title: Acute ethanol gavage attenuates hemorrhage/resuscitation-induced hepatic oxidative stress in rats.
abstract: Acute ethanol intoxication increases the production of reactive oxygen species (ROS). Hemorrhagic shock with subsequent resuscitation (H/R) also induces ROS resulting in cellular and hepatic damage in vivo. We examined the role of acute ethanol intoxication upon oxidative stress and subsequent hepatic cell death after H/R. 14 h before H/R, rats were gavaged with single dose of ethanol or saline (5 g/kg, EtOH and ctrl; H/R_EtOH or H/R_ctrl, resp.). Then, rats were hemorrhaged to a mean arterial blood pressure of 30 ± 2 mmHg for 60 min and resuscitated. Two control groups underwent surgical procedures without H/R (sham_ctrl and sham_EtOH, resp.). Liver tissues were harvested at 2, 24, and 72 h after resuscitation. EtOH-gavage induced histological picture of acute fatty liver. Hepatic oxidative (4-hydroxynonenal, 4-HNE) and nitrosative (3-nitrotyrosine, 3-NT) stress were significantly reduced in EtOH-gavaged rats compared to controls after H/R. Proapoptotic caspase-8 and Bax expressions were markedly diminished in EtOH-gavaged animals compared with controls 2 h after resuscitation. EtOH-gavage increased antiapoptotic Bcl-2 gene expression compared with controls 2 h after resuscitation. iNOS protein expression increased following H/R but was attenuated in EtOH-gavaged animals after H/R. Taken together, the data suggest that acute EtOH-gavage may attenuate H/R-induced oxidative stress thereby reducing cellular injury in rat liver.
authors.affiliation: Department of Trauma Surgery, Goethe University Frankfurt am Main, 60590 Frankfurt, Germany. info@bornarelja.com
authors.forename: B
authors.initials: B
authors.lastname: Relja
authors.forename: K
authors.initials: K
authors.lastname: Wilhelm
authors.forename: M
authors.initials: M
authors.lastname: Wang
authors.forename: D
authors.initials: D
authors.lastname: Henrich
authors.forename: I
authors.initials: I
authors.lastname: Marzi
authors.forename: M
authors.initials: M
authors.lastname: Lehnert
mesh_terms: D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D053181:Caspase 8 / Q000235:genetics / Q000378:metabolism; D000431:Ethanol / Q000633:toxicity*; D005260:Female; D006470:Hemorrhage / Q000378:metabolism / Q000473:pathology*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D017382:Reactive Oxygen Species / Q000378:metabolism; D012151:Resuscitation; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: D000447:Aldehydes; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; C002744:3-nitrotyrosine; D000431:Ethanol; D014443:Tyrosine; D052247:Nitric Oxide Synthase Type II; D053181:Caspase 8; C027576:4-hydroxy-2-nonenal