Galactosamine-induced sensitization to the lethal effects of endotoxin.

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Abstract
Treatment of rabbits, rats and mice with D-galactosamine increased their sensitivity to the lethal effects of lipopolysaccharide [from Salmonella abortus equi] several thousand-fold. The susceptibility of the animals was highest when the lipopolysaccharide was injected together with galactosamine and decreased successively when injection was carried out 1, 2 and 3 h later. Sensitization was absent when the lipopolysaccharide was administered 1 h before or 4 h after galactosamine. The onset of lethality after treatment with galactosamine and lipopolysaccharide occurred faster than with lipopolysaccharide alone; usually all animals died 5-9 h later. The galactosamine-induced sensitization to lipopolysaccharide could be reversed by uridine, which inhibits the early biochemical alterations induced by the amino sugar in the hepatocytes. Although galactosamine exhibits hepatotoxic activity, inducing ultimate necrosis of the hepatocytes, the data suggest that the sensitization to lipopolysaccharide is related only to the early metabolic effects of the hexosamine.