Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present investigation an attempt was made to ascertain whether nonviral liver impairment in rats affects the THelper/TSuppressor ratio. Two hepatotoxic agents were used: (i) galactosamine (GA), which causes a drug-induced hepatitis-like damage, and (ii) orotic acid (OA), which induces fatty changes. Since these two substances act as antidotes to one another they were administered to rats either separately or simultaneously. GA caused severe liver damage documented by a 104-, 48-, and 1.6- fold rise in the plasma concentrations of ALT, AST, and ALP and by multiple foci of hepatocyte necrosis. This was followed by a drop in TH/TS ratio from 2.25 observed in the controls to 0.89 in the GA-treated rats. All of these phenomena were prevented by concurrent administration of GA and OA. OA alone did not show an effect on the liver with respect to changes in plasma enzyme concentrations and by light microscopic analysis. However, OA caused a drop in the TH/TS ratio from 2.25 to 1.55. Neither GA nor OA produced a change in TH/TS ratios in in vitro experiments.
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PMID:The effect of nonviral liver damage on the T-lymphocyte helper/suppressor ratio. 296 93

The reported cytoprotective effects of prostaglandins against noxious stimuli in the liver was the basis for the present investigations of the effects of prostacyclin (PGI2) and a prostaglandin analogue (BW 245C) in an animal model of severe liver failure. Rats were given galactosamine at two dose levels and the prostaglandins were given in repeated doses from 0 to 6 h during the development of the liver damage or in another group from 24 to 30 h at the time of maximal liver injury. For PGI2 significant cytoprotection was found as assessed by a reduction in blood Normotest at 24, 48 and 72 h (P less than 0.05) and the plasma level of aspartate aminotransferase at 24 and 48 h (P less than 0.02) and the lysosomal markers N-acetyl-beta-glucosaminidase at 24, 48 and 72 h (P less than 0.001) and cathepsin D at 48 h (P less than 0.005) as compared to appropriate controls. Early administration of PGI2 reduced the mortality rate from 63% in the control group to 0% (P less than 0.01) in the treated group, but no significant effects were found when either compound was given later in the 24-h to 30-h period.
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PMID:Effect of prostacyclin (PGI2) and a prostaglandin analogue BW 245C on galactosamine-induced hepatic necrosis. 351 86

Serum proteolytic activity was determined in galactosamine-treated rats and in controls. Injection of the hepatotoxin at a dose of 400 mg/kg resulted in a 3.4-fold elevation in the serum proteolytic activity, while AST (aspartate aminotransferase), ALT (alanine aminotransferase) and bilirubin were increased by factors of 3.9, 8.8 and 4.5, respectively. Studies with proteinase inhibitors revealed that the serum proteolytic activity was partially metal-dependent as well as puromycin and antipain sensitive. Differences in susceptibility to a combination of N-ethylmaleimide and antipain indicated presence of different proteolytic systems in the sera of liver damaged and control rats. Separation of serum proteinases by gel filtration showed that the galactosamine-intoxicated rat serum contained activity which did not appear in the control serum. This activity was partially metal dependent, antipain and N-ethylmaleimide sensitive, and was more susceptible to dithiothreitol than the control activity. These findings demonstrate that hepatocellular damage induced by galactosamine caused not only an increase in serum proteinases, but was also associated with the appearance of enzymes not normally released by the liver of untreated animals.
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PMID:Quantitative and qualitative changes of serum proteolytic activity in rats with liver damage induced by galactosamine. 353 Jan 92

Although copper is believed to be hepatotoxic in Wilson's disease and Indian Childhood Cirrhosis (ICC), the rat shows only minimal hepatic damage on copper-loading. To investigate the possibility that copper deposition may potentiate the effects of a superimposed hepatitis, D-galactosamine (GalN) was given to copper-loaded and control rats. In the non-copper-dosed rats, GalN 0.85 g/kg i.p. produced elevated serum AST (3731 +/- 545 IU/l; normal 64.8 +/- 2.1), ALT (2090 +/- 190 IU/l; normal 18.0 +/- 0.7), and OCT (16.7 +/- 2.6 mmol/min/ml; normal 0.12 +/- 0), and liver cell necrosis with portal infiltration. In rats whose liver copper was elevated to 1298 +/- 169 micrograms/g (control 18.7 +/- 1.7) by oral copper supplementation, GalN produced much smaller increases in AST (825 +/- 122 IU/l), ALT (103 +/- 15 IU/l) and OCT (0.27 +/- 0.02 mmol/min/ml) and minimal histological damage. Viable bacterial cell counts from faecal homogenates showed that the anaerobically cultured bacteria were reduced on copper-dosing of rats. Therefore the protective effect of copper may be due to a decrease in gut-derived endotoxin acting on the liver, or to an impaired prostaglandin synthesis or perhaps to synthesis of acute phase reactants.
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PMID:Copper protects against galactosamine-induced hepatitis. 365 8

The effects of supplementation with fibronectin on liver damage and survival in rats with galactosamine-induced liver failure were studied. In rats with acute liver failure induced by a low dose of galactosamine, supplementation with purified plasma fibronectin at 3 hr after the administration of galactosamine provided significant increase of plasma fibronectin levels and augmentation of reticuloendothelial system function at 4 hr, significantly higher plasma fibronectin levels and significant protection of liver damage with shorter prothrombin times, lower AST and less histological damage at 48 hr as compared to control animals. Plasma fibronectin levels were inversely correlated with both plasma prothrombin times and AST. Fibronectin supplementation at 6 hr also resulted in the significant decrease of liver damage at 48 hr as evaluated histologically. When rats with liver failure, induced by a high dose of galactosamine, were supplemented with fibronectin at 3 hr, the survival rate was significantly higher than that of control rats. The results indicate that fibronectin supplementation in the early stages of acute liver failure could reduce liver damage and improve the survival of rats with galactosamine-induced liver failure.
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PMID:Protective effects of fibronectin in galactosamine-induced liver failure in rats. 379 10

The effects of minimal acute liver injury on circulating ferritin levels have been examined in the rat both in vivo and in the isolated perfused liver. Liver damage produced by 6 mmol/kg of D-galactosamine (GalN) in vivo resulted in a marked rise in plasma ferritin levels 4 h after administration, 2 h before any significant increase in plasma aspartate transaminase. In the isolated perfused liver, damage produced by 5mM GalN introduced into the perfusate also produced an early increase in circulating ferritin before any evidence of release of intracellular enzymes, or alteration in liver histology as assessed by light microscopy was apparent. It is concluded that minimal acute liver damage results in a pronounced increase in circulating ferritin levels before other evidence of liver dysfunction. This is unlikely to be due solely to increased release from damaged cells but may rather result from an alteration in the mechanism responsible for ferritin homeostasis.
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PMID:The effect of acute liver damage on circulating ferritin levels in vivo and in the isolated perfused rat liver. 398 31

1. In confirmation of previous work, administration of d(+)-galactosamine (0.5-0.75g/kg body wt.) to rats caused a hepatitis with histological evidence of liver damage and a 9-fold rise in aspartate aminotransferase activity in serum. 2. There was a significant elevation of blood lactate and pyruvate concentrations in 24h-starved rats treated with galactosamine but no change in the [lactate]/[pyruvate] ratio. 3-Hydroxybutyrate and acetoacetate concentrations in blood were decreased. 3. The changes in the concentrations of lactate, pyruvate and ketone bodies in the freeze-clamped liver were parallel to those observed in the blood. 4. In the livers of 24h-starved galactosamine-treated rats there were large increases in the concentrations of alanine (3-fold), citrate (5-fold), 2-oxoglutarate (4-fold), with smaller increases in malate, glutamate and aspartate. There was a 4-fold rise in the value of the mass-action ratio of the alanine aminotransferase system in the livers of galactosamine-treated rats when compared to controls. 5. There was a significant decrease in the activities of aspartate and alanine aminotransferases in the cytoplasm and the soluble fraction of sonicated homogenates of the livers of rats treated with galactosamine. The activity of phosphoenolpyruvate carboxylase was decreased by 75% of the control value. 6. Glucose synthesis from lactate in perfused livers from galactosamine-treated rats was inhibited 39% when compared with controls. 7. The results indicate that the conversion of lactate into glucose is decreased in the livers of galactosamine-treated rats and that this decrease may be due to the loss of phosphoenolpyruvate carboxylase from damaged hepatocytes.
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PMID:Metabolic studies in experimental liver disease resulting from D(+)-galactosamine administration. 465 44

The effects of allyl alcohol, galactosamine, bromobenzene, and corn oil administration were evaluated in male Fischer 344 rats at 4 to 5, 14 to 15, and 24 to 25 months of age to determine if susceptibility to hepatotoxic injury is modified as a consequence of aging. Parameters measured were (1) severity of hepatocellular necrosis as judged by light microscopy of liver sections, (2) activity of alanine aminotransferase and aspartate aminotransferase in serum, and (3) hepatic microsomal cytochrome P-450 content and NADPH-cytochrome P-450 reductase activity. Allyl alcohol toxicity was more severe in middle-aged and old rats than in young-adult rats. In contrast, galactosamine and bromobenzene toxicities were slightly decreased or unchanged in old rats. The results demonstrate that aging has effects on some types of chemically induced hepatotoxicity.
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PMID:Influence of aging on the susceptibility of rats to hepatotoxic injury. 671 May 24

In order to test the possibility of metallothionein (MT) transfer from liver to kidney, experimental hepatic disorders produced by hepatotoxins were examined to study the release of MT from liver. 109Cd exposed rats were treated with carbon tetrachloride (CCl4) and the distribution of cadmium (Cd) in the body was studied. Hepatic Cd was significantly decreased corresponding to the dose of CCl4. Cd in plasma, kidney, and urine was increased remarkably in contrast with the decrease of hepatic Cd. No remarkable changes in Cd of other tissues and feces were observed. These phenomena were produced by other hepatotoxins like galactosamine and ethionine, and long-term administration of Cd, too. In every case that plasma Cd increased markedly, plasma levels of glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), and lactate dehydrogenase (LDH) rose simultaneously, and a significant, positive correlation between Cd concentration and each of enzyme activities in plasma was observed. Cd in hepatic supernatant of CCl4 treated rats was bound mostly to MT fraction, and in kidney, plasma or urine, Cd was also in the form of MT. These results suggest that hepatic MT can be released into blood in the same manner as hepatic enzymes and transported to kidney and urine in some types of hepatic disorders.
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PMID:Effects of hepatic disorder on the fate of cadmium in rats. 705 69

The complex cell-wall polysaccharide, C-substance, was isolated from Streptococcus pneumoniae type 1 and purified by DEAE-cellulose (HCO3(-) form) and Sephadex column chromatography. The complete structure of this antigen was obtained by the application of methylation and 1H NMR and 13C NMR spectroscopic techniques to a series of oligosaccharide fragments obtained by the selective degradation of the N-acetylated antigen. Native C-substance is composed of the following repeating unit: beta-D-Glup-1 leads to 3-alpha-AAT-Galp-1 leads to 4-alpha-D-GalNAcp-1 leads to 3-beta-D-GalNH2p-1 leads to 1'-ribitol-5-phosphate where AATGal is 2-acetamido-4-amino-2,4,6-trideoxygalactose. Phosphocholine substituents are situated at O(6) of the unacetylated galactosamine residues, and the repeating units are linked through a diphosphate ester from ribitol to O(6) of the beta-D-glucopyranose residue. This structure has also been shown to be common to C-substances prepared from a number of other pneumococcal types based on the criterion of their identical 13C NMR spectra.
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PMID:Structure of the complex polysaccharide C-substance from Streptococcus pneumoniae type 1. 742 24


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