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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The protective effect of dietary L-glutamine against the hepatotoxic action of D-galactosamine (GaIN) was investigated by model experiments with rats. Rats fed with 20% casein diets containing 10% free amino acids were injected with GaIN, and the serum aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase activities and the hepatic glycogen content were assayed 20 hours after the injection. These enzyme activities in the group fed with 10% L-glutamine diet for 8 days were lower than those in the groups fed with the control, 10% L-glutamic acid and 10% L-alanine diets for 8 days. The more prolonged the feeding period with the 10% L-glutamine diet was, the more the serum activity levels of such enzymes were decreased. Although neomycin also lowered these enzyme activities, its simultaneous ingestion with neomycin did not show any additive or synergistic effect. The hepatic glycogen content in the 10% glutamine group still remained high after the GaIN treatment. It is therefore assumed that the effectiveness of glutamine intake would have been mediated by glycogen metabolism rather than by uridine metabolism.
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PMID:Effect of dietary L-glutamine on the hepatotoxic action of D-galactosamine in rats. 898 89

Dimaprit, a selective histamine H2 receptor agonist, was examined in experimental models of endotoxin shock and hepatitis in mice. Injection of lipopolysaccharide (8 mg/kg i.v.) into Balb/c mice resulted in an elevation of plasma tumor necrosis factor-alpha (TNF-alpha), reaching the maximal level at 1 h post-lipopolysaccharide (1147 U/ml). Oral administration of dimaprit 200 mg/kg, 1 h prior to lipopolysaccharide challenge, inhibited the increase in plasma TNF-alpha by 71% and also the survival rate was increased to 62.5% from 8.3% in the disease control. In a mouse hepatitis model, simultaneous injection of galactosamine (700 mg/kg i.v.) and lipopolysaccharide (3 micrograms/kg i.v.) into Balb/c mice caused an increase in plasma TNF-alpha, peaking at 1 h, followed by an elevation of L-alanine aminotransferase (E.C.2.6.1.2) activity at 4 h onward. Oral administration of dimaprit 200 mg/kg, 1 h prior to galactosamine and lipopolysaccharide, reduced the increase in plasma TNF-alpha by 99% and L-alanine aminotransferase by 82%. In vitro, dimaprit dose dependently inhibited the production of TNF-alpha in mouse peritoneal macrophages and human peripheral blood monocytes stimulated with lipopolysaccharide with IC50 values of 1 microM. The decrease in TNF-alpha production by dimaprit was reversed by cimetidine, a histamine H2 receptor antagonist. Dimaprit dose dependently suppressed TNF-alpha mRNA in human peripheral blood monocytes. These results suggest that activation of the histamine H2 receptor downregulates the production of TNF-alpha, and that histamine may be an important regulator in pathological conditions in which TNF-alpha plays an important role.
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PMID:Efficacy of a selective histamine H2 receptor agonist, dimaprit, in experimental models of endotoxin shock and hepatitis in mice. 908 75

Using transmission electron microscopy and biochemical analysis, the effect of cuban red propolis against hepatitis induced by 1,000 mg kg-1 of galactosamine in rats was studied. An ethanolic extract of propolis was prepared and it was given to rats at doses of 10, 50 and 100 mg kg-1, 30 min before the hepatotoxin. Propolis extract prevented hepatocytes alterations induced by galactosamine. It was mainly seen in rough endoplasmic reticulum, Golgi complex, nucleus and plasma membrane of hepatocytes. Propolis extract induced reversion of the increased activity of alanine aminotransferase and malondialdehyde concentration in the serum of rats treated with galactosamine. The probable role of antioxidant activity of propolis in the prevention of hepatitis is discussed in this paper.
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PMID:Effects of Cuban red propolis on galactosamine-induced hepatitis in rats. 914 8

Dietary supplementation with powder of a green tea extract suppressed the enhancement of plasma alanine aminotransferase and aspartate aminotransferase activities induced by D-galactosamine, but not by carbon tetrachloride, in a dose-dependent manner in rats. The minimum dose to cause a significant effect was 1 to 2%. Drinking green tea also suppressed plasma enzyme activities. These results indicate that green tea had a liver injury-preventive effect.
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PMID:Green tea suppresses D-galactosamine-induced liver injury in rats. 957 96

Liver injury accompanied by apoptosis of hepatocytes was provoked in mice by an intravenous injection of recombinant tumor necrosis factor-alpha (rTNF-alpha) (1.0 microg/kg) together with an intraperitoneal injection of D-galactosamine (D-gal) (500 mg/kg). Injection of various doses of dibutyryl cAMP (DBcAMP) protected mice from TNF-alpha/D-gal-induced liver injury as assessed by serum alanine aminotransferase (ALT) levels, histological examination and DNA fragmentation. DBcAMP significantly enhanced the Hsp70 expression in the hepatocytes of D-gal/TNF-alpha-injected mice in close correlation with suppression of liver injury. DBcAMP induced Hsp70 expression in the hepatocyte in vitro. These results suggest that increase in Hsp70 expression by DBcAMP is involved in protective mechanisms by DBcAMP against TNF-alpha-induced liver injury in D-gal-sensitized mice.
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PMID:Dibutyryl cyclic adenosine monophosphate protects mice against tumor necrosis factor-alpha-induced hepatocyte apoptosis accompanied by increased heat shock protein 70 expression. 967 46

Picrorhiza kurroa (Pk), a known hepatoprotective plant, was studied in experimental and clinical situtations. The standardization of active principles--Picroside 1 and 2 was done with High Performance Liquid Chromatography. Picroside 1 ranged from 2.72 to 2.88 mg/capsule and picroside 2 from 5.50 to 6.00 mg/capsule. In the galactosamine-induced liver injury in rats, Pk at a dose of 200 mg/kg p.o. showed a significant reduction (p < 0.05) in liver lipid content, GOT and GPT. In a randomised, double-blind placebo controlled trial in patients diagnosed to have acute viral hepatitis (HBsAg negative), Pk root powder 375 mg three times a day was given for 2 weeks (n = 15) or a matching placebo (n = 18) was given. Difference in values of bilirubin, SGOT and SGPT was significant between placebo and Pk groups. The time in days required for total serum bilirubin to drop to average value of 2.5 mg% was 75.9 days in placebo as against 27.44 days in Pk group. The present study has shown a biological plausability of efficacy of Pk as supported by clinical trial in viral hepatitis, hepatoprotection in animal model and an approach for standardizing extracts based on picroside content.
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PMID:Picrorhiza kurroa (Kutaki) Royle ex Benth as a hepatoprotective agent--experimental & clinical studies. 971 10

Endotoxin (ET) induces neutrophil sequestration in hepatic sinusoids, the activation of proinflammatory transcription factors (nuclear factor KB [NF-kappaB]) with up-regulation of adhesion molecules on sinusoidal endothelial cells and hepatocytes. However, if galactosamine (Gal) is co-administered with ET, neutrophils transmigrate and attack parenchymal cells. This suggests that a signal from parenchymal cells triggers neutrophil transmigration. In this study, we tested the hypothesis that parenchymal cell apoptosis may induce neutrophil transendothelial migration in the Gal/ET model. Treatment of C3Heb/FeJ mice with 700 mg/kg Gal and 100 microg/kg ET induced tumor necrosis factor alpha (TNF-alpha) formation (13.25 +/- 0.75 ng/mL) and hepatic NF-kappaB activation at 90 minutes; the generation of the C-X-C chemokine KC (2.86 +/- 0.30 ng/mL at 5 hours); sinusoidal neutrophil sequestration (380 +/- 21 polymorphonuclear leukocytes/50 high-power fields) and apoptosis (925% +/- 29% increase of DNA fragmentation; and a 45-fold increase of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells) at 6 hours, followed by transmigration of neutrophils and development of substantial necrosis (38% +/- 3% of hepatocytes; alanine transaminase [ALT]: 1,500 +/- 300 U/L) at 7 hours. Administration of uridine (1,000 mg/kg) did not reduce plasma levels of TNF-alpha and KC, NF-kappaB activation, or polymorphonuclear leukocyte sequestration, but attenuated apoptosis by 90% to 94%. In these livers, neutrophils did not transmigrate and liver injury was prevented (necrosis: < 5%; ALT: 40 +/- 3 U/L). However, massive apoptosis and liver injury initiated by the anti-Fas antibody, Jo2, did not recruit neutrophils into the liver. We conclude that excessive parenchymal cell apoptosis represents an important signal for transmigration of primed neutrophils sequestered in sinusoids during endotoxemia in vivo. However, apoptosis per se does not cause neutrophil sequestration in the liver vasculature.
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PMID:Parenchymal cell apoptosis as a signal for sinusoidal sequestration and transendothelial migration of neutrophils in murine models of endotoxin and Fas-antibody-induced liver injury. 973 84

The effects of dietary oligosaccharides on the hepatotoxic action of D-galactosamine (GalN) were investigated in this study. Male Wistar rats fed with 20% casein diets containing 10% oligosaccharide or D-galactose (Gal) for 2 weeks were injected with GalN (1,900 mg/kg of body weight), and the plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and the hepatic glycogen concentration were examined 20 hours after the injection. The plasma AST and ALT activities in experiment 1 for the Gal + neomycin (NEO) group were significantly lower than those for the control (C), NEO, raffinose (RAF) + NEO and galacto-oligosaccharide (GA-LO) + NEO groups. In experiment 2, these activities were significantly lower in the Gal, Gal + NEO and RAF groups than in the RAF + NEO group when the groups were treated with GalN. On the other hand, in respect of the hepatic glycogen concentration in experiment 1, that of the Gal + NEO group was higher than that of the C, NEO, RAF + NEO or GALO + NEO groups. In experiment 2, this parameter was significantly higher in the Gal, Gal + NEO and RAF groups than in the RAF + NEO group after the GalN treatment. As a result, it is suggested that the GalN-hepatitis-suppressive effects of indigestible oligosaccharides such as RAF or GALO is mediated by the action of intestinal bacteria.
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PMID:Effect of indigestible oligosaccharides on the hepatotoxic action of D-galactosamine in rats. 975 56

Experimental hepatitis induced by tumor necrosis factor in D-(+)-galactosamine-sensitized mice or by an agonistic anti-Fas antibody in normal mice is accompanied by dramatic apoptosis of hepatocytes. Apoptosis is the final result of activation of a cascade of caspases. We used caspase-1-/- mice, generated by gene targeting, to study the role of this protease in TNF- and anti-Fas-induced lethal hepatitis. We found that mutant mice exhibited the typical caspase-1-/- phenotype, since they resisted to a lethal injection of LPS and released no interleukin-1beta in the circulation, in contrast to wild-type littermates. When caspase-1-/- mice were challenged with different doses of tumor necrosis factor/D-(+)-galactosamine or with anti-Fas, no increased survival was observed compared with control mice. Furthermore, apoptosis in the livers of these mice and serum levels of alanine aminotransferase were not reduced. These data indicate that caspase-1 deficiency does not lead to reduced apoptosis in these models, either because caspase-1 is irrelevant in this model or because of functional redundancy.
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PMID:Caspase-1 is not involved in experimental hepatitis in mouse. 1006 84

The protective effects of various kinds of dietary amino acids against the hepatotoxic action of D-galactosamine (GalN) were examined. Male Wistar rats fed with 20% casein diets containing 10% or 5% amino acid for one week were injected with GalN (800 mg/kg body weight), and the serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) activities, the hepatic glycogen concentration, and the serum glucose-level were examined 20 hours after the injection. In the groups with the 10% amino acid diets, activities of AST, ALT, and LDH in serum of 10% L-glutamine (Gln), 10% L-asparagine (Asn), and 10% L-serine (Ser) groups were significantly lower than those of the control group, and in the groups with the 5% amino acid diets, those activities of 5% L-histidine (His), 5% L-tyrosine (Tyr), 5% L-lysine (Lys), and 5% L-glycine (Gly) groups were also lower than those of the control group. The concentration of liver glycogen of 10% Gln-, 10% Asn-, and 10% Ser- groups and those levels of 5% His-, 5% Tyr-, 5% Lys-, and 5% Gly-groups were also significantly higher than that of the control group. As a result, it was found that some kinds of dietary amino acid such as L-Ser, L-Asn, L-His, L-Lys, L-Tyr, and L-Gly, in addition to L-Gln were effective to protect the rats from GalN-induced injury.
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PMID:Effects of various kinds of dietary amino acids on the hepatotoxic action of D-galactosamine in rats. 1019 13


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