Recent studies demonstrated remote effects of renal ischemia/reperfusion (IR) injury on some organs such as brain, liver, and lungs.Apoptosis is reported in remote lung, liver and myocardial injury after acute kidney injury. These data suggest a possible remote effect of renal IR injury on pancreas. So, we postulated that renal IR may affect distant organs such as pancreas and that oxidative stress and mitochondrial mediated apoptosis may play role in this injury. The aim of this study is to investigate the effects of kidney IR on pancreatic exocrine and endocrine function, antioxidant enzymes activity, apoptosis and the protective effect of vitamin C in a rat model of IR injury. The animals were submitted to non-traumatic bilateral renal IR, Sham operation or treated with vitamin C after IR. In three groups, rats were sacrificed on the 1st, 3rd, and 7th days of the experiment to evaluate the parameters of oxidative stress (catalase, lipid peroxidase, reduced glutathione and superoxide dismutase), pancreatic endocrine and exocrine function (amylase, insulin and fasting blood glucose), renal functions (serum creatinine and BUN), cell injury and apoptotic markers (Bcl-2, Bax and caspase-3). The results suggest that bilateral renal ischemia caused significant impairment of pancreatic functions and structure as indicators of acute pancreatitis. Apoptosis and enhanced oxidative stress was evident, on the other hand, vitamin C appeared to play a cyto-protective role. This might be due to their effect on oxidative stress with concomitant decrease in pancreatic apoptotic markers after ischemia/reperfusion injury.