Oxygen free radical activity and inhibition were examined in experimental pancreatitis. Twenty-Ji've rats were randomized to five groups: controls received intravenous saline, to simulate pancreatitis one group receitied intravenous caerulein (5 pg kg -' h -'), and three groups received sodium taurocholate via the pancreatic duct (0.2 ml, 5 per cent), either alone, Jollowing allopurinol or immediately before superoxide dismutase. Chernilurninescence ( a phenomenon based on the emission of light during chemical reactions and which is dependent on oxygen free radical activity) u~as used as an index of oxygen free radical activity and was measured in tissue samples at 5-min intervals following induction of pancreatitis. The control mean(s.e.m.) serum amylase level I h after induction of pancreatitis was 635(13) units. It was significantly elevated in caerulein-induced pancreatitis, 1833( 118) units (P < 0.0.5) and exceeded 3000 units in all taurocholate-infused animals. Mean(s.e.m.) chemilurninescence ranged from 44 (8) m V 100 mg -' at time zero to 404( 113) mV 100 mg-' at 1 h in controls. In caeruleininduced pancreatitis mean(s.e.m.) chemiluminescence peaked at 20 rnin (1399(239) m V 100 mg -', P < 0.02) and in taurocholate-induced pancreatitis at 15 rnin (2316(95) m V 100 m y -', P <0.004). Superoxide dismutase signijicantly reduced chemiluminescence and hyperamylasaemia in taurocholate groups. Increasing oxygen free radical activity paralleled evolving pancreatitis. Superoxide dismutase may have a therapeutic role in pancreatitis.