Background/aims: One of the most important complications of acute pancreatitis is the secondary bacterial infections of the pancreas and gut. Translocation of bacteria from the gut is accepted as being responsible for the development of septic complications in acute pancreatitis. In this study, our aim was to investigate the effect of PARP inhibition via 3-aminobenzamide on the bacterial translocation in acute pancreatitis. Methods: 45 male Sprague-Dawley rats were randomly allocated into three groups. Group I (Sham+saline) received normal saline infusion into the common biliopancreatic duct. Acute pancreatitis was induced in Group II (acute pancreatitis+saline) and Group III (acute pancreatitis+3-aminobenzamide) by the retrograde injection of taurocholate into the common biliopancreatic duct. Six hours after induction of pancreatitis, the rats in Group I and II were treated with saline (1 ml, every 12 hours), while the rats in Group III were treated with 3-aminobenzamide (10 mg/kg/day every 12 hours), intraperitoneally. In the 54(th) hour of the study, blood and tissue samples were taken for biochemical, microbiological and histopathological analysis. Results: Acute pancreatitis developed in Groups II and III. Pathologic score [median (25-75% percentiles). of the pancreatitis in Group III [8 (7-9)] was significantly lower than in Group II [19 (18-21)] (p<0.001). Bacterial translocation to mesenteric lymph node (53.3%), peritoneum (60%) and pancreas (46.7%) in Group III was significantly lower than in Group II (100% for all) (p<0.02, p<0.03, p<0.005, respectively). Pancreatic tissue glutathione peroxidase, superoxide dismutase, and malondialdehyde levels were better in Group III compared to Group II (p<0. 001 for all). Comparison of Groups II and III demonstrated reduced severity of inflammation of the gut in Group III (p>0.05). Improvement in bacterial translocation was correlated with reducing oxidative stress. Conclusions: We demonstrated that 3-aminobenzamide therapy improved histopathologic score and oxidative stress in experimental pancreatitis. In addition, it was demonstrated microbiologically and histopathologically that 3-aminobenzamide therapy improves bacterial translocation. Further survival studies demonstrating the efficacy of 3-aminobenzamide therapy and explaining the potential mechanisms of bacterial translocation prevention in acute necrotizing pancreatitis will be beneficial.