The purpose of the study is to establish the effectiveness of remaxol in the correction of endogenous intoxication in patients with acute peritonitis. Material and methods. The work is based on the results of clinical and laboratory studies. The clinic examined 55 patients with acute moderate peritonitis as complication of various diseases (acute appendicitis, perforated gastric or duodenal ulcer, acute intestinal obstruction, acute destructive cholecystitis). Before surgical operation and in the early postoperative period we evaluated the severity of endogenous intoxication by the level of hydrophilic and hydrophobic toxic products. The content of molecular products of lipids peroxidation - oxidative stress, phospholipase activity were determined in the blood plasma. In the study group (n = 28) in the postoperative therapy additionally included remaxol (400 ml intravenous fluids). Results. Research established that the occurrence of endogenous intoxication syndrome in patients with acute peritonitis associated with the activation of oxidative stress and phospholipases, high intensity of which is maintained even after elimination of the source of peritonitis with manifestation on the 1st day after surgery. Remaxol include leads to a significant reduction in the severity of intoxication syndrome in patients with acute peritonitis. Positive effect of the drug on the correction of endogenous intoxication is largely determined by its ability to significantly reduce oxidative stress and the activity of phospholipases, as the most important membrane destabilizing agents. The greatest detoxication effect of the drug is recorded when it is applied already at the preoperative stage of patients when its ability to reduce the activity of trigger agents of catabolic processes implemented to the greatest extent. Conclusion. In acute moderate peritonitis, remaxol use before surgery or in the early postoperative period in complex therapy leads to a significant correction of factors contributing to the development and preservation of the intensification of catabolic processes - one of the sources of endogenous intoxication.