Escherichia coli (E. coli) endotoxin and E. coli L-asparaginase produced diarrhea, rapid respiration and nasal discharge. L-asparaginase caused a greater incidence of tremors, muscle fasciculations and ultimate convulsions than endotoxin. The maximal incidence of L-asparaginase toxicity (40–45 %) occurred after 800 or 1,400 IU/kg. Endotoxin toxicity was observed within 24 h, whereas L-asparaginase intoxication developed after 24 h. The blood pressure in animals displaying severe L--asparaginase toxicity was similar to that monitored in the control animals, whereas severe hypotension was found in endotoxin-intoxicated animals. L-asparaginase and endotoxin induced increases in blood glucose and urea nitrogen. The blood urea nitrogen levels returned to control levels by 72 h in surviving animals. Endotoxin also produced elevations in serum glutamic pyruvic transaminase and serum glutamic oxaloacetic transaminase levels. Endotoxin and L-asparaginase produced some histopathological changes in the lung, kidney, liver and spleen. The alterations in the liver and kidney appeared to be more severe after endotoxin treatment. Significant decreases in plasma levels of calcium and magnesium and an increase in plasma phosphorus levels were noted in L-asparaginase-intoxicated animals. These plasma ions were not altered by endotoxin treatment. Thus, the pharmacological effects of L-asparaginase observed in rabbits appear to differ in many respects from that of endotoxi