Show item record

dc.contributor.authorBosoi, Cristina R.
dc.contributor.authorYang, Xiaoling
dc.contributor.authorHuynh, Jimmy
dc.contributor.authorParent-Robitaille, Christian
dc.contributor.authorJiang, Wenlei
dc.contributor.authorTremblay, Mélanie
dc.contributor.authorRose, Christopher
dc.date.accessioned2013-04-28T21:24:31Z
dc.date.available2013-04-28T21:24:31Z
dc.date.issued2012-04
dc.identifier.urihttp://hdl.handle.net/1866/9595
dc.description.sponsorshipCIHR- MOP-82839en
dc.subjectAllopurinolen
dc.subjectBile-duct ligationen
dc.subjectEncéphalopathie hépatiqueen
dc.subjectEspèces réactives de l'oxygèneen
dc.subjectHepatic encephalopathyen
dc.subjectHyperammonemiaen
dc.subjectHyperammoniémieen
dc.subjectPortacaval anastomosisen
dc.subjectReactive oxygen speciesen
dc.titleSystemic oxidative stress is implicated in the pathogenesis of brain edema in rats with chronic liver failure
dc.typeArticleen
dc.contributor.affiliationUniversité de Montréal. Faculté de médecinefr
dc.contributor.affiliationUniversité de Montréal. Faculté de médecine. Centre de recherche du CHUMfr
dc.identifier.doi10.1016/j.freeradbiomed.2012.01.006
dcterms.abstractChronic liver failure leads to hyperammonemia, a central component in the pathogenesis of hepatic encephalopathy (HE); however, a correlation between blood ammonia levels and HE severity remains controversial. It is believed oxidative stress plays a role in modulating the effects of hyperammonemia. This study aimed to determine the relationship between chronic hyperammonemia, oxidative stress, and brain edema (BE) in two rat models of HE: portacaval anastomosis (PCA) and bile-duct ligation (BDL). Ammonia and reactive oxygen species (ROS) levels, BE, oxidant and antioxidant enzyme activities, as well as lipid peroxidation were assessed both systemically and centrally in these two different animal models. Then, the effects of allopurinol (xanthine oxidase inhibitor, 100mg/kg for 10days) on ROS and BE and the temporal resolution of ammonia, ROS, and BE were evaluated only in BDL rats. Similar arterial and cerebrospinal fluid ammonia levels were found in PCA and BDL rats, both significantly higher compared to their respective sham-operated controls (p<0.05). BE was detected in BDL rats (p<0.05) but not in PCA rats. Evidence of oxidative stress was found systemically but not centrally in BDL rats: increased levels of ROS, increased activity of xanthine oxidase (oxidant enzyme), enhanced oxidative modifications on lipids, as well as decreased antioxidant defense. In PCA rats, a preserved oxidant/antioxidant balance was demonstrated. Treatment with allopurinol in BDL rats attenuated both ROS and BE, suggesting systemic oxidative stress is implicated in the pathogenesis of BE. Analysis of ROS and ammonia temporal resolution in the plasma of BDL rats suggests systemic oxidative stress might be an important "first hit", which, followed by increases in ammonia, leads to BE in chronic liver failure. In conclusion, chronic hyperammonemia and oxidative stress in combination lead to the onset of BE in rats with chronic liver failure.en
dcterms.languageengen
UdeM.VersionRioxxVersion acceptée / Accepted Manuscript
oaire.citationTitleFree radical biology and medicine
oaire.citationVolume52
oaire.citationIssue7
oaire.citationStartPage1228
oaire.citationEndPage1235


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show item record

This document disseminated on Papyrus is the exclusive property of the copyright holders and is protected by the Copyright Act (R.S.C. 1985, c. C-42). It may be used for fair dealing and non-commercial purposes, for private study or research, criticism and review as provided by law. For any other use, written authorization from the copyright holders is required.