Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two methods of inducing liver cirrhosis in the rat were studied. Intragastric administration of CCl4 for 16 weeks according to Proctor and Chatamra was compared to the administration of thioacetamide in the drinking water (0.3 g/l) for the same period. CCl4 administration induced micronodular cirrhosis in 6/8 animals with a 27% mortality. Thioacetamide induced cirrhosis in 6/8 animals without mortality. The histologic pictures differed somewhat in that the CCl4 group exhibited more necrosis and cellular swelling while the thioacetamide group had more nuclear atypias and proliferation. Biochemically both groups had elevated plasma levels of aspartate aminotransferase. The lysosomal enzyme beta-hexosaminidase (beta-NAG) showed a transient increase in the thioacetamide animals, while beta-glucuronidase decreased. CCl4-induced cirrhosis led to an increase in beta-NAG. Plasma zinc decreased in both groups as well as liver zinc content in the CCl4 group, while there was a continuous elevation of liver zinc in the thioacetamide group. We conclude that oral administration of thioacetamide is a simple and reliable method of inducing experimental liver cirrhosis. The differences in histological appearances and some biochemical parameters may be caused by the different mechanisms of action of thioacetamide and CCl4.
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PMID:Thioacetamide- and carbon tetrachloride-induced liver cirrhosis. 276 88

To study the relationship between lipid peroxidation (LPO) and the release of lysosomal enzymes as markers of liver injury three compounds were chosen which evoke lipid peroxidation (cumene hydroperoxide, CHP), hepatocellular injury (thioacetamide, TAA) or both (carbon tetrachloride, CCl4). Premitochondrial supernatants of phenobarbital-induced rat liver homogenates were incubated in the presence of either agent and an NADPH-regenerating system. Then, lipid peroxidation was assessed by measurement of malondialdehyde (MDA) formation and, after centrifugation at 105 000 g, released beta-glucuronidase was measured in the supernatant. While CCl4 and CHP promoted both events in a time and concentration dependent manner, TAA did not evoke either LPO or lysosomal enzyme release. Glutathione, dithiocarb and (+)-catechin inhibited both effects. Though LPO and lysosomal enzyme release proved to be related events, no strict correlation with the hepatotoxicity was found.
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PMID:Interrelation between lipid peroxidation and lysosomal enzyme release in the presence of carbon tetrachloride, cumene hydroperoxide or thioacetamide. 630 41