Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Different groups of rats suffering from galactosamine hepatitis or ANIT-cholestasis received 200 mg galactose either by 5 minutes intravenous infusion or via a gastric tube. Blood galactose concentrations were measured for a time period of 1.5 hrs. after intravenous administration and the galactose elimination capacity (GEC) was calculated. After oral administration the galactose blood concentrations were determined for a period of 3.5 hrs. and the oral galactose clearance was estimated. After termination of both types of galactose loading the activity of the galactokinase (EC 2.7.1.6.) was determined in total liver homogenate and compared either to the GEC or to the oral galactose clearance in vivo. Galactokinase activity in the liver increased in the group of animals with experimental cholestasis and was significantly reduced in the galactosamine treated group. In vivo these changes could be estimated much better by the GEC than by determination of the oral galactose clearance.
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PMID:[Intravenous and oral galactose loading of rats suffering from galactosamine hepatitis and ANIT-cholestasis; comparison of the kinetics in vivo and the galactose metabolism in the liver in vitro (author's transl)]. 52 47

We studied the effects of acute and chronic ethanol feeding on hepatic regeneration in rats after partial hepatectomy and toxic liver injury produced by D-galactosamine. Ethanol, when administered as a single dose (6 g/kg), inhibited 3H-thymidine incorporation into hepatic DNA; this effect depended in part on the time of ethanol feeding after partial hepatectomy. Multiple ethanol feedings produced an even greater inhibition, which persisted for at least 48 hr after partial hepatectomy. Rats chronically fed ethanol for 30 days also failed to achieve a hepatic proliferative response to either partial hepatectomy or D-galactosamine-induced hepatitis, comparable with isocaloric pair-fed controls. These investigations suggest that there may be a certain metabolic state in the hepatocyte cell cycle that is most susceptible to the action(s) of ethanol; inhibition of liver regeneration by acute or chronic ethanol consumption may result in delayed recovery from prior or coincident liver injury.
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PMID:Inhibition of hepatic regeneration in rats by acute and chronic ethanol intoxication. 57 15

Galactosamine caused changes in the livers of rats that were similar to those seen in human viral hepatitis. In hamsters the changes were characteristic of a typical toxic hepatitis. The response by the liver to galactosamine was very variable in both the rat and the hamster and there was a degree of correlation between the raised transaminase levels and the liver cell damage.
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PMID:A comparison between the morphologic changes in the livers of hamsters and rats after galactosamine treatment and their correlation with altered serum transaminase levels. 57 38

The i.p. application of 400 mg/kg D-galactosamine to rats induces liver damage which histologically resembles hepatitis. As also shown in the present investigation, the transaminases SGOT and SGPT in the serum of the damaged animals strongly increase already within 24 h. In the present investigation part of the animals (rats) was treated with 15, 30, 60, 125, 250 and 500 mg/kg of a new hepatoprotective preparation alpha,alpha-dithio-dicapronic acid (ES 914, Lipexal Berna) 2 h before and 6 h after the application of the liver damaging substance D-galactosamine (dose 400 mg/kg). ES 914 was applied p.o. whereas D-galactosamine was injected i.p. The transaminases were estimated at the beginning of the experiments as well as 24 h after the injection of D-galactosamine. The statistical evaluation of the results showed an increasing protective effect depending on the increasing dosage of the preparation ES 914. The protective effect begins at the latest with the dose of 30 mg/kg ES 914 and with 60 mg/kg it is highly significant (p less than or equal to 0.001). With a dosage of 500 mg/kg ES 914 the increase of SGOT and SGPT values is virtually abolished.
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PMID:[Effect of the liver protecting compound ES 914 on D-galactosamine induced experimental hepatitis in the rat]. 58 21

1. The metabolism of protein and phospholipid in rat liver plasma membranes isolated by the method of Neville [(1960) J. Biophys. Biochem. Cytol. 8, 413-422] was investigated 3 and 6 h after the injection of D-galactosamine in vivo. During this time, all the biochemical and morphological alterations associated with hepatitis developed. 2. After the injection of D-galactosamine the concentration of sphingomyelin in the plasma membrane decreased to below 60% of the control values. 3. The activity of 5'-nucleotidase (EC 3.1.3.5), which has been purified as a sphingomyelin-protein complex, decreased in the total homogenate as well as in the plasma-membrane fraction of livers of rats treated with galactosamine, to about 60% of the control values. 4. Protein synthesis, as measured by the incorporation of [14C]leucine into plasma membranes, was decreased to 45% of that of the controls. However, only small differences were observed in the amino acid composition of the plasma membrane after D-galactosamine treatment. 5. The protein composition of the plasma membranes was determined by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis. The results showed a change from low- to high-molecular-weight proteins after the injection of galactosamine. 6. These results demonstrate different metabolic processes of the plasma membrane altered during the induction of galactosamine hepatitis.
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PMID:Studies on rat liver plasma membrane. Altered protein and phospholipid metabolism after injection of D-galactosamine. 59 40

In order to elucidate the role of lysosomes in experimental hepatitis caused by D-galactosamine in rats the activities of cathepsin A and D and acid carboxypeptidase were measured. Enzyme activities were assayed in liver homogenate, lysosomal supernatant fraction and lysosomal sediment fraction. Lysosomal enriched fractions were prepared according to De Duve. Vitamin A in high doses aggravates the morphological alterations observed in galactosamine treated rats. At the same time the labilization of lysosomes increases substantially. This effect was induced by doses of retinyl-palmitate that normally caused only an activation of Kupffer cells and no significant liberation of lysosomal peptidehydrolases. The activities of cathepsin A and D increased 2-fold in liver homogenate after combined treatment with galactosamine and vitamin A, whereas the activity of acid carboxypeptidase decreased markedly.
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PMID:Effect on vitamin A on the development of galactosamine-induced hepatitis in rats. 70 84

With D-galactosamine hydrochloride severe hepatitis was induced in rats and the water content of cerebrum, cerebellum and brain stem determined. The animals showed a parallel increase in cerebral water content and occurrence of cerebral symptoms.
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PMID:Cerebral edema in the rat with galactosamine induced severe hepatitis. 72 Apr 86

Ammonia toxicity and the protective effect of arginine thereon were investigated in rats after single and repeated doses of galactosamine. Urea cycle enzymes and ornithine-oxo-acid transaminase activities were measured in rat liver homogenates. Ammonium acetate proved to be less toxic in rats treated with single or repeated doses of galactosamine than in untreated animals. Urea cycle enzyme activities of galactosamine-treated rats were clearly lowered. The protective effect of arginine against lethal ammonia intoxication was found in animals that had been treated with galactosamine as well as in untreated rats. Since the toxicity of ammonium acetate is lower in rats with galactosamine hepatitis, in which the activities of the liver urea cycle enzymes are reduced, it seems likely that ammonia detoxication in galactosamine-poisoned rat liver partly bypasses the urea cycle.
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PMID:[Toxicity of ammonium acetate in rats with acute and subacute galactosamine-induced hepatitis (author's transl)]. 76 43

In patients suffering from acute viral hepatitis (n = 12) an about 50 per cent decrease of serum diamine oxidase (DAO, histaminase, E.C.N. 1.4.3.6) was detected as compared to a healthy control group (n = 24). Normally, the intravenous injection of heparin is promptly followed by a marked rise of plasma DAO. In viral hepatitis, however, after application of heparin (200 IU/kg b.w., i.v.) the enzyme release from the visceral organs into the plasma was markedly decreased. There was an inverse correlation between the serum glutamic pyruvic transaminase (SGPT) and the postheparin enzyme. Normalization of SGPT occurred before the normalization of post-heparin diamine oxidase (PHD). In galactosamine "hepatitis" of rats (800 mg Gal-N/kg b.w., i.p.), in contrary to human viral hepatitis plasma DAO increased about 5-fold after heparin application. This increased PHD in plasma of Gal-N rats was correlated to enhanced animal's endogenous plasma DAO activity (r=0.685, p less then 0.0005, n = 54). The cause of these enzyme activity changes and its possible pathophysiological meaning are still unknown. It is concluded from these experiments that in Gal-N "hepatitis" of rats plasmatic DAO level changes are mediated by endogenous heparin, released from disrupted mast cells. Increased basal DAO levels correspond to the enhanced release after heparin application, both possibly induced by less stable binding of the enzyme to the cells of the small intestine in inflammation. Both, decreased endogenous and post-heparin DAO levels in human hepatitis would correspond to a depletion of the enzyme containing organs.
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PMID:Serum level changes of endogenous and postheparin diamine oxidase (histaminase) in clinical and experimental hepatitis. 81 62

The course of galactosamine hepatitis induced by 1.0 g/kg i.p. injected galactosamine (Ga1N) was investigated a sequential study in normal rats, in colectomized rats, and in rats being endotoxin resistent against both exogenous and endogenous endotoxin. Clinical symptoms of Ga1N-hepatitis such as pyrogen reaction, disseminated intravascular coagulation, arterial hypotension, and hypoglycaemia correlated significantly with the development of endotoxaemia, which was detected by means of the limulus gelation test (L.G.T.) Ga1N refractoriness was found after colectomy, a situation, in which gram negative bacterias and their endotoxins were eliminated. Ga1N refractoriness was also observed in case of endotoxin resistence. It is concluded that endotoxins contribute significantly to the pathogenesis of "Ga1N-hepatitis" and its clinical symptoms.
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PMID:Significance of endotoxaemia in experimental "galactosamine-hepatitis" in the rat. 85 60


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