Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subacute thyroiditis is generally thought to be a self-limited inflammatory disease of the thyroid gland. This paper describes serial observations on the clinical course of a typical patient with subacute thyroiditis. This patient showed specific features of destructive thyrotoxicosis with increases in the serum levels of acute phase reactants and in the erythrocyte sedimentation rate. She also showed signs of liver dysfunction [slightly increased alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (gamma-GTP), and leucine aminopeptidase (LAP)], slight anemia, glucose intolerance, increased pancreatic enzymes, splenomegaly, and an increase in peripheral Leu 7 positive (NK/K) cells. These abnormalities all improved with recovery from disease. These findings indicate that in this patient with subacute thyroiditis inflammation is not limited to the thyroid gland but also involves the liver, pancreas and spleen. Thus the subacute thyroiditis in this patient may be a systemic multi-organ disease.
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PMID:Subacute thyroiditis associated with systemic multi-organ disorders. 263 13

Analysis of data on 9 cases with active cytomegalovirus infection in patients with kidney grafts showed a positive association of serum leucine aminopeptidase activity concentration with the appearance of plasmacytoid lymphocytes in blood. Additional studies indicate that like the liver, the lymphocytes contain leucine aminopeptidase in relatively large quantities and that this enzyme is increased about 3-fold in plasmacytoid lymphocytes when compared with the activity in normal lymphocytes. In contrast, the 'hepatic' enzyme alanine aminotransferase is practically absent in both lymphocytes and plasmacytoid cells. Therefore, the difference in serum between the relative increases of leucine aminopeptidase and alanine aminotransferase may be attributed to proliferating plasmacytoid lymphocytes. Earlier observations on a large number of cases of acute viral hepatitis A or B lend credence to this assumption. However, in this disease, the serum enzyme changes reflect the much greater involvement of the liver and the relatively slight, but significant, proliferation of plasmacytoid lymphocytes. Our hypothesis is confirmed by the recent observation of 3 cases of acute EBV infection (infectious mononucleosis) in otherwise healthy individuals showing greatly elevated leucine aminopeptidase in contrast to normal or slightly raised alanine aminotransferase in serum.
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PMID:Serum leucine aminopeptidase for monitoring viral infections with plasmacytoid reaction. 287 29

An in vivo model of liver hyperplastic noduligenesis was induced in rats by long-term administration of thioacetamide (TAM) (50 mg/kg/day i.p.). Three doses of 50 mg/kg of an antitumoral Rh(III) complex were administered at 14, 9 and 5 days before the end of TAM treatment. Plasma and urine were obtained from either TAM or Rh(III) complex or TAM plus Rh(III) complex treated rats to determine the interactions of both substances with the biochemical parameters related to liver function. The rise in alkaline phosphatase (ALP), leucine aminopeptidase (LAP), gamma-glutamyl transferase (GGT) and the unchanged activities in the aspartate and alanine aminotransferases (AST, ALT) in plasma of TAM-treated rats indicated that the disease induced by this substance can be considered as a chronic obstructive biliary disease with indices of cell proliferation and tumors. The increased concentration of bilirubin both in the plasma and urine of TAM-treated rats suggested liver cholestasis and hepatobiliary obstruction. The very low values of creatinine clearance indicated that there was some degree of kidney failure due to the effect of TAM. The increased concentration of ammonia both in plasma and urine were probably a consequence of the decreased flux in the urea cycle in the liver. The Rh(III) complex alone did not produce significant changes in the plasma enzyme activities. The only significant changes were found in the concentrations of uric acid and ammonia in the urine. When the Rh(III) complex was administered to TAM-treated rats, significant restoration of the following parameters were observed: plasma enzymatic activities, blood bilirubin and ammonia, uric acid and creatinine in the urine and the creatinine clearance. These results suggest that the altered liver function induced by TAM can be restored by Rh(III) complex. The mechanisms by which this complex acts to counteract the TAM-induced changes are not yet established.
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PMID:Effect of a rhodium complex on alterations of hepatic function in thioacetamide-induced hyperplastic noduligenesis in rats. 288 38

Oral administration of L-triiodothyronine (L-T3) (0.015-1 mg/kg) for 30 days to mature rats or cynomolgus monkeys resulted in both species in a high mortality at 1 mg/kg (after 2 weeks of treatment) and a progressive loss in body weight. Dose-related elevations in plasma marker enzymes occurred, mainly after 1-2 weeks of treatment. The approximate no-effect dose for these changes was around 0.015-0.020 mg/kg for both rat and primate. The large elevations of leucine aminopeptidase (LAP) at 1 mg/kg L-T3 in monkey indicated hepatocellular toxicity although in the rat such large increases in alanine aminotransferase (ALT) and glutamate dehydrogenase (GLDH) were not seen. L-T3 also showed little toxicity to rat hepatocytes in vitro. High concentrations of L-T3 (7 x 10(-9) to 7 x 10(-7) M) had minimal effects on parameters of cell viability such as lactate dehydrogenase (LDH) leakage, chromium-51 release and [3H]leucine incorporation. Urinary enzymes in the rat showed a similar profile to those in plasma. Large rises in alkaline phosphatase (AKP) and N-acetyl glucosaminidase (NAG) at 1 mg/kg indicated possible proximal tubular damage although this was not supported histologically. Clinically, in both species L-T3 appeared more toxic to males than females but this was not supported histologically. The histological lesions observed were different in the 2 species. In the monkeys there was extensive lipid vacuolation of hepatocytes and changes in thyroid and adrenal cortex. In the rat there was fine, non-lipid vacuolation of hepatocytes and thyroid changes. In the rat, 2 previously unreported lesions were also noted. There were multinucleated cells in the renal distal tubular epithelium, and focal fibroplasia of serosal surfaces of abdominal viscera.
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PMID:Comparison of the toxicity of orally administered L-triiodothyronine (T3) in rat and cynomolgus monkey. 320 78

Secretory immunoglobulin A (sIgA) in serum was measured in patients with various liver diseases using enzyme immunoassay specific to sIgA. Marked elevation of the serum sIgA concentrations was found in liver diseases especially in intrahepatic or extrahepatic cholestasis. In chronic hepatitis and liver cirrhosis serum sIgA correlated significantly with leucine aminopeptidase (r = 0.69), GOT (r = 0.66), alkaline phosphatase (r = 0.55), and direct bilirubin (r = 0.42). In acute hepatitis their levels correlated significantly with total bilirubin (r = 0.59) and GPT (r = 0.55). In acute hepatitis and acute exacerbation of chronic hepatitis the major peaks of serum sIgA were observed later than those of liver enzymes. These results suggest two mechanisms working to elevate the serum sIgA levels in liver diseases. In chronic hepatitis, liver cirrhosis, and intrahepatic and extrahepatic cholestasis the raised serum sIgA probably reflects reflux of bile, a rich source of secretory component and sIgA, into circulation. In acute or chronic massive liver necrosis elevation of sIgA may be associated with liver regeneration. Serial measurement of serum sIgA with other conventional parameters will contribute much to the understanding of the pathophysiology of liver diseases.
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PMID:Serum levels of secretory immunoglobulin A in liver disease. 388 22

The pesticide dichlorvos inhibits not only cholinesterase but also alkaline phosphatase, lactate dehydrogenase and glutamate dehydrogenase competitively. A mixed type inhibition of glutamic-oxaloacetic transaminase is in contrast to the increased activity of glutamic-pyruvic transaminase after dichlorvos application. The activity of leucine aminopeptidase is not affected by the substance. After administering rats an acutely toxic dose of dichlorvos (70 mg per kg b.w.) in vitro-inhibitions other than that of cholinesterase could not be found.
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PMID:Enzyme activities after in vitro and in vivo application of dichlorvos. 400 35

The effect of a single oral dose of endosulfan (5 mg/kg body weight) on the uptake of certain nutrients and brush-border enzymes has been studied in rat intestine. The uptake of glucose and alanine was elevated but that of leucine was decreased in endosulfan-fed rats. There was no change in the uptake of phenylalanine and lysine in insecticide-fed rats. The activities of brush-border sucrase and alkaline phosphatase were considerably increased while the activity of Na+ K+ ATPase was reduced in endosulfan-exposed animals. The leucine aminopeptidase activity was unaffected in pesticide-treated rats. There was a significant decrease in cellular LDH and GOT activities with no change in GPT activity. Neither was there a considerable increase in the cellular glucose-6-phosphatase activity (P less than 0.01) in the pesticide-fed rats. These results suggest that endosulfan toxicity induces certain functional changes in the intestine.
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PMID:Effect of a single oral dose of endosulfan on intestinal uptake of nutrients and on brush-border enzymes in rats. 618 May 24

Activities of 12 enzymes (amylase, lipase, cholinesterase, nonspecific carboxyl esterase, lactate dehydrogenase (LDH), alkaline phosphatase, glutamate-oxalacetate transaminase (GOT), glutamate-pyruvate transaminase (GPT), gamma-glutamyl transferase (gamma-GT), leucine aminopeptidase (LAP), malate dehydrogenase (MDH) and peroxidase) were determined in the perienteric fluid and homogenate of Ascaris suum. With the exception of amylase, all activities were higher in the homogenate than in the perienteric fluid. The enzyme activities in the perienteric fluid were then compared with those in the human serum. Comparable activities were demonstrated for LDH, LAP, lipase and alkaline phosphatase, markedly higher activities in perienteric fluid were demonstrated for MDH, GOT, GPT and amylase, and much lower for cholinesterase. No gamma-GT activity was detected in the perienteric fluid.
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PMID:Activities of some enzymes in the perienteric fluid of Ascaris suum. 619 63

The aim of this work is to evaluate the concentration of serum bile acids (SBA) as an index of impaired liver function in systemic lupus erythematosus (SLE) patients versus usual laboratory tests of hepato-biliary system diseases. In patients with SLE the mean fasting SBA concentration was 9.6 +/- 1.4 mumol/L; in normal subjects the concentration was 2.9 +/- 0.6 mumol/L (P less than 0.01). In patients with SLE, mean gamma-glutamyl transpeptidase (GGTP) concentration was 31.5 +/- 5.9 mU/ml versus 10.05 +/- 1.1 mU/ml in controls (P less than 0.01). The bromsulphalein (BSP) excretion test, 45 minutes after injection, was 6.8 +/- 1% in SLE patients versus 2.8 +/- 0.4% in controls (P less than 0.02). No significant difference was found between these two groups of subjects with respect to leucine aminopeptidase (LAP), alkaline phosphatase (AlPh), glutamic-oxalacetic transaminase (SGOT), glutamic-pyruvic transaminase (SGPT), bilirubin serum rates. SBA rate was abnormal in 50% of the SLE patients; GGTP rate and the BSP excretion test were abnormal in 38% and 27% respectively. Our findings show the presence of an actual liver impairment in SLE patients, significantly demonstrated by fasting SBA concentration, GGTP rate and BSP excretion test. Other liver function tests are less useful in evaluating hepatic damage in SLE.
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PMID:Concentration of serum bile acids as an index of hepatic damage in systemic lupus erythematosus. 646 63

The aminopyrine breath test, postprandial serum bile acids, and routine liver tests were assessed as indicators of liver dysfunction in 38 patients with porphyria cutanea tarda. In 17 patients needle biopsy specimens of the liver were obtained. Bile acids were increased in almost all the patients studied (97%) but impairment of aminopyrine demethylation was found in only 45%. More than 50% of cases had elevated activities of serum alanine aminopeptidase, leucine aminopeptidase, gammaglutamyl transpeptidase (GGTP), and alanine aminotransferase (ALAT). All liver biopsy specimens showed fluorescence characteristic of porphyrins. Histologic examination of biopsy material revealed cellular lesions in all cases, the most common pathological findings being fatty degeneration of varying degree and iron accumulation. The most frequent electronmicroscopic changes in the liver were fat droplets, granules containing bile material, and siderosomes in the cytoplasm of hepatocytes. However, there was no evident relationship between morphological and functional liver changes.
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PMID:The function and morphology of the liver in porphyria cutanea tarda. 650 22


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