Regulatory Toxicology and Pharmacology 42 (2005) 260–264 www.elsevier.com/locate/yrtph 0273-2300/$ - see front matter  2005 Elsevier Inc. All rights reserved. doi:10.1016/j.yrtph.2005.04.008 EVect of interleukin-10 on pancreatic damage caused by organophosphate poisoning I. Ikizceli a,¤ , Y. Yurumez b , L. Avsarofullari a , C. Kucuk c , E.M. Sozuer a , I. Soyuer d , Y. Yavuz b , S. Muhtaroglu e a Erciyes University Medical Faculty, Department of Emergency Medicine, Kayseri, Turkey b Kocatepe University Medical Faculty, Department of Emergency Medicine, Afyon, Turkey c Erciyes University Medical Faculty, Department of Surgery, Kayseri, Turkey d Erciyes University Medical Faculty, Department of Pathology, Kayseri, Turkey e Erciyes University Medical Faculty, Department of Biochemistry, Kayseri, Turkey Received 7 March 2005 Abstract Organophosphate poisoning is a common cause of severe morbidity and mortality in emergency departments. Acute pancreatitis is a frequently reported consequence of organophosphate poisoning, but preventing this potentially severe complication has not been the subject of much research. We tested whether interleukin-10, a cytoprotective agent, could prevent or diminish pathological signs of acute pancreatitis caused by organophosphate poisoning. Thirty rats were divided into three equal groups. Group 1 did not receive any agent during the experiment. Group 2 received 0.8 g/kg fenthion intraperitoneally, followed by 6 ml/kg intraperitoneal normal saline 30 min and 3 h later. Group 3 received 0.8 g/kg fenthion intraperitoneally, followed by 2 g/kg of interleukin-10 intra- peritoneally 30 min and 3 h later. All rats underwent laparotomy and thoracotomy while still under anesthesia at 6 h, and tissue sam- ples were obtained from the pancreas. After blood samples were taken by cardiac puncture, the animals were sacriWced. Organophosphate poisoning resulted in signiWcant elevations of serum amylase and glucose. Interleukin-10 signiWcantly reduced pancreatic damage as determined by pathologic scoring, but not by enzyme elevations. Interleukin-10 should be considered for larger studies in other animal models to conWrm its ability to decrease pancreatic damage after organophosphate poisoning treatment with interleukin-10.  2005 Elsevier Inc. All rights reserved. Keywords: Organophosphate; Poisoning; Pancreatic damage; Treatment; Interleukin-10 1. Introduction Organophosphates (OP) are widely used as insecti- cides in both urban and rural settings. In vivo, these agents bind irreversibly to cholinesterase, and thus the clinical manifestations are those of increased cholinergic activity (Panieri et al., 1997; Zweiner and Ginsburg, 1988). Acute pancreatitis is a well known complication of OP poisoning (Panieri et al., 1997), whose pathoge- netic mechanism may be excess cholinergic stimulation within the pancreas and ductular hypertension (Dressel et al., 1982; Hsiao et al., 1996; Sahin et al., 2002). The inXammation and necrosis seen in acute pancreatitis may be mediated by proinXammatory cytokines (Van Laethem et al., 1995). Interleukin-10 (IL-10) was discovered in 1989 and was originally named “cytokine synthesis inhibitory fac- tor.” It is produced by Th2 cells, macrophages/mono- cytes and B cells (Fiorentino et al., 1989). Macrophages, once activated by antigenic stimuli, release a variety of * Corresponding author. Fax: +90 352 437 52 73. E-mail address: ikizceli@erciyes.edu.tr (I. Ikizceli).