Galactosamine-induced sensitization to the lethal effects of endotoxin (lipopolysaccharide) was studied in rabbits, rats, and mice. Treatment with D-galactosamine significantly increased the animals' sensitivity to endotoxin, with susceptibility highest when administered together and decreasing over time. Sensitization was absent when endotoxin was given 1 hour before or 4 hours after galactosamine. The onset of lethality was faster when galactosamine and endotoxin were administered together, with all animals dying 5–9 hours later. Uridine reversed the sensitization, indicating that the early metabolic effects of galactosamine were responsible for the increased sensitivity. Galactosamine is a hepatotoxic agent that causes liver injury through early metabolic changes, leading to cell damage and death. These changes are inhibited by uridine. The study showed that galactosamine treatment increased the sensitivity of animals to endotoxin by thousands of times, with the effect being most pronounced in rabbits, rats, and mice. The sensitivity was short-lived, with maximum effect when endotoxin was administered immediately after galactosamine. The study also demonstrated that galactosamine sensitized mice to lipid A, a component of endotoxin, to an extent similar to that seen with complete lipopolysaccharide. The findings suggest that the sensitization to endotoxin is related to the early metabolic effects of galactosamine, not to the later necrosis of liver cells. The study provides a model for investigating the mechanisms of endotoxin toxicity, as the biochemical changes induced by galactosamine are well understood. The results indicate that temporary metabolic changes can render the organism susceptible to small amounts of endotoxin, highlighting the importance of early metabolic alterations in endotoxin sensitivity. The study also shows that the liver plays a key role in the initiation of endotoxin activities, in addition to its role in clearing endotoxin. The model is useful for studying endotoxin mechanisms, as it involves well-defined biochemical changes in liver cells.Galactosamine-induced sensitization to the lethal effects of endotoxin (lipopolysaccharide) was studied in rabbits, rats, and mice. Treatment with D-galactosamine significantly increased the animals' sensitivity to endotoxin, with susceptibility highest when administered together and decreasing over time. Sensitization was absent when endotoxin was given 1 hour before or 4 hours after galactosamine. The onset of lethality was faster when galactosamine and endotoxin were administered together, with all animals dying 5–9 hours later. Uridine reversed the sensitization, indicating that the early metabolic effects of galactosamine were responsible for the increased sensitivity. Galactosamine is a hepatotoxic agent that causes liver injury through early metabolic changes, leading to cell damage and death. These changes are inhibited by uridine. The study showed that galactosamine treatment increased the sensitivity of animals to endotoxin by thousands of times, with the effect being most pronounced in rabbits, rats, and mice. The sensitivity was short-lived, with maximum effect when endotoxin was administered immediately after galactosamine. The study also demonstrated that galactosamine sensitized mice to lipid A, a component of endotoxin, to an extent similar to that seen with complete lipopolysaccharide. The findings suggest that the sensitization to endotoxin is related to the early metabolic effects of galactosamine, not to the later necrosis of liver cells. The study provides a model for investigating the mechanisms of endotoxin toxicity, as the biochemical changes induced by galactosamine are well understood. The results indicate that temporary metabolic changes can render the organism susceptible to small amounts of endotoxin, highlighting the importance of early metabolic alterations in endotoxin sensitivity. The study also shows that the liver plays a key role in the initiation of endotoxin activities, in addition to its role in clearing endotoxin. The model is useful for studying endotoxin mechanisms, as it involves well-defined biochemical changes in liver cells.