Acute Ethanol Gavage Attenuates HemorrhageResuscitation-Induced Hepatic Oxidative Stress in Rats

Abstract EN

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.