Redox state and the potential role of antioxidant compounds in liver ischemia/reperfusion injury

Maria I. Korontzi^1*, Apostolos Papalois², Ilias Kouerinis¹, Andreas C. Lazaris³,

George Theodoropoulos¹ and George Zografos¹

¹First Department of Propaideutic Surgery, Hippocration Hospital, Athens Medical School, Athens, Greece.

²Experimental Research Center ELPEN, Athens, Greece.

³Department of pathology, Laiko Hospital, Athens Medical School, Athens, Greece.

*Corresponding author. E-mail: markorontzi@gmail.com. Tel: +306932662229.

Accepted 12 April 2010

 Abstract

Hepatic ischemia/reperfusion (I/R) injury consists of a sequel of cellular and humoral events that finally leads to parenchymal and nonparenchymal cell death. It is of utmost importance as regards the outcome of liver transplantation and liver resections. There is ample evidence that the key role in the inflicted injury is ascribed to reactive oxygen species (ROS) generated mainly by Kupffer cells and neutrophils during reperfusion, with the participation of endothelial cells and hepatocytes. ROS can procure serious damage to cellular membranes and genomic material. The disaster culminates with the initiation of several inflammatory mediators. On the other hand, cells posses a very potent, enzymatic and non enzymatic antioxidant system capable to mitigate oxidant stress or scavenge ROS, thus preserving to some extent cellular redox state. When the imbalance between oxidant stress and antioxidant systems predominates, cell death ensues. The spectre of liver I/R injury therapeutic options includes a plethora of antioxidant agents, natural or synthetic, and extends to genetic modifications. The aim of this article is to review the current knowledge on the generation and mode of action of ROS and to give a further insight on the antioxidant compounds that comprise the therapeutic quiver of this complicated syndrome.  

Key words: Reactive oxygen species, oxidant stress, liver ischemia reperfusion, redox state, inflammation, antioxidants.