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)

Twelve patients with primary biliary cirrhosis (PBC), stages I to III, received long-term therapy with a combination of 600 mg ursodeoxycholic acid (UDCA) and 1 mg colchicine given daily for more than 2 years. Drug toxicity was mild; one patient experienced diarrhoea that was probably due to colchicine. Serum levels of bilirubin, alkaline phosphatase (ALPase), gamma-glutamyl transpeptidase and alanine aminotransferase decreased by more than 50% of the initial values. Serum albumin and cholesterol levels also improved, but immunoglobulins and anti-mitochondrial antibody titre did not change. Histologic features in the eight patients who received serial liver biopsies before and 2 years after the beginning of treatment were evaluated. Piecemeal necrosis and portal inflammation were improved, but there was no change in portal fibrosis. Patients were divided into two groups; the first received both drugs from the outset, and the second group were started on UDCA for 3 months followed by the addition of colchicine. After 3 months, the improvement in serum bilirubin and ALPase in the first group was greater than in the second. However, in the second group, the ALPase levels had decreased significantly when measured at 6 and 9 months after the treatment compared with the levels at 3 months. These findings suggest that UDCA and colchicine may have a synergistic effect. This combination therapy appears to be safe and effective, both clinically and histologically, for treating PBC.
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PMID:Combination therapy with ursodeoxycholic acid and colchicine for primary biliary cirrhosis. 161 Oct 15

Results of routine hematologic and serum biochemical analyses from 12 healthy adult male dogs that were given prednisone (0.55 mg/kg of body weight, PO, q 12 h) for 35 days were compared with those of a control group of 6 dogs that were given gelatin capsules. Analyses were performed at 2-week intervals during and after prednisone administration. Lymphocyte and eosinophil counts were significantly (P less than 0.005) decreased after 2 and 4 weeks of prednisone treatment, compared with controls. Two weeks after treatment, eosinophil counts in prednisone-treated dogs were similar to those of control dogs, whereas lymphocyte counts remained low 4 weeks after treatment in treated dogs (1,869 +/- 145 cells/microliters), compared with that in control dogs (3,662 +/- 548 cells/microliters). Neutrophil and monocyte counts did not significantly change during glucocorticoid administration. Mean platelet volume significantly (P less than 0.001) decreased after 4 weeks of prednisone treatment, but returned to pretreatment values by 2 weeks after treatment. Four weeks of prednisone treatment did not cause significant increased activity in serum alanine transaminase, total alkaline phosphatase or the steroid-induced isoenzyme of alkaline phosphatase. Significant increases in serum albumin (P less than 0.001) and total protein (P less than 0.05) concentrations were detected after 4 weeks of treatment, but mean values were not significantly different from those of controls 2 weeks after treatment ended. Results of our study indicate that eosinophil and lymphocyte counts are the most sensitive indicators of long-term glucocorticoid administration at anti-inflammatory dosages of 1.1 mg/kg daily.
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PMID:Hematologic and serum biochemical effects of long-term administration of anti-inflammatory doses of prednisone in dogs. 162 72

Serum samples from 254 wild-caught Aotus nancymai were analyzed to determine the reference intervals for serum chemistry parameters in this species. Findings show values of total bilirubin, creatinine, alkaline phosphatase, alanine aminotransferase, urea nitrogen, serum albumin, and gamma glutamic transpeptidase having a non-normal distribution. Based on nonparametric tests, significant differences between male and female values were observed for cholesterol, serum calcium, and gamma glutamic transpeptidase. Males were significantly heavier than females. The reference intervals presented were estimated by the nonparametric percentile method.
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PMID:Serum chemistry of the wild caught karyotype I night monkey (Aotus nancymai). 165 42

Prothrombin time, serum albumin, aminotransferases and liver size were evaluated in 40 consecutive cases of kwashiorkor. Eleven (27.5%) of the 40 patients died. Eight out of the 11 patients who died had a prolonged prothrombin time of more than 3 s above the control compared to only 4 out of the 29 who survived (p = 0.005). Mean serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) albumin, globulin and liver size were abnormal but similar in both groups. These results may indicate a predictive mortality value of prothrombin time in kwashiorkor.
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PMID:Prothrombin time as an index of mortality in kwashiorkor. 169 50

The present study was undertaken to investigate the effects of acute 2,4-dichlorophenoxyacetic acid (2,4-D) intoxication (0.6 g/kg, po) on lactate dehydrogenase, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, amylase, creatinine, glucose, total protein and albumin levels in rats. Serum levels of lactate dehydrogenase, alkaline phosphatase and creatinine increased from 1- to 4-fold at 5, 8 and 24 h after 2,4-D administration, whereas serum levels of aspartate and alanine aminotransferase were higher only at 8 and 24 h. Amylase levels were only increased 8 h after administration of 2,4-D and then returned to normal levels. In contrast, 2,4-D reduced the serum levels of glucose and total protein 5, 8 and 24 h and serum albumin levels 5 h after herbicide intoxication. Thus, acute intoxication with 2,4-D disrupts serum levels of several enzymes and components which are considered to be indicators of tissue injury. Most likely these alterations mainly reflect hepatic and muscle tissue damage induced by the herbicide, but significant pancreatic and kidney toxicity may also have occurred.
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PMID:Effects of acute 2,4-dichlorophenoxyacetic acid intoxication on some rat serum components and enzyme activities. 172 51

The effects of administration of dec-2-ynol and dec-2-ynoic acid on the hepatic glutathione (GSH) content and hepatic microsomal trans-2-enoyl-CoA reductase activity were examined in rat. Both compounds, when administered ip, caused a marked depletion of GSH levels and a corresponding inactivation of trans-2-enoyl-CoA reductase activity in both a time- and dose-dependent manner. The dec-2-ynoic acid caused greater hepatotoxicity than dec-2-ynol based on serum alanine transaminase activity. Based on the observations that (a) the alcohol did not interact with GSH in the presence or absence of cytosol, (b) the spectral manifestation of the interaction between GSH and the alcohol occurred only when NAD+ was added to the reaction mixture containing the cytosol and reactants, and (c) a similar absorbance spectrum was obtained following the interaction between aldehyde and GSH, it was concluded that dec-2-ynol is converted to an electrophile, dec-2-ynal, which causes depletion of GSH. The decrease in GSH content following administration of the acid appears to be due to activation of the acid to the electrophile, dec-2-ynoyl CoA, which then interacts with GSH, resulting in its depletion, based on the in vitro observations that (a) the acid did not interact with GSH in the presence or absence of cytosol, and (b) the spectral manifestation of interaction between GSH and dec-2-ynoyl CoA occurred both nonenzymatically and enzymatically in the presence of rat liver glutathione S-transferase (Sigma). Bovine serum albumin stimulated the enzymatic reaction. Comparable to the effects on GSH were the effects of dec-2-ynol, dec-2-ynal, dec-2-ynoic acid, and dec-2-ynoyl CoA on the microsomal trans-2-enoyl-CoA reductase activity in vitro. While the alcohol had no effect on the enzyme activity, its electrophilic product, the aldehyde, was a potent inhibitor. Similarly, the acid did not inhibit the enzyme activity unless the acid was present at high concentration; however, its electrophilic product, the CoA thioester, was a very potent inhibitor at very low concentration.
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PMID:Depletion of rat hepatic glutathione and inhibition of microsomal trans-2-enoyl-CoA reductase activity following administration of a dec-2-ynol and dec-2-ynoic acid. 173 41

The medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration less than or equal to 2.2. g/dl in 12 dogs, serum alkaline phosphatase activity greater than or equal to 169 U/L in 18 dogs, serum alanine transaminase activity greater than or equal to 57 U/L in 15 dogs, and total bilirubin concentration greater than or equal to 1 mg/dl (in the absence of lipemia) in 7 dogs. Serum phenobarbital concentration was greater than or equal to 40 micrograms/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations greater than 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration greater than or equal to 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, PO. Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.
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PMID:Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989). 174 13

The value of the aminoterminal procollagen-III-peptide (P-III-P) in predicting death or survival was evaluated in a group of 43 patients with proven postnecrotic or alcoholic cirrhosis. Patients were followed-up prospectively for 2 years. The prognostic value of P-III-P was compared with the Child classification, fasting and postprandial serum bile acids, and standard laboratory tests such as bilirubin, prothrombin index, pseudocholinesterase, albumin, GOT, GPT, gamma-GT, and clinical findings such as ascites, encephalopathy (assessed with the number connection test = NCT), and nutritional status. Between patients who died and those who survived the following 2 years, there were significant differences in the following parameters at the time of inclusion in the study: encephalopathy judged by NCT (p = 0.001), serum albumin (p = 0.0012), postprandial serum bile acids (p = 0.0024), fasting serum bile acids (p = 0.0025), pseudocholinesterase (p = 0.0044), GOT (p = 0.015), bilirubin (p = 0.016), and prothrombin index (p = 0.01). None of the other parameters investigated, including SP-III-P (p = 0.46), revealed any statistically significant differences between patients who died and survivors. The prognostic significance of laboratory tests and recorded clinical findings was evaluated, either alone or in combination with life-table analysis using the Cox model. SP-III-P, alone or in combination with other parameters, failed to improve prediction of mortality in patients with cirrhosis. In comparison to the Child classification (p = 0.0004) the combination of NCT and postprandial serum bile acids showed a similar ability (p = 0.0003) to predict patient survival.
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PMID:Predictive value of serum procollagen-III-peptide for the survival of patients with cirrhosis. 180 22

The effects of lipid peroxide on protein catabolism after severe burn injury are studied. Burned rats (30% TBSA III) were divided randomly into two groups: group A (N = 120) received I. M. injection of bovine serum albumin (BSA) served as control; group B (N = 146), the treated group, receiving I. M. injection of superoxide dismutase (SOD) and catalase (CAT). It was found that in PBD 5, 7, 9, 11, 3-Methyl histidine (3-Mehis) excretion was significantly lower in group B than in group A (P less than 0.01); and that in group B cumulative urinary nitrogen (UN) excretion and cumulative nitrogen balance in the eleven-day period after burns were significantly lower than in group A (P less than 0.01); On PBD 12, serum GOT and GPT were higher significantly in group A than that in group B (P less than 0.05). Besides, in group B the total nitrogen content in liver and gastrocnemius muscle on PBD 12 was significantly higher than in group A (P less than 0.05). These findings suggest that a certain relationship exists between lipoperoxide and increased protein catabolism after severe burns. SOD and CAT, the oxygen radical scavengers, can reduce protein catabolism to a certain extent, and protect the hepatic function from being injured.
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PMID:[Effect of lipoperoxide on catabolism of protein in burns in rats]. 181 69

Nine women with symptomatic precirrhotic primary biliary cirrhosis have been treated with oral pulse methotrexate, 15 mg/wk, for 12-34 months. Three women had pruritus, two fatigue, and four pruritus and fatigue. Itching disappeared and fatigue lessened or disappeared in all within 4-11 months after starting methotrexate. All who itched were able to discontinue cholestyramine (five) or antihistamines (two). Biochemical tests of liver function improved in all patients and then worsened in three when methotrexate was discontinued or the dose lowered. Mean serum alkaline phosphatase decreased from 471 to 171 U/L (P less than 0.01), serum bilirubin from 0.99 to 0.59 mg/dL (P less than 0.05), and serum alanine aminotransferase from 132 to 61 U/L (P = 0.02), and serum cholesterol fell from 265 to 213 mg/dL (NS). The decrease in serum cholesterol was significant, P = 0.05, if data were used just from the six women whose baseline serum cholesterol levels were elevated. Serum albumin remained normal in all. The serum bilirubin levels became normal in three of four patients with elevated levels. The serum alkaline phosphatase levels became normal in four patients and the alanine aminotransferase levels in three. Liver histology improved in five patients and was stable in the remaining four based on a quantitative evaluation of coded liver biopsy specimens. The improvement in histology was primarily due to decreased portal inflammation and bile duct injury. The titer of antimitochondrial antibody decreased in seven patients. The data suggest that methotrexate may be effective treatment for precirrhotic primary biliary cirrhosis. Controlled trials are needed to evaluate long-term efficacy and toxicity.
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PMID:Treatment of primary biliary cirrhosis with low-dose weekly methotrexate. 193 16


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