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)

Acute toxic hepatic necrosis is common and may be fatal. Predicting clinical outcome may be aided by following serum markers that could indicate recovery or may signify massive (substantial) destruction of functional liver mass. Previously, in a published case of chloroform poisoning, we serially assayed serum biomarkers of hepatocellular necrosis (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase) and markers of hepatocellular regeneration (alpha-fetoprotein, retinol-binding protein, gamma-glutamyl transferase, and des-gamma-carboxyprothrombin). We noted a decline in necrotic markers and a synchronous elevation in regenerative markers, which could be suggestive of a favorable outcome in similar cases. We now report 6 Amanita mushroom poisonings with favorable outcome and 2 fatal acetaminophen poisonings in which the same markers were observed. Our results further support our hypothesis that a sustained decline in serum markers of hepatocyte necrosis with a concurrent elevation in regenerative markers could aid in prediction of favorable outcome in patients with acute liver injury.
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PMID:Biomarkers of liver regeneration allow early prediction of hepatic recovery after acute necrosis. 1047 40

Arylsulfotransferase (AST, EC 2.8.2.22), an enzyme capable of sulfating a wide range of phenol-containing compounds was purified from a Clostridium innocuum isolate (strain 554). The enzyme has a molecular weight of 320 kDa and is composed of four subunits. Unlike many mammalian and plant arylsulfotransferases, AST from Clostridium utilizes arylsulfates, including p-nitrophenyl sulfate, as sulfate donors, and is not reactive with 3-phosphoadenosine-5'-phosphosulfate (PAPS). The enzyme possesses broad substrate specificity and is active with a variety of phenols, quinones and flavonoids, but does not utilize primary and secondary alcohols and sugars as substrates. Arylsulfotransferase tolerates the presence of 10 vol% of polar cosolvents (dimethyl formamide, acetonitrile, methanol), but loses significant activity at higher solvent concentrations of 30-40 vol%. The enzyme retains high arylsulfotransferase activity in biphasic systems composed of water and nonpolar solvents, such as cyclohexane, toluene and chloroform, while in biphasic systems with more polar solvents (ethyl acetate, 2-pentanone, methyl tert-butyl ether, and butyl acetate) the enzyme activity is completely lost. High yields of AST-catalyzed sulfation were achieved in reactions with several phenols and tyrosine-containing peptides. Overall, AST studied in this work is a promising biocatalyst in organic synthesis to afford efficient sulfation of phenolic compounds under mild reaction conditions.
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PMID:Arylsulfotransferase from Clostridium innocuum-A new enzyme catalyst for sulfation of phenol-containing compounds. 1211 26

Chloroform extract of Prunus africana (Hook f. (Rosaceae) did not cause clinical signs or pathology in rats at daily oral doses of up to 1,000 mg/kg for 8 weeks. The extract caused marked clinical signs, organ damage and a 50% mortality rate at a dose of 3.3 g/kg for 6 days. The main lesions observed at this dose were marked centrilobular hepatocellular degeneration and necrosis, diffuse nephrosis, myocardial degeneration, lymphocytic necrosis and neuronal degeneration. The morphological damage in these tissues caused a corresponding rise in blood biochemical parameters namely, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, creatine kinase and blood urea nitrogen. The target organs of toxicity of this extract are the liver, kidney and heart. Overt toxicity occurred only after the administration of multiple doses of 3.3 g/kg body weight. These findings confirm the suitability of this extract for therapeutic use, since the doses used in the therapy of prostate gland are much lower than those used in this study and would therefore not be expected to cause pathological changes.
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PMID:Toxicity of chloroform extract of prunus africana stem bark in rats: gross and histological lesions. 1216 69

The diethyl ether, chloroform, acetone and methanol extract of Nerium indicum leaf were evaluated for their piscicidal activity against common freshwater air breathing predatory fish Channa punctatus. The rank of order of toxicity (LC50) of the leaf extract was, diethyl ether extract (17.34 mg/l)>acetone (40.01 mg/l)>chloroform (40.61 mg/l)>and methanol (106.37 mg/l). There was a significant negative correlation between LC50 values and exposure periods. Thus increase in exposure period, LC50 decreases from 17.34 mg/l (24 h) to >13.58 mg/l (96 h) in the diethyl ether extract. Similar trends were also observed in acetone, chloroform and methanol extracts. Exposure of sub-lethal doses (40% and 80% of LC50) of the diethyl ether extract of N. indicum leaf (which has maximum piscicidal activity) for 24 or 96 h caused significant alteration in the level of total protein, total free amino acid, nucleic acid, glycogen, pyruvate, lactate and activity of enzyme protease, phosphatases, alanine aminotransferase, aspartate aminotransferase and acetylcholinesterase in liver and muscle tissue. The alterations in all the above biochemical parameters were significantly (P<0.05) time and dose dependent. There was a significant recovery in all the above biochemical parameters, in both liver and muscle tissues of fish after the seventh day of the withdrawal of treatment. Thus, the leaf extracts of N. indicum have potent piscicidal activity against fish C. punctatus and also significantly affect both aerobic and anaerobic pathway of respiration in fish.
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PMID:Control of common freshwater predatory fish, Channa punctatus, through Nerium indicum leaf extracts. 1450 8

Terminalia catappa L. leaves have been shown to protect against acute liver injury produced by some hepatotoxicants, but the active components and mechanisms are not clear. This study was designed to characterize the protective effects of the chloroform fraction of the ethanol extract of T. catappa leaves (TCCE) against carbon tetrachloride (CCl4)-induced hepatotoxicity in mice, and analyze the changes in expression level of interleukin-6 (IL-6) in the process. It was found that TCCE pretreatment (10 or 30 mg/kg, ig) protected mice from CCl4 toxicity, as evidenced by the reversed alterations in serum alanine aminotransferase (sALT) and serum aspartate aminotransferase (sAST) activities. Additionally liver tissues were subjected to RT-PCR, Western blot and immunohistochemistry to analyze changes in IL-6 expression. It was found that TCCE markedly suppressed the CCl4-induced over-transcription of IL-6 gene. Consistent with the result, the expression of IL-6 protein was also blocked by TCCE in CCl4-stimulated mice, especially in the area around central vein on liver tissue section. In conclusion, TCCE is effective in protecting mice from the hepatotoxicity produced by CCl4, and the mechanisms underlying its protective effects may be related to the inhibition on the overexpression of IL-6 mainly around terminal hepatic vein.
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PMID:Inhibitory effect of TCCE on CCl4-induced overexpression of IL-6 in acute liver injury. 1551 51

The aim of this study was to evaluate the effect of the chloroform extract of Terminalia catappa L. leaves (TCCE) on carbon tetrachloride (CCl(4))-induced acute liver damage and D-galactosamine (D-GalN)-induced hepatocyte injury. Moreover, the effects of ursolic acid and asiatic acid, two isolated components of TCCE, on mitochondria and free radicals were investigated to determine the mechanism underlying the action of TCCE on hepatotoxicity. In the acute hepatic damage test, remarkable rises in the activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) (5.7- and 2.0-fold) induced by CCl(4) were reversed and significant morphological changes were lessened with pre-treatment with 50 and 100 mg kg(-1) TCCE. In the hepatocyte injury experiment, the increases in ALT and AST levels (1.9- and 2.1-fold) in the medium of primary cultured hepatocytes induced by D-GalN were blocked by pre-treatment with 0.05, 0.1, 0.5 g L(-1) TCCE. In addition, Ca(2+)-induced mitochondrial swelling was dose-dependently inhibited by 50-500 microM ursolic acid and asiatic acid. Both ursolic acid and asiatic acid, at concentrations ranging from 50 to 500 microM, showed dose-dependent superoxide anion and hydroxyl radical scavenging activity. It can be concluded that TCCE has hepatoprotective activity and the mechanism is related to protection of liver mitochondria and the scavenging action on free radicals.
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PMID:Hepatoprotective activity of Terminalia catappa L. leaves and its two triterpenoids. 1552 53

The hepatoprotective activity of aerial parts of Tridax procumbens was investigated against d-Galactosamine/Lipopolysaccharide (d-GalN/LPS) induced hepatitis in rats. d-GalN/LPS (300 mg/kg body weight/30 microg/kg body weight)-induced hepatic damage was manifested by a significant increase in the activities of marker enzymes (aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase and gamma glutamyl transferase) and bilirubin level in serum and lipids both in serum and liver. Pretreatment of rats with a chloroform insoluble fraction from ethanolic extract of Tridax procumbens reversed these altered parameters to normal values. The biochemical observations were supplemented by histopathological examination of liver sections. Results of this study revealed that Tridax procumbens could afford a significant protection in the alleviation of d-GalN/LPS-induced hepatocellular injury.
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PMID:Hepatoprotective activity of Tridax procumbens against d-galactosamine/lipopolysaccharide-induced hepatitis in rats. 1592 95

The protective effects of chloroform extracts of Terminalia catappa L. leaves (TCCE) on carbon tetrachloride (CCl4)-induced liver damage and the possible mechanisms involved in the protection were investigated in mice. We found that increases in the activity of serum aspartate aminotransferase and alanine aminotransferase and the level of liver lipid peroxidation (2.0-fold, 5.7-fold and 2.8-fold) induced by CCl4 were significantly inhibited by oral pretreatment with 20, 50 or 100 mg/kg of TCCE. Morphological observation further confirmed the hepatoprotective effects of TCCE. In addition, the disruption of mitochondrial membrane potential (14.8%), intramitochondrial Ca2+ overload (2.1-fold) and suppression of mitochondrial Ca2+-ATPase activity (42.0%) in the liver of CCl4-insulted mice were effectively prevented by pretreatment with TCCE. It can be concluded that TCCE have protective activities against liver mitochondrial damage induced by CCl4, which suggests a new mechanism of the hepatoprotective effects of TCCE.
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PMID:Effective protection of Terminalia catappa L. leaves from damage induced by carbon tetrachloride in liver mitochondria. 1616 7

Mycelia of Antrodia cinnamomea were extracted with chloroform and hot water. A neutral polysaccharide named ACN2a separated from the water extract was purified using 10% CCl3COOH, and repeated column chromatography on HW-65 and DE-52 cellulose. Its structure was determined by chemical and spectroscopic analyses. ACN2a was composed of Gal, Glc, Fuc, Man and GalN (in the ratio 1:0.24:0.07:0.026:faint), in which an alpha-D-(1-->6)-Gal linkage accounted for 73% of all linkages. The ratio of branch points was about 16% of the total residual numbers, and branches were attached to C-2 of galactosyl residues of the main chain. ACN2a had an average molecular weight of 12.9x10(5) Daltons, [alpha]D25=+115 degrees (c=0.44, H2O); [eta]=0.0417dl.g-1, Cp=0.2663 cal/(g. degrees C). The hepatoprotective effect of ACN2a was evaluated using a mouse model of hepatic injury that was induced by Propionibacterium acnes (P. acnes) and lipopolysaccharide (LPS). The administration of ACN2a (0.4, 0.8 g/kg/d, p.o.), significantly prevented increases in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzyme activities in mice treated with P. acnes-LPS, indicating hepatoprotective activity in vivo.
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PMID:Protective effects of a neutral polysaccharide isolated from the mycelium of Antrodia cinnamomea on Propionibacterium acnes and lipopolysaccharide induced hepatic injury in mice. 1659 52

Oral administration of alcoholic extracts of Schouwia thebica Webb showed that extracts are safe for human use. The studied extracts are considered safe, since they failed to induce death of mice in doses up to 4000 mg/kg body weight. Hepatoprotective activity was studied for the total alcoholic extracts. The total extract was fractionated in turn with diethyl ether, chloroform, ethyl acetate, and n-butanol, respectively. These extracts were tested for possible hepatoprotective activity. It was found that the ethyl acetate and n-butanol extracts of S. thebica Webb showed hepatoprotective activity. These extracts significantly reduced the increase in activities of ALT, AST, and GGT, and levels of glucose, triglycerides, and cholesterol in serum of CCl(4)-treated rats. The extracts showing activity were found to contain flavonoids; one new compound, chrysoeriol-7-O-xylosoide- (1,2)-arabinofuranoside (2), in addition to another known four compound chrysoeriol (1), quercetin (3), quercetin-7-O-rhamnoside (4), and kaempferol-3-O-beta-D-glucoside (5). The isolated new compound was mainly found to be responsible for this activity when tested on animals in the laboratory. The structures were established by melting point, UV spectroscopy, EI-Mass, Fab-Mass, and 1D and 2D NMR spectroscopic techniques on a 600MHz instrument.
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PMID:Hepatoprotective activity of Schouwia thebica webb. 1679 83


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