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)

A 2-year-old spayed female Siamese cat was presented with clinical liver disease characterized by anorexia; depression; elevations in serum levels of alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase; hyperbilirubinemia; and icterus. Liver biopsy diagnosed hepatocellular degeneration with marked centrilobular hepatocellular accumulation of rhodanine-positive brown granules. Subsequent postmortem examination revealed similar granular material in the epithelium of the proximal convoluted tubules and collecting ducts of the kidney and alveolar epithelium and macrophages in the lung. The liver and kidney copper concentrations were 4,074 and 792 ppm dry weight, respectively. Hepatic degeneration in this cat apparently was due to excessive accumulation of copper.
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PMID:Hepatopathy associated with excessive hepatic copper in a Siamese cat. 748 20

This is a case report of a boy with a combination of two rare disorders:growth hormone deficiency (GHD) and Wilson disease. To our knowledge, no comparable case has yet been published in the literature. GHD was diagnosed at the age of 4.5 years (height standard deviation score (SDS) -4.85). However, because of a difficult family background, growth hormone (GH) therapy could not be started. The boy was not seen again until the age of 7.7 years (height SDS -4.77), when GHD was reconfirmed and GH therapy could be initiated (dose 0.6 IU/kg/week). At that time, elevated liver enzymes (GPT 128 U/l, GOT 67 U/l, gamma-GT 28 U/l) confused diagnostic procedures. On GH, growth velocity SDS increased from -1.86 to +4.50 in the first year and +3.87 in the second year, and height SDS increased to -4.26 and -3.59. However, serum IGF-I levels did not normalize (max. 67 ng/ml), and liver enzymes were still elevated. At the age of 10 years, Wilson disease was diagnosed in view of low concentration of serum ceruloplasmin, elevated urinary copper excretion and high copper content in a liver biopsy sample. Under a combined therapy with D-penicillamine and GH, serum liver enzymes decreased, and IGF-I levels increased to normal. Height SDS for chronological age has improved constantly.
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PMID:Effect of growth hormone on IGF-I levels in a patient with growth hormone deficiency and Wilson disease. 764 26

In the present work the influence of the administration of industrial emissions from a zinc and copper plant on aspartate aminotransferase (AST), alanine aminotransferase, gammaglutamyl transferase, creatine phosphokinase (CK), total bilirubin, serum zinc levels and the genetic apparatus was studied on seven ewes. Each animal was given a dose of 31.99 g of emissions per day. The first and the last animals died of zinc intoxication on days 42 and 58, respectively. Significantly increased zincemia could be observed from day 8 of the experiment (P < 0.01). In the enzymes under investigation, the most pronounced effects of the emission were seen in AST and CK activities. In comparison with the starting levels, AST values revealed significant differences on days 37 and 58 (P < 0.05 and P < 0.01, respectively), and CK on day 58 (P < 0.01). Significantly increased bilirubinemia (P < 0.01) could be observed from day 8 of the experiment. In the period prior to the first gavage of emission and day 30 of administration no significant increase of chromosome breaks per cell was observed in the experimental sheep. The genotoxic effect of the emission was also stated on the basis of recombination frequency visualized by means of the sister chromatid exchange test; on day 30, the increase of these disturbances revealed statistical significance (P < 0.01).
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PMID:Effects on enzymes and the genetic apparatus of sheep after administration of samples from industrial emissions. 786 91

A number of biochemical events accompany the development of chronic liver disease and its evolution into hepatic cancer. Low plasma zinc and high plasma copper levels have been observed in individuals with advanced hepatocellular liver disease. Moreover, many investigators have demonstrated an increase in serum estradiol levels in individuals with chronic liver disease and hepatocellular carcinoma (HCC). In the present study, the relationship between these biochemical events and HCC was investigated in an animal model. Specifically, carbon tetrachloride (CCL4) was administered intragastrically to 20 female Sprague Dawley rats for 30 weeks. All 20 animals developed cirrhosis. Six (30%) developed HCC. Significantly higher serum estradiol, zinc and copper levels were observed in the rats developing HCC as compared with those with cirrhosis alone (P < or = 0.05, 0.01 and 0.001, respectively). A trend toward increased serum levels of progesterone, ALT and total bilirubin (0.1 > or = P < or = 0.05) was found in the animals developing HCC. No differences in serum testosterone and alkaline phosphatase levels were noted between animals with and without HCC. These studies demonstrate that in animals with experimental CCL4-induced cirrhosis and HCC serum levels of estradiol, zinc and copper are increased, as is the case in man.
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PMID:CCL4-induced liver cirrhosis and hepatocellular carcinoma in rats: relationship to plasma zinc, copper and estradiol levels. 795 73

This study was planned to investigate the effects of copper (Cu) deficiency on liver and bone metabolism in malnourished children. Serum total calcium (Ca), inorganic phosphorus (P), Ca/P, Cu/Ca, Cu/P ratios and alkaline phosphatase (ALP) activity values were analyzed. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyltransferase (GGT) enzyme activities and the ALT/AST (De Ritis) ratio as well as their correlations with Cu were tested to determine liver function. The results of the study showed that Cu deficiency directly affects the organic matrix formation, and by the suppression of ALP activity, indirectly causes decalcification. In the liver, however, no direct effect of Cu deficiency was seen. Deterioration in liver function and Cu deficiency increased parallel with the severity of malnutrition. Thus we concluded that a correlation exists between Cu and the parameters that indicate liver function.
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PMID:Effect of copper on liver and bone metabolism in malnutrition. 797 11

In order to assess the liver protective activity and the antioxidant properties of a new silybin complex (IdB1016), we carried out a short-term pilot study on 20 patients with chronic active hepatitis (CAH), randomly assigned to 240 mg of silybin b.i.d. (10 patients, 4 m/6 f, mean age: 50 years) or placebo (10 patients, 2 m/8 f, mean age: 55 years). Blood samples were collected before and after 7 days of treatment for liver function tests (LFTs), malonaldehyde (MDA) as an index of lipid peroxidation, and copper (Cu) and zinc (Zn), two trace elements involved in protecting cells against free radical-mediated lipid peroxidation. In the treated group, there was a statistically significant reduction of mean (+/- SEM) serum concentrations of aspartate aminotransferase (AST) from 88.0 (+/- 13.3) to 65.9 (+/- 7.5) u/l, (p < 0.01), of alanine aminotransferase (ALT) from 115.9 (+/- 12.9) to 82.5 (+/- 10.6) u/l (p < 0.01), of gamma-glutamyltranspeptidase (gamma-GT) from 51.4 (+/- 9.3) to 41.3 (+/- 4.2) u/l (p < 0.02) and of total bilirubin (TB) from 0.76 (+/- 0.08) to 0.53 (+/- 0.04) mg/dl (p < 0.05). Alkaline phosphatase (AP) fell slightly from 143.4 (+/- 6.4) to 137.5 (+/- 7.8) u/l. There were no significant changes in MDA, Cu or Zn serum concentrations. These results show that IdB1016 may improve LFTs related to hepatocellular necrosis and/or increases membrane permeability in patients affected by CAH.
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PMID:A pilot study on the liver protective effect of silybin-phosphatidylcholine complex (IdB1016) in chronic active hepatitis. 822 95

1. Over an 8-year period, 19 biochemical parameters have been determined at various ages in the blood serum of 92 clinically healthy Lechwe waterbucks (Kobus leche), 33 males and 59 females. 2. Significant differences have been noted with age. In neonates, the lowest values of total proteins, glucose, creatinine, urea, AST, ALT and iron have been noted; the highest ones have been seen for cholesterol, alkaline phosphatase, calcium and phosphorus. 3. With regard to sex, raised values of glucose, urea, alkaline phosphatase and ALT, and lowered values of cholesterol, have been noted in juvenile females compared with males of the same age. 4. In adult females, higher levels of urea and cholesterol and lower levels of glucose, triglycerides and natrium have been recorded compared with males. 5. With sex and age, no significant changes have been found in the levels of GGT, magnesium, chlorides and copper. 6. Our findings are discussed with those abstracted from the literature for related species.
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PMID:Serum chemistry profiles for Lechwe waterbucks (Kobus leche): variations with age and sex. 840 53

Fischer rats were a fed diet supplied with copper chloride (150-600 ppm) for 60 d from weaning. Serum (glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) activities were increased with the increase of Cu concentration in the diet. Biliary excretion of Cu was related to the dietary Cu level. Depositions of hepatic and renal Cu were also related to the dietary Cu level in a dose-dependent manner. In particular, hepatic (155.2 +/- 13.3 micrograms/g) and renal (44.9 +/- 4.4 micrograms/g) Cu concentrations increased abruptly in the Cu-600 ppm group. In the liver, about 60% of Cu was distributed in the soluble fraction (100,000 g supernatant). In the Cu-600 ppm group, 25% of cystosolic Cu was bound to metallothionein (MT). Our results suggest that chronic exposure to Cu appears to have a deleterious effect on the hepatic function, and further, that even in rats with normal biliary Cu excretion, clearance of Cu from the liver may be marginal when dietary Cu is near the 600-ppm level. Although Cu is an essential nutrient, an overload of Cu should be avoided.
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PMID:Response of hepatic function to hepatic copper deposition in rats fed a diet containing copper. 856 84

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.
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PMID:[Evaluation of the combined effect of cupric chloride and sodium nitrite on selected biochemical parameters in rat plasma (subchronic exposure)]. 861 20

Trientine dihydrochloride (trientine) is an alternative medicinal copper chelating agent for patients with Wilson's disease of penicillamine intolerance. We examined the effects of trientine on the spontaneous development of hepatitis and hepatic tumors, by its short-term and long-term administration to Long-Evans cinnamon (LEC) rats with an accumulation of copper in the liver, as animal models of Wilson's disease. Male rats were given trientine in their drinking water at 1500 ppm for 18 weeks, from 6 weeks to 24 weeks of age in short-term experiment, and 1500 ppm for 27 weeks then 750 ppm for 52 weeks, from 8 to 87 weeks of age in the long-term experiment. Development of hepatitis was observed in the control LEC rats at 18 weeks of age. They had high levels of plasma transaminases (glutamic oxaloacetic transaminase [GOT], glutamic pyruvic transaminase [GPT]), and on pathological examination, hepatocyte destruction was observed. Histological findings revealed that short-term administration of trientine inhibited the development of hepatitis remarkably. The plasma GOT and GPT levels of treated animals were only slightly higher than those of normal LEA (Long-Evans with agouti coat color) rats, a sibling line of LEC rats. Copper levels in the liver were decreased by a maximum of 50 percent. In the long-term administration of trientine, the incidence of hepatic cell carcinoma (HCC) in the treated rats was 67 percent that of the untreated LEC rats, and the number of HCCs per rat in the treated group was 0.7 +/- 0.5, being significantly lower as compared with 4.7 +/- 3.5 in the untreated rats. Additionally, the development of cholangiofibrosis in LEC rats was completely prevented by long-term administration of the agent. The copper level in the liver of treated rats was reduced by 33 percent at 87 weeks of age. Development of HCC in LEC rats might be partly, but not totally, because of copper accumulation. No effects on the levels of copper, iron, or zinc in the liver of LEA rats was detected, and no adverse effects were detected in either LEC or LEA rats after both short- and long-term administration of trientine in drinking water.
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PMID:Inhibition of hereditary hepatitis and liver tumor development in Long-Evans cinnamon rats by the copper-chelating agent trientine dihydrochloride. 866 30


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