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)

An experimental model of toxic liver injury in rats was employed to assay the effect of Nifedipine (a calcium antagonist blocker) and S-Adenosylmethionine (a precursor of glutathione). An important decrease in both perivenular fibrosis and cirrhosis was found. Furthermore, a significant decrease in lactic acid levels was found in the group of animals treated with pharmacologic therapy, although no correlation was seen between lactic acid levels and the different degrees of perivenular fibrosis. No significant variations in ALT and AST enzymes were observed between both groups, as opposed to a significant decrease in LDH enzyme in the Nifedipine+S-Adenosylmethionine group. The results indicate an improvement in the histologic picture of the liver in rats treated by means of pharmacological association, without any change in inflammatory infiltrate and with a slight decrease in necrosis, indicating an action mechanism via creeping fibrosis (instead of a hepatitis pathway).
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PMID:Effect of nifedipine and S-adenosylmethionine in the liver of rats treated with CCl4 and ethanol for one month. 151 99

Endotoxin administration causes liver injury. Patients with alcoholic liver disease frequently have portal vein and systemic endotoxemia, and some investigators have suggested that endotoxin plays an etiologic role in alcoholic liver injury. Many of the metabolic effects of endotoxin are mediated by the cytokine tumor necrosis factor (TNF). It was the purpose of this study to determine whether TNF plays a role in ethanol-enhanced endotoxin liver injury. Rats were fed either a diet in which 36% of the calories were from ethanol or an isocaloric control diet. After 6 weeks, groups of 10 rats were intravenously injected with either saline, 1 mg/kg endotoxin, or 30 micrograms/kg of a prostaglandin E1 (PGE1) analogue + 1 mg/kg endotoxin 24 hr prior to sacrifice. Ethanol/endotoxin-treated rats had significantly higher liver enzyme levels (ALT: 1064 +/- 355 IU/liter, AST: 2024 +/- 515 IU/liter) compared with isocaloric/endotoxin controls (ALT: 237 +/- 54 IU/liter, AST: 602 +/- 80 IU/liter). Ethanol/endotoxin rats also had significantly higher peak serum TNF concentrations (992 +/- 200 units/ml) compared with isocaloric/endotoxin controls (344 +/- 96 units/ml). Pretreatment of ethanol/endotoxin rats with PGE1 caused significant attenuation of liver injury (ALT: 267 +/- 64 IU/liter, AST: 612 +/- 77 IU/liter) and a diminished serum TNF response. In contrast to chronic ethanol administration, acute gavage with 2 mg/kg ethanol (30% w/v) followed by intravenous injection of 2 mg/kg endotoxin produced significantly lower peak serum TNF concentrations (401 +/- 76 units/ml) than gavage with distilled water (1152 +/- 208 units/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tumor necrosis factor in alcohol enhanced endotoxin liver injury. 153 Jan 27

Serum human hepatocyte growth factor levels were measured using a newly developed enzyme-linked immunosorbent assay kit in patients with liver diseases. Serum human hepatocyte growth factor levels were increased in correlation with derangements of prothrombin time, total bilirubin and other parameters reflecting hepatocellular dysfunction in 112 patients with chronic liver disease. The levels were positively correlated with serum AST and ALT levels in 59 of these patients whose prothrombin times were within the normal range. Abnormally increased serum human hepatocyte growth factor levels were found in 100% of the determinations in 16 patients with fulminant hepatic failure and in 80% of the determinations in 16 patients with chronic hepatic failure. The levels greater than 1 ng/ml, however, were found in 94% of determinations in the former group, but only in 16% of the determinations in the latter group. This difference was seen irrespective of prothrombin time or hepatic coma grades. In patients with fulminant hepatic failure serum human hepatocyte growth factor levels were increased immediately after plasma exchange using heparin as the anticoagulant in 71% of the determinations. This increase disappeared 12 hr after discontinuation of plasma exchange. In 17 of 39 patients with chronic renal failure who had no liver disease, serum human hepatocyte growth factor levels were abnormally increased before hemodialysis using heparin, and the levels were elevated immediately after hemodialysis in all the patients. The increase of serum human hepatocyte growth factor levels in hepatic failure may be the result of hepatocellular dysfunction and necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of serum human hepatocyte growth factor levels in patients with hepatic failure. 153 Jul 86

To assess the effect of prolonged administration of midazolam or isoflurane on hepatocellular integrity, we measured the concentrations of glutathione transferase (EC 2.5.1.18) B1 subunit and the activities of alanine aminotransferase (ALT; EC 2.6.1.2) and aspartate aminotransferase (AST; EC 2.6.1.1) in 40 patients who required long-term sedation with low-dose midazolam or isoflurane. Blood samples were collected before and 24 h after the start of the sedation and 0, 24, 72, 120, and 172 h after the last dose. ALT and AST activities did not change appreciably, but the glutathione transferase B1 concentration decreased significantly (P less than 0.03) at all times studied. The patients who received isoflurane and those who received midazolam showed no significant differences in any of the enzyme tests. We conclude that long-term sedation with midazolam or isoflurane is unlikely to affect hepatocellular integrity.
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PMID:Aspartate aminotransferase, alanine aminotransferase, and glutathione transferase in plasma during and after sedation by low-dose isoflurane or midazolam. 156 9

In patients with thalassemia intermedia in whom hyperabsorption of iron may result in serious organ dysfunction, an orally effective iron-chelating drug would have major therapeutic advantages, especially for the many patients with thalassemia intermedia in the Third World. We report reduction in tissue iron stores and normalization of serum ferritin concentration after 9-month therapy with the oral chelator 1,2-dimethyl-3-hydroxypyrid-4-one (L1) in a 29-year-old man with thalassemia intermedia and clinically significant iron overload (SF 2,174 micrograms/L, transferrin saturation 100%; elevated AST and ALT, abnormal cardiac radionuclide angiogram) who was enrolled in the study with L1 75 mg/kg/day after he refused deferoxamine therapy. L1-Induced 24-hour urinary iron excretion during the first 6 months of therapy was (mean +/- SD, range) 53 +/- 30 (11 to 109) mg (0.77 mg/kg), declining during the last 3 months of L1 to 24 +/- 14 (13-40) mg (0.36 mg/kg), as serum ferritin decreased steadily to normal range (present value, 251 micrograms/L). Dramatic improvement in signal intensity of the liver and mild improvement in that of the heart was shown by comparison of T1-weighted spin echo magnetic resonance imaging with images obtained immediately before L1 administration was observed after 9 months of L1 therapy. Hepatic iron concentration decreased from 14.6 mg/g dry weight of liver before L1 therapy to 1.9 mg/g liver after 9 months of therapy. This constitutes the first report of normalization of serum ferritin concentration in parallel with demonstrated reduction in tissue iron stores as a result of treatment with L1. Use of L1 as a therapeutic option in patients with thalassemia intermedia and iron overload appears warranted.
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PMID:Reduction of tissue iron stores and normalization of serum ferritin during treatment with the oral iron chelator L1 in thalassemia intermedia. 158 21

Most laboratories in Pakistan use expensive imported clinical chemistry reagent kits resulting in high cost/test to the patients. To reduce these costs, reagents were prepared from basic chemicals, substrates and enzymes imported from Sigma Chemical Company U.K. This reduced the cost/test by up to 500% in some reagents. The quality of these reagents was tested by Wellcome External, Q.C. Locally prepared reagents were comparable to or better than commercial reagents systems in terms of accuracy and precision. This paper describes the preparations according to I.F.C.C., costs and quality control of some of the reagents i.e., glucose, calcium, bilirubin, albumin, total protein, urea, ALT, AST and LDH and their comparisons with equivalent commercial kits.
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PMID:Economy and quality assessment of home made clinical chemistry reagents. 159 26

Egyptian scorpion venom was collected by electrical stimulation of the telson. Rats were injected with the lyophilized venom in 3 different doses (100, 200 and 400 micrograms/kg). Blood samples were drawn by heart puncture before and 4 h after venom administration. Serum was separated and collected for determination of glucose, blood urea nitrogen (BUN), creatinine, uric acid (UA), total proteins, cholesterol, sodium, potassium, calcium, inorganic phosphorus, alkaline phosphatase, aspartate aminotransferase (AST, GOT), alanine aminotransferase (ALT, GPT), lactate dehydrogenase and creatine phosphokinase (CPK). Serum glucose, creatinine, GOT, GPT and LDH were increased significantly in all treatments. At the same time serum BUN and CPK were elevated significantly with a dose-response relationship. On the other hand, serum total proteins, uric acid, cholesterol, calcium and potassium were significantly decreased 4 h after administration of the 3 doses. These changes in clinical chemistry parameters are most probably related to the toxic effect of the venom on the target organs.
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PMID:Effect of scorpion Leiurus quinquestriatus (H&E) venom on the clinical chemistry parameters of the rat. 160 45

1. Intact trophozoites of Giardia duodenalis (clone P1C10) took up and metabolised L-[U14C-] aspartate to 14CO2 at rates of 10.27 +/- 0.76 and 27.6 +/- 2.07 ng hr-1 10(-6) cells in a simple maintenance medium (MM) and in a complex bile supplemented (BIS-33) medium respectively. 2. Intact trophozoite of G. duodenalis (clone P1C10) also took up and metabolised L-[U14C-] alanine to 14CO2 at rates of 20.6 +/- 1.1 and 91.4 +/- 17.5 ng hr-1 10(-6) cells in the simple (MM) and complex (BIS-33) medium respectively. 3. trophozoite sonicates contained significant levels of aspartate-2-oxoglutarate transaminase (AST; EC 2.6.1.1) and alanine-2-oxoglutarate transaminase (ALT; EC 2.6.2.2.). Specific activities (at 23 degrees C) were 95.1 +/- 11.3 and 87.3 +/- 9.8 nmol (min)-1 (mg protein)-1 respectively. 4. These observations suggest that Giardia has the capacity to utilise aspartate and alanine and possibly other amino acids as alternative sources of energy. 5. The extrusion or uptake of alanine by Giardia trophozoites may be dictated by the intracellular redox-status of the protozoan parasite or components in the external mileu.
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PMID:The uptake and conversion of L-[U14C-] aspartate and L-[U14C-] alanine to 14CO2 by intact trophozoites of Giardia duodenalis. 161 34

The role of clinical (biliary pain and/or jaundice), laboratory (discriminant function (DF) calculated using AST, ALT, AlkPh and GGT serum values) and ultrasonographic (US)(dilation and/or stone of common bile duct (CBD)) findings in identification of the biliary etiology of acute pancreatitis (AP) was studied in 60 patients. AP biliary etiology was defined by ERCP executed in the early phase of the disease (lithiasis and/or stenosis of CBD; endoscopic features of forced papilla in patients with gallstone). US showed the best values of sensitivity (84.6%) and diagnostic efficacy (76.7%); DF showed the best results of specificity (62.5%) and of test positive predictive value (92.8%). The statistical evaluation (McNemar test) showed a significant increase of sensitivity for US vs clinical findings and of specificity for DS vs clinical findings (p less than 0.05). The sensitivity, specificity, accuracy, test negative and positive predictive value were improved to 96.1, 87.5, 96.6, 77.1 and 92% by the combination of US and DF. Therefore the association of US and DF can provide the best non invasive method in rapidly detecting CBD pathology as an etiological factor in AP and then the enough accurate indication to early operative ERCP.
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PMID:[The role of clinical, biochemical and echographic data in identifying the biliary pathogenesis of acute pancreatitis]. 162 15

Six-month chronic oral toxicity studies of 7-chloro-3-[1-(2, 4-dichlorophenyl)-2-(1H-imidazol-1-yl)ethoxy-methyl] benzo[b]thiophene (sertaconazole, FI-7045, CAS 99592-32-2) were carried out in rats and ferrets. The dose levels used were 50, 150 and 300 mg/kg in rats and 50, 150 and 250 mg/kg in ferrets. There was no mortality associated with the drug in either of the two species. The results obtained show that the toxic effects may be summarized as a smaller body weight increase in rats at 150 and 300 mg/kg and in male ferrets at 250 mg/kg. Food consumption decreased significantly in rats at 300 mg/kg, and was not proportional to the doses of 150 and 50 mg/kg. In serum biochemistry, increases in alkaline phosphatase in rats, ALT in male ferrets at 150 and 250 mg/kg and AST only at 250 mg/kg were observed. BUN increased at 150 and 250 mg/kg in ferrets.
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PMID:Chronic toxicity studies of sertaconazole after oral administration to rats and ferrets. 162 94


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