The liver is particularly susceptible to ischaemia/reperfusion injury, which is evident after conditions such as shock, trauma, transplantation, and surgical hepatectomy. Poly (ADP-ribose) polymerase (PARP) is a nuclear enzyme activated by strand breaks in DNA, which are caused by ROS. Activation of PARP is a consequence of ischemic injury in the brain, retina, heart, kidney, skeletal muscle and liver [1]. Here we investigate the role of a water-soluble PARP inhibitor in a model of hepatic ischemia/reperfusion. Male Wistar rats (280–350 g) were pre-treated with PJ-34 (1 mg/kg, i.v.) 5 minutes prior partial hepatic ischaemia (performed after animals were anaesthetised with pentobarbital sodium 60 mg/kg, i.p.). A midline incision was made in order to expose the organ and a vascular microclamp was used to interrupt the blood supply to 3/4 of the liver during 30 minutes, followed by 2 hours of reperfusion. Biochemical markers of liver injury (AST, ALT and LDH) and kidney dysfunction (urea and creatinine) were determined. Results were compared by one-way ANOVA followed by a Bonferroni post-hoc test (P

Keywords: liver ischemia, PARP, 5-aminoisoquinoline, Rat