Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present research was conducted to evaluate the effect of mitogen pre-exposure on CCl4-induced hepatotoxicity. Male Wistar rats were administered a single i.p. injection of CCl4 (0.3 ml kg-1 in corn oil) 48 h following either a single dose of lead nitrate (0.33 mg kg-1) or distilled water via i.v. injection. Hepatotoxicity, as measured by serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, was monitored 6, 24, 48, 72 and 120 h after CCl4 exposure. The lead nitrate-pretreated rats displayed markedly lower serum ALT and AST levels at 24, 48 and 72 h than rats pretreated with distilled water. However, treatment with the antimitotic agent colchicine did not alter the lead-induced protection. These findings suggest that the lead-induced protection is not associated with the major mitogenic response of lead, despite its strong temporal association. A critical review of the available toxicological data also argues against the lead protection being a function of its capacity to inhibit cytochrome P-450.
 ...
PMID:Decrease in hepatotoxicity by lead exposure is not explained by its mitogenic response. 778 58

The study was performed on 4 groups of male Wistar rats, receiving p.o. through 3 months every day: 1). Sodium nitrite in dose 30 mg/kg b.w. x day (0.2 LD50); 2). Cupric chloride in dose 4.67 mg/kg b.w. x day (0.03 LD50); 3 ). Cupric chloride and sodium nitrite in amounts as above, and 4). Control group--received dest. water. The activity of alanine aminotransferase (AlAT), aspartate aminotransferase (AspAT), gamma-glutamyltransferase (GGTP-ase) and creatinine and urea level in blood plasma were determined 24 hours after the last application of compounds. There was showed, that every day rats' intoxication with sodium nitrate during 90 days caused the significant increase of gamma-glutamyltransferase activity and decrease of urea level in the blood plasma. Subchronic exposure to copper and copper with sodium nitrate causes no effect on biochemical parameters were studied.
 ...
PMID:[Evaluation of the combined effect of cupric chloride and sodium nitrite on selected biochemical parameters in rat plasma (subchronic exposure)]. 861 20

To evaluate the role of nitric oxide (NO) in hepatic microcirculation and liver injury during endotoxemia, we studied O2 transport in the hepatic microcirculation of endotoxin-infused rats. Rats were continuously infused with Escherichia coli lipopolysaccharide (LPS) (0.8 mg/kg/h) for 7 hours. LPS increased the plasma levels of NO2- + NO3- and aspartate transaminase (AST), and decreased the bile flow rate and hepatic adenosine triphosphate (ATP) level. Hepatic microcirculation was evaluated by two methods: reflectance spectrophotometry showed a decrease in the oxygenation of hemoglobin (Hb) in the liver, and dual-spot microspectroscopy indicated that LPS administration decreased blood velocity, the oxygenation of Hb, and O2 release from sinusoids to hepatocytes. The observed decreases in the O2 transport parameters were prominent in pericentral sinusoids. All of these phenomena were further aggravated by the administration of N(w)-nitro-L-arginine methyl ester (L-NAME) (5 mg/kg/h) plus LPS, and by aminoguanidine (AMG) (5 mg/kg/h) plus LPS, and these could be reversed by the concomitant administration of L-arginine (L-Arg) (100 mg/kg/h). These results suggest that deterioration of hepatic oxygen transport and liver function induced by endotoxin can be ameliorated by NO.
 ...
PMID:Role of nitric oxide in oxygen transport in rat liver sinusoids during endotoxemia. 925 43

1 Here we compared the effects of various inhibitors of the activity of protein tyrosine kinase on (i) the expression of the activity of the inducible isoform of nitric oxide (NO) synthase (iNOS) caused by endotoxin (lipopolysaccharide, LPS) in cultured macrophages, (ii) the induction of iNOS and cyclooxygenase 2 (COX-2) protein and activity in rats with endotoxaemia, and (iii) the circulatory failure and organ dysfunction caused by LPS in the anesthetized rat. 2 Activation of murine cultured macrophages with LPS (1 microgram ml-1) resulted, within 24 h, in a significant increase in nitrite (an indicator of the formation of NO) in the cell supernatant. This increase in nitrate was attenuated by the tyrphostins AG126, AG556, AG490 or AG1641 or by genistein in a dose-dependent fashion (IC50: approximately 15 microM). In contrast, tyrphostin A1 (an analogue of tyrphostin AG126) or daidzein (an analogue of genistein) had no effect on the rise in nitrite caused by LPS. 3 Administration of LPS (E. coli, 10 mg kg-1, i.v.) caused hypotension and a reduction of the pressor responses elicited by noradrenaline (NA, 1 microgram kg-1, i.v.). Pretreatment of rats with the tyrphostins AG126, AG490, AG556, AG1641 or A1 attenuated the circulatory failure caused by LPS. Although genistein attenuated the vascular hyporeactivity to NA, it did not affect the hypotension caused by LPS. Daidzein did not affect the circulatory failure caused by LPS. 4 Endotoxaemia for 360 min resulted in rises in the serum levels of (i) urea and creatinine (indicators of renal failure), (ii) alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin and gamma-glutamyl transferase (gamma GT) (indicators of liver injury/dysfunction), lipase (an indicator of pancreatic injury) as well as lactate (an indicator of tissue hypoxia). None of the tyrosine kinase inhibitors tested had a significant effect on the rise i the serum levels of urea, but the tyrphostins AG126, AG556 or A1 significantly attenuated the rises in the serum level of creatinine caused by LPS. In addition, all tyrphostins and genistein attenuated the liver injury/failure, the pancreatic injury, the hypoglycaemia and the lactic acidosis caused by LPS. In contrast, daidzein did not reduce the organ injury/dysfunction or the lactic acidosis caused by LPS. 5 Injection of LPS resulted (within 90 min) in a substantial increase in the serum level of tumor necrosis factor alpha (TNF alpha), which was attenuated by pretreatment of LPS-rats with any of the tyrphostins used. Genistein, but not daidzein, also reduced the rise in the serum levels of TNF alpha caused by LPS. Endotoxaemia for 6 h also resulted in a substantial increase in the expression of iNOS and COX-2 protein and activity in the lung, which was attenuated by pretreatment of LPS-rats with the tyrphostins AG126, AG556 or genistein, but not by daidzein. 6 Thus, tyrphostins (AG126, AG556, AG1641 or A1) and genistein, but not daidzein (inactive analogue of genistein), prevent the (i) circulatory failure, (ii) the multiple organ dysfunction (liver and pancreatic dysfunction/injury lactacidosis, hypoglycaemia), as well as (iii) the induction of iNOS and COX-2 protein and activity in rats with endotoxic shock.
 ...
PMID:Effects of tyrphostins and genistein on the circulatory failure and organ dysfunction caused by endotoxin in the rat: a possible role for protein tyrosine kinase. 929 29

The activity of aspartate aminotransferase, glutamate dehydrogenase in the liver of rats in 1, 7 and 15 days after gamma irradiation effect of the dose of 0.5 Gy on the background of consumption by animals of sodium nitrate, sodium nitrite and nitrosodiethylamine was studied. The combined influence of chemical agents and gamma irradiation modified the effects of nitro compounds-xenobiotics on processes of the synthesis and dissociation of the glutamic acid as well as the intensity of transamination of the reamination by aspartate aminotransferase.
 ...
PMID:[The combined action of ionizing radiation and nitro compounds on the activity of the basic enzymes of glutamic acid metabolism]. 968 35

Nitric oxide, a free radical inter- and intracellular messenger molecule, is important in exercise physiology. This study tested the hypothesis that serum nitric oxide concentrations change after strenuous exercise with severe generalized muscle cramps. The study group consisted of 77 professional football players in preseason training. All players' concentrations of serum nitrite and of other serum chemicals were determined during their preseason evaluations and compared with the concentrations in 40 serum samples taken from 25 of those same players who required intravenous rehydration for severe generalized muscle cramps after a training session. Player weight and percentage of body fat were significantly higher in players who received intravenous fluids than in players who did not. The serum of players requiring intravenous hydration showed evidence of skeletal muscle breakdown (increases in lactate dehydrogenase, creatinine phosphokinase, aspartate aminotransferase, and alanine aminotransferase) and of dehydration (elevations in protein, blood urea nitrogen, and cholesterol). The major finding, however, was a nearly 300% increase in serum nitrite concentrations in players requiring rehydration. There were no correlations between concentrations of nitrate and of any of the other serum chemicals. These data support the hypothesis that large amounts of nitric oxide are synthesized in professional football players after strenuous exercise with severe muscle cramps. The study design did not allow us to determine whether this increase in nitric oxide was due to exercise or muscle cramps or both, but it does provide a basis for evaluating these relationships.
 ...
PMID:Postexercise increase in nitric oxide in football players with muscle cramps. 1049 91

Two alpha-amylase-producing strains of Aspergillus oryzae, a wild-type strain and a recombinant containing additional copies of the alpha-amylase gene, were characterized with respect to enzyme activities, localization of enzymes to the mitochondria or cytosol, macromolecular composition, and metabolic fluxes through the central metabolism during glucose-limited chemostat cultivations. Citrate synthase and isocitrate dehydrogenase (NAD) activities were found only in the mitochondria, glucose-6-phosphate dehydrogenase and glutamate dehydrogenase (NADP) activities were found only in the cytosol, and isocitrate dehydrogenase (NADP), glutamate oxaloacetate transaminase, malate dehydrogenase, and glutamate dehydrogenase (NAD) activities were found in both the mitochondria and the cytosol. The measured biomass components and ash could account for 95% (wt/wt) of the biomass. The protein and RNA contents increased linearly with increasing specific growth rate, but the carbohydrate and chitin contents decreased. A metabolic model consisting of 69 fluxes and 59 intracellular metabolites was used to calculate the metabolic fluxes through the central metabolism at several specific growth rates, with ammonia or nitrate as the nitrogen source. The flux through the pentose phosphate pathway increased with increasing specific growth rate. The fluxes through the pentose phosphate pathway were 15 to 26% higher for the recombinant strain than for the wild-type strain.
 ...
PMID:Identification of enzymes and quantification of metabolic fluxes in the wild type and in a recombinant aspergillus oryzae strain 987 53

Abamectin is widely used as an insecticide and an anthelmintic. A previous report indicated that abamectin was used to commit suicide and led to death in Taiwan. This investigation focused on the toxicological effects of abamectin on serum aspartate aminotransferase (AST) and nitrate/nitrite (NO) levels in rats. After rats were gavaged with abamectin ranging from 1 to 20 mg/kg/body weight, AST and NO levels were examined within 12 h. AST and NO levels were elevated in abamectin-dosed rats in a dose-dependent manner. The least increase of AST corresponded to the highest enhancement of NO release at 6 h. A negative correlation coefficient (r=-0.55) between AST and NO was found. Both NG-nitro-L-arginine-methyl ester and aminoguanidine, inhibitors of nitric oxide synthase, increased the AST level induced by abamectin. These findings suggest that NO may be involved in the alteration of AST release induced by abamectin in rats.
 ...
PMID:Abamectin effects on aspartate aminotransferase and nitric oxide in rats. 1152 77

The effects of betaine or taurine on hepatotoxicity induced by lipopolysaccharide (LPS) were examined in adult male SD rats. Rats were provided with drinking water containing either 1% betaine or taurine for 2 weeks prior to challenge with LPS (5 mg/kg, iv). Supplementation with betaine or taurine protected the animals from induction of LPS hepatotoxicity as measured by changes in aspartate aminotransferase (AST), alanine aminotransferase (ALT) activities and total bilirubin levels in serum, and hepatic glutathione contents. LPS challenge increased serum TNF-alpha and nitrate/nitrite in rats, which were reduced by betaine or taurine intake. Taurine depletion induced by supply of drinking water containing 3% beta-alanine for 7 days did not enhance the LPS-induced hepatic damage or the decrease in hepatic glutathione level. The results indicate that intake of betaine or taurine attenuates the LPS-induced hepatotoxicity resulting from activation of Kupffer cells.
 ...
PMID:Attenuation of bacterial lipopolysaccharide-induced hepatotoxicity by betaine or taurine in rats. 1189 13

In a recent study in rats, alanine aminotransferase (ALT), the preferred plasma biomarker of hepatocellular injury in rats, was ineffective at detecting marked hepatic necrosis produced by acetaminophen (Human and Experimental Toxicology 19, 277-83, 2000). In contrast, glutamate dehydrogenase (GLDH) was markedly elevated. Accordingly, these enzymes were comprehensively evaluated as plasma biomarkers of hepatocellular injury in rats using several other models of hepatic injury, including partial hepatectomy and exposure to methapyrilene, dexamethasone, cyproterone, isoniazid, lead nitrate, and Wyeth-14643. Other enzymes also evaluated were aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH), and the hepatobiliary marker alkaline phosphatase (ALP). Compared to plasma ALT increases, plasma GLDH increases were up to 10-fold greater, up to 3-fold more persistent, and occurred at times following hepatocellular injury when plasma ALT was not increased. Plasma GLDH activity was not inhibited by the test compounds, whereas ALT was substantially inhibited by both isoniazid and lead nitrate. While plasma GLDH activity was unaffected by induction, ALT was induced by cyproterone and dexamethasone, and ALP was induced by Wyeth-14643 and partial hepatectomy. GLDH was concluded to be a more effective biomarker of acute hepatic injury than ALT, AST, SDH or ALP in the rat, based primarily on the large increase following hepatocellular injury, prolonged persistence in the blood following injury, high sensitivity for detection of injury (including pre-necrotic injury), high tissue specificity, and lower susceptibility to inhibition or induction.
 ...
PMID:Advantages of glutamate dehydrogenase as a blood biomarker of acute hepatic injury in rats. 1214 42


<< Previous 1 2 3 4 5 6 7 8 9 Next >>