina
Cádiz, Nicolás
Bastías, Daniela
Román, Sebastián
Tapia, Gladys
Videla, Luis A.
author_facet Fernández, Virginia
Vargas, Romina
Castillo, Valentina
Cádiz, Nicolás
Bastías, Daniela
Román, Sebastián
Tapia, Gladys
Videla, Luis A.
author_sort Fernández, Virginia
collection PubMed
description The role of iron (Fe)-induced prooxidant status in Fe preconditioning against ischemia (1 h)-reperfusion (20 h) induced liver injury was assessed using N-acetylcysteine (NAC) (1 g/kg) before Fe (50 mg/kg), given to male Sprague Dawley rats on alternate days during 10 days. IR significantly increased serum aspartate transaminase (AST) and alanine transaminase (ALT) levels, with drastic changes in liver histology, hepatic glutathione depletion, and nuclear factor-κB (NF-κB) p65 diminution (P < 0.05) (ELISA). Fe-induced liver oxidative stress, as evidenced by higher protein carbonyl/glutathione content ratios (P < 0.05) at days 11 and 12 after treatment, was abolished by NAC. Under these conditions, short-term Fe administration exerted significant protection against IR liver injury, as shown by 85% and 60% decreases in IR-induced serum AST and ALT (P < 0.05), respectively, and normalization of hepatic histology, glutathione levels, and NF-κB activation, changes that were suppressed by NAC administration prior to Fe. Results of this study indicate that NAC administration prior to an iron protocol reestablishes IR liver injury, supporting the role of Fe-induced transient oxidative stress in hepatoprotection and its potential clinical application.
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spelling pubmed-38263212013-11-28 Reestablishment of Ischemia-Reperfusion Liver Injury by N-Acetylcysteine Administration prior to a Preconditioning Iron Protocol Fernández, Virginia Vargas, Romina Castillo, Valentina Cádiz, Nicolás Bastías, Daniela Román, Sebastián Tapia, Gladys Videla, Luis A. ScientificWorldJournal Research Article The role of iron (Fe)-induced prooxidant status in Fe preconditioning against ischemia (1 h)-reperfusion (20 h) induced liver injury was assessed using N-acetylcysteine (NAC) (1 g/kg) before Fe (50 mg/kg), given to male Sprague Dawley rats on alternate days during 10 days. IR significantly increased serum aspartate transaminase (AST) and alanine transaminase (ALT) levels, with drastic changes in liver histology, hepatic glutathione depletion, and nuclear factor-κB (NF-κB) p65 diminution (P < 0.05) (ELISA). Fe-induced liver oxidative stress, as evidenced by higher protein carbonyl/glutathione content ratios (P < 0.05) at days 11 and 12 after treatment, was abolished by NAC. Under these conditions, short-term Fe administration exerted significant protection against IR liver injury, as shown by 85% and 60% decreases in IR-induced serum AST and ALT (P < 0.05), respectively, and normalization of hepatic histology, glutathione levels, and NF-κB activation, changes that were suppressed by NAC administration prior to Fe. Results of this study indicate that NAC administration prior to an iron protocol reestablishes IR liver injury, supporting the role of Fe-induced transient oxidative stress in hepatoprotection and its potential clinical application. Hindawi Publishing Corporation 2013-10-27 /pmc/articles/PMC3826321/ /pubmed/24288495 http://dx.doi.org/10.1155/2013/607285 Text en Copyright © 2013 Virginia Fernández et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Fernández, Virginia
Vargas, Romina
Castillo, Valentina
Cádiz, Nicolás
Bastías, Daniela
Román, Sebastián
Tapia, Gladys
Videla, Luis A.
Reestablishment of Ischemia-Reperfusion Liver Injury by N-Acetylcysteine Administration prior to a Preconditioning Iron Protocol
title Reestablishment of Ischemia-Reperfusion Liver Injury by N-Acetylcysteine Administration prior to a Preconditioning Iron Protocol
title_full Reestablishment of Ischemia-Reperfusion Liver Injury by N-Acetylcysteine Administration prior to a Preconditioning Iron Protocol
title_fullStr Reestablishment of Ischemia-Reperfusion Liver Injury by N-Acetylcysteine Administration prior to a Preconditioning Iron Protocol
title_full_unstemmed Reestablishment of Ischemia-Reperfusion Liver Injury by N-Acetylcysteine Administration prior to a Preconditioning Iron Protocol
title_short Reestablishment of Ischemia-Reperfusion Liver Injury by N-Acetylcysteine Administration prior to a Preconditioning Iron Protocol
title_sort reestablishment of ischemia-reperfusion liver injury by n-acetylcysteine administration prior to a preconditioning iron protocol
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826321/
https://www.ncbi.nlm.nih.gov/pubmed/24288495
http://dx.doi.org/10.1155/2013/607285
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