[Antioxidative effect of N2-mercaptopropionylglycine (N2 MPG) in experimental acute pancreatitis].

The N2-Mercaptopropionylglycine (N2-MPG) is a potent antioxidant by inhibiting the abnormal production of xantina-oxidase. The aim of this research is to analyze the antioxidant capacity of this tiol compound by offering some protection to pancreatic tissue in the acute pancreatitis (AP). The induction of AP was obtained through two methods: a) supramaximal dose of cerulein; b) infusion of 2.5% sodium taurocholate into the biliopancreatic duct of the rat. Thirty-six male Wistar rats (220-270 g) were divided into four groups. AP with cerulein (Two parenteral doses of 20 micrograms/kg; one hour interval): in two groups: GI: nineteen rats previously treated with N2-MPG (100 mg/kg) ten minutes before AP. GII (control): seventeen animals which received saline 0.9%. AP with taurocholate (0.5 ml into the main biliopancreatic duct): in other two groups: GIII: eleven rats previously treated with N2-MPG (100 mg/kg) ten minutes before AP. GIV (control): fifteen animals which received saline 0.9%. The albumin leakage into the cell interstice as an inflammatory parameter was measured through Evans-Blue (EB) colorimetry, that links totally with serum albumin after injection into the pancreatic tissue, immediately before induction of AP. The rats were sacrificed one hour after. Water tissue content was also measured. There was a relevant reduction of EB leakage in GI (344 +/- 27 micrograms/gtissue) when compared to GII (729 +/- 84 micrograms/gtissue), p < 0.01, and in GIII (386 +/- 52 micrograms/gtissue) when compared to GIV (543 +/- 53 micrograms/gtissue), p < 0.05. There was no difference in tissue water content between GI (88.2 +/- 0.6%) and GII (87.4 +/- 0.9%), but certainly between GIII (77.7 +/- 2.1%) and GIV (82.8 +/- 1.2%), p < 0.05. The amilase levels didn't show any difference among the four groups. These results suggest that the use of the antioxidant N2-MPG offers a protective action, at least in rats, reducing the severity of AP induced by supramaximal dose of cerulein, and even in a more severe AP such as produced by sodium taurocholate at 2.5%, although apparently not interfering with its pathogenesis. It also strengthens the actual participation of free radicals of oxygen in the physiopathology of acute pancreatitis.