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Summary: The incorporation of [35S]sulfate into total and specific glycosaminoglycans of the liver of rats injured acutely by a singie intraperitoneal dose of either jD-galactosamine (700 and 350 mg/kg body weight, respectively) or thioacetamide (100 mg/kg body weight) was studied in vivo and in liver slices. Regardless of the chemical nature of the hepatotoxic agent and its mechanism of action the incorporation of isotope in vivo is changed biphasically: a rapidly occurring and strong Inhibition is followed by pronounced elevation in later stages of injury. In contrast to the dose-dependent Inhibition of heparan sulfate formation the production of chondroitin sulfate and dermatan sulfate is only slightly and for a rather short period of time diminished. The synthesis of the latter glycosaminoglycans is stimulated 3 to 4 fold 8 to 24 h after onset of liver damage, fhat of heparan sulfate about 2 fold. Impaired synthesis of heparan sulfate occurs before the elevation of the activities of aspartate aminotransferase, alanine aminotransferase, and leucine arylamidase in serum. The specific radioactivity of 3'-phosphoadenosine-5'-phosphosulfate remains nearly constant in galactosamine-damaged livers. Similar time-dependent changes of [3S S]sulfate incorporation into heparan sulfate, chondroitin sulfate and dermatan sulfate were measured in slices from livers injured in vivo for various times with -D-galactosamine or thioacetamide. Neither serum from normal nor galactosaniine-treated rats influences the total amount and the pattern of glycosaminoglycans synthesized in normal or injured liver slices. Hepatic glycosaminoglycan formation of 3.5 and 33 months old rats responds quantitatively and qualitatively in a simuar way to £>-galactosamine; 50% Inhibition is reached with about 80 mg/kg of the hepatotoxin. The Inhibition of heparan sulfate synthesis in early injured livers could not be reversed by addition of p-nitrophenyl-/3-Z)-xylopyranoside to the medium (final concentration l mmol/1), but in rats treated with diethyldithiocarbamate or the flavonoid (+)-cianidanol-3, prior to injection of Z)-galactosamine, a partial restoration of the diminished synthesis of total glycosaminoglycans and of heparan sulfate is achieved.

The Sequence of Changes in the Biosynthesis of Sulfated Glycosaminoglycans in Acute, Experimental Liver Disease