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)

The hepatoprotective effect of Ban-zhi-lian was investigated in three kinds of experimental models. The animals were treated with Ban-zhi-lian (300 mg/kg, p.o.) at 2,4, and 10 hours after carbon tetrachloride (32 l/kg, i.p.), acetaminophen (600 mg/kg, i.p.), and beta-D-galactosamine (188 mg/kg, i.p.) administration. Significant protective effects from these hepatotoxins were expressed. This protection was evidenced by comparing the serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), and histopathologic examination in animals treated and untreated with Ban-zhi-lian. Serum enzyme activities were significantly lower in Ban-zhi-lian-treated groups. In the histopathologic observation, liver damage induced by three hepatotoxins was markedly improved in Ban-zhi-lian treated animals. These results demonstrated that Ban-zhi-lian has a protective effect against experimental liver damage induced by various hepatotoxins.
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PMID:Protective and therapeutic effects of ban-zhi-lian on hepatotoxin-induced liver injuries. 803 Jun 17

Acute hepatic failure was induced in 50 male rabbits by D-galactosamine HCl (1 g per kg bw), and the effects of prostaglandin E1 on this model were investigated. Twelve hours after the administration of D-galactosamine HCl, a continuous infusion of prostaglandin E1 (2 micrograms.kg-1.h-1 or 20 micrograms.kg-1.h-1) was started. Ten animals in each group were observed until the time of death and mean survival times were compared between the groups. Five animals in each group were used for the determination of regional blood flows and brain water content. After the injections of D-galactosamine HCl, serum aspartate transaminase and alanine transaminase activity rose markedly and prothrombin time was prolonged. The administration of prostaglandin E1 did not affect these levels. However, the survival time in the prostaglandin E1 20 micrograms.kg-1.h-1 group (48.2 +/- 10.4 h) was significantly longer (p < 0.005, p < 0.01) than those in the untreated group (24.9 +/- 5.0 h) and the prostaglandin E1 2 micrograms.kg-1.h-1 group (28.1 +/- 5.8 h). Prostaglandin E1 20 micrograms.kg-1.h-1 inhibited elevations of blood urea nitrogen and creatinine and significantly inhibited the decrease of urine volume and urinary sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of prostaglandin E1 on experimental acute hepatic failure in rabbits: prostaglandin E1 prevents the development of multiple-organ failure. 805 85

Endogenous lipopolysaccharide has been implicated as a cofactor in the hepatocellular injury and death resulting from toxic liver injury. To prevent this lipopolysaccharide-induced injury and to further understand the mechanism of this effect, an anti-lipopolysaccharide antibody was administered to rats in which toxic hepatocellular injury was induced. Rats were given the hepatotoxin galactosamine together with an isotypic control antibody B55 or the anti-lipopolysaccharide antibody E5. E5 treatment resulted in reductions of serum AST levels of 43% at 36 hr (p < 0.02) and 60% at 48 hr (NS) after galactosamine administration. These decreases in AST values were accompanied by diminished histological evidence of injury and inflammation. In carbon tetrachloride-induced liver injury, E5 similarly reduced serum AST levels at 36 and 48 hr by 47% (p < 0.04) and 54% (p < 0.03), respectively. E5 treatment was equally effective in reducing AST levels 48 hr after administration of carbon tetrachloride, whether the initial dose of antibody was given 1 hr before or 3 or 6 hr after the administration of this toxin. To understand the mechanism of this E5 effect, the activation of the toxic cytokine tumor necrosis factor-alpha and the chemotactic cytokine monocyte chemoattractant protein 1 was examined by Northern-blot analysis of RNA from rat livers after galactosamine-induced injury and treatment with B55 or E5. Despite E5's efficacy in reducing hepatocellular damage, E5 treatment did not affect the timing or magnitude of tumor necrosis factor-alpha or monocyte chemoattractant protein 1 activation during galactosamine-induced injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipopolysaccharide-neutralizing antibody reduces hepatocyte injury from acute hepatotoxin administration. 817 53

Effects of electrical stimulation of the hepatic nerves on acute liver damage were examined using isolated rat liver perfused in situ, 24 hours after intraperitoneal injection with D-galactosamine (800 mg/kg). The leakage of lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) from the liver was used as markers of acute liver damage. In perfused livers after treatment with galactosamine, nerve stimulation (20 V, 20 Hz, 2 ms) increased the leakage of LDH and AST about 3-fold over the basal level accompanied by the decrease in flow rate, whereas with control livers the leakage of LDH and AST into the effluent was almost undetectable throughout the perfusion. The rapid increase in the leakage of LDH and AST was observed during nerve stimulation even under conditions where perfusion flow was maintained constant. Such effects of hepatic nerve stimulation on galactosamine-treated livers were mimicked well by infusion of noradrenaline or phenylephrine, and inhibited by the alpha1-antagonist bunazosin. Artificial reduction of perfusion flow alone did not induce the rapid leakage of LDH and AST into the effluent. On the other hand, low concentration (10 nmol/L) of noradrenaline only minimally decreased the flow rate but apparently augmented liver cell damage. The acute liver damage augmented by noradrenaline was dependent on extracellular Ca2+. These results indicate that in the liver, already having been injured slightly, the activation of hepatic sympathetic nerves and circulating catecholamines exaggerates acute liver damage through an action on liver cells, which depends on the influx of extracellular Ca2+.
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PMID:Exaggeration of acute liver damage by hepatic sympathetic nerves and circulating catecholamines in perfused liver of rats treated with D-galactosamine. 861 32

The effects of dietary protein on the elevation of activities of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in D-galactosamine-injected rats were investigated. The rats fed with experimental diets containing test protein sources for 2 weeks were injected with D-galactosamine (0.8 g.kg-1 body weight). The activities of AST and ALT in serum were assayed after 20 h. According to the results, these enzyme activities in the rats fed 40% casein diet were higher than those of 5, 10, or 20% casein groups. In the 40% gluten group, these enzyme activities were lower than in the 40% casein group. This difference was not considered to be caused by the deficit of L-lysine and L-threonine in gluten. The extent of the reduction of UTP and UDP-glucose in liver by D-galactosamine was almost the same in the 40% gluten and 40% casein groups. These results suggest that levels and quality of dietary protein affect the susceptibility of animals to the hepatotoxin D-galactosamine and dietary gluten was found to alleviate the elevation of serum transaminases in rats by the drug.
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PMID:Dietary wheat gluten alleviates the elevation of serum transaminase activities in D-galactosamine-injected rats. 878 Sep 70

Ayurvedic and other 'traditional' medical practitioners in Sri Lanka use the mature leaves of the plant Osbeckia octandra for its hepatoprotective properties. In this study the effects of an aqueous extract of Osbeckia octandra against injury induced by D-galactosamine and tert-butyl hydroperoxide (TBH) were investigated in freshly isolated rat hepatocytes. The plant extract (500 micrograms/ml) significantly reduced the inhibition of protein synthesis (as assessed by the incorporation of 14C-leucine into protein) in hepatocytes incubated for 1 h with 10 mM galactosamine by a mean of 25.6 +/- 3.6% and decreased the release of cellular lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) enzyme activities into the medium by 55.3% and 32.8%, respectively. With TBH, the plant extract decreased lipid peroxidation (estimated from malondialdehyde formation) by a mean of 29.9 +/- 1.1% together with a 46.8% and 54.7% decrease in the release of LDH and AST, respectively into the incubation medium. Significant protection was also obtained when the Osbeckia extract was added to the incubation medium up to 30 min after pre-exposure of the hepatocytes to either galactosamine or, to a lesser extent, TBH. The results support the use of Osbeckia as a hepatoprotective agent.
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PMID:Protective effects of Osbeckia octandra against galactosamine and tert-butyl hydroperoxide induced hepatocyte damage. 884 86

Acute liver failure is accompanied by a high rate of bacterial and septic complications. Arginine has a potent effect on the immune system and modulates bacterial clearance in septic models. We studied the effect of oral arginine supplementation on the extent of liver injury and the associated bacterial translocation in an acute liver injury model in rats. Sprague-Dawley rats were divided into normal, liver injury, and arginine supplemented groups. In the arginine group, 2% arginine was supplemented daily through a nasogastric tube for 8 d. Acute liver injury was induced on the eighth day by intraperitoneal injection of D-galactosamine (1.1 g/kg body wt). Samples were collected 24 h after the liver injury. In the arginine-supplemented group, alkaline phosphatase, bilirubin, and aspartate aminotransferase were reduced significantly compared with the acute liver injury control group. The results of bacterial translocation in the arginine-supplemented group showed a significantly reduced number of translocated bacteria to the liver and mesenteric lymph nodes than occurred in the acute liver injury group. The histological study of the liver in arginine-supplemented group showed scattered areas of hepatocellular necrosis and inflammatory cell infiltration, and in the acute liver injury group there were more and widespread hepatocellular necrosis and inflammatory cell infiltration. Oral supplementation of arginine in an acute liver injury model improves significantly the state of the liver injury and reduces bacterial translocation to the liver and mesenteric lymph nodes.
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PMID:Oral arginine supplementation in acute liver injury. 887 48

This study was done to clarify the effects of dietary wheat gluten on the hepatotoxic action of D-galactosamine (GalN) and endotoxin (Etx). Male Wistar rats fed a high casein or high gluten (supplemented with L-Lys and L-Thr) diet were injected with GalN or Etx, and the plasma glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, and lactase dehydrogenase activities were examined 20 h later. In rats fed the high gluten diet, these enzyme activities were lower than in the high casein group after injection of 800 mg/kg of GalN. But such a difference between the casein and gluten groups was not clear when they were treated with 400 mg/kg of GalN nor observed even after injection of Etx or Etx+GalN (400 mg/kg). Similarly these was no difference in the plasma concentrations of Etx, tumor necrosis factor-alpha, or interferon-gamma in the rats receiving an injection of 800 mg/kg of GalN between both dietary groups. These results suggest that dietary gluten affords protection against hepatic injury by a high dose of GalN but not by a low dose of GalN and/or Etx.
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PMID:Effects of dietary gluten on the hepatotoxic action of galactosamine and/or endotoxin in rats. 890 Nov 1

The effect of high-dose alanine on survival and liver function in rats with acute liver failure caused by a lethal dose of D-galactosamine (D-gal) was studied. Greater than 90% of control animals died within 5 days after D-gal injection, but alanine significantly decreased mortality, even when treatment was started at 12 hours after D-gal injection. Alanyl-glutamine had a slight effect, but glucose produced no improvement. There was marked elevation of the plasma aspartate transaminase (AST) level, prolongation of the prothrombin time, and a decrease of the arterial ketone body ratio (AKBR) and hepatic adenosine triphosphate (ATP) content within 12 hours after D-gal injection. The AKBR decreased in parallel with the decrease of the hepatic ATP content. These parameters were significantly improved in alanine-treated rats at 48 hours after the induction of liver damage, which was just before control rats began to die. The hepatic ATP content was significantly greater in alanine-treated rats than in the other rats (including normal controls), but glucose pretreatment had no effect. It was also found that the liver labeling index of partially hepatectomized rats was significantly elevated by alanine administration at 3 hours before measurement. In conclusion, alanine is effective for the treatment of experimental acute liver failure, probably caused by promotion of ATP synthesis. Ala may be a good candidate for clinical application because of its preventive effect on hepatocyte necrosis and its promotive effect on liver regeneration.
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PMID:Effect of alanine on D-galactosamine-induced acute liver failure in rats. 890

The hepatoprotective effect of Huanglian-Jie-Du-Tang (HLJDT), a Chinese medicinal prescription, was investigated in three kinds of experimental models. The animals were treated with HLJDT (300 mg/kg, p.o.) thrice at 2, 4 and 10 hours after administration with carbon tetrachloride (32 microliters/kg, i.p.), acetaminophen (600 mg/kg, i.p.) and beta-D-galactosamine (188 mg/kg, i.p.). Significant hepatoprotective effects on carbon tetrachloride and acetaminophen induced liver injuries were noted, but no significant effect on beta-D-galactosamine induced liver injury was observed. These hepatoprotective effects were evidenced by comparing the serum glutamate oxaloacetate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT) levels in HLJDT treated and untreated groups. Serum enzyme activities in the carbon tetrachloride and acetaminophen experiments were significantly lower in the treated groups while the herbal prescription has no effect on the beta-D-galactosamine experiment. These results demonstrated that Huanglian-Jie-Du-Tang has a hepatoprotective effect against experimental liver injuries induced by specific hepatotoxins, and therefore may be useful in treating some, but not all, liver injuries.
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PMID:Protective and therapeutic effects of huanglian-jie-du-tang on hepatotoxin-induced liver injuries. 898 34


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