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:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of copper chelation was studied in a group of children with intrahepatic cholestasis of childhood (IHCC) and increased liver copper levels. Initial therapy was D-penicillamine (10 mg/kg/day), being replaced by triethylenetetramine dihydrochloride (20 mg/kg/day) when side-effects of D-penicillamine occurred. Eight children completed two years of copper chelation. Pruritus remained the main symptom and did not improve. Two patients developed D-penicillamine side-effects - one patient after nine months (marked anorexia, lassitude) and one other patient after 19 months (thrombocytopenia). Two patients died during the study, in one of these normal hepatic copper concentration was achieved. Hepatic copper concentrations decreased in seven of eight patients from 8.6 (2.7 +/- 16.2) mumol/g to 3.4 (0.6-16.5) mumol/g (median and range (0.05 less than 0.01) and serum aspartate transaminase increased in seven of eight patients (p less than 0.05). Histological assessment of serial liver sections revealed increased fibrosis and cholestasis despite reductions in hepatic copper levels during the study. This study showed that D-penicillamine therapy was associated with significant side-effects, while marked clinical, biochemical, or histological improvement did not follow effective copper chelation therapy in intrahepatic cholestasis of childhood.
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PMID:Copper chelation therapy in intrahepatic cholestasis of childhood. 684 32

Copper toxicity occurred in North Ronaldsay sheep fed on a diet of terrestrial herbage relatively high in molybdenum. Five sheep were taken from the island of North Ronaldsay, Orkney to the veterinary investigation centre at Thurso and fed solely on the herbage of the laboratory paddocks, supplemented in winter by hay made from these paddocks. The level of copper, molybdenum, zinc and total sulphur in the terrestrial herbage was analysed, together with the seaweeds which form the major part of the diet on North Ronaldsay. Serum copper, vitamin B12 and serum aspartate aminotransferase levels were obtained. Four of the five sheep died on this diet of terrestrial herbage and had liver copper levels of 1379, 1723, 2279 and 2281 mg/kg. The susceptibility of the North Ronaldsay breed of Orkney sheep to copper poisoning when first introduced to a diet of purely terrestrial herbage is demonstrated by the high liver copper levels of the four dead sheep compared to the normal serum copper levels and unimpaired health of two other breeds of sheep and a north country Cheviot cross North Ronaldsay ram.
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PMID:Copper poisoning in sheep from North Ronaldsay maintained on a diet of terrestrial herbage. 714 42

In primary biliary cirrhosis (PBC) liver copper retention occurs as a complication of cholestasis. By analogy with Wilson's disease, it has been suggested that copper retention is hepatotoxic in PBC, and this has been the rationale for the use of D-penicillamine in this disease. The hypothesis that copper is hepatotoxic in PBC has not been tested and in this study we have evaluated the role of liver copper retention in the pathogenesis of PBC. Sixty-four patients with PBC have been studied. Fifty-four had increased liver copper concentrations. Liver cell synthetic function was well preserved. All the patients had normal prothrombin times, and only two had subnormal serum albumin concentrations. There was no correlation between liver copper concentrations and the degree of liver cell damage assessed biochemically (aspartate transaminase), and histologically. Electron microscopy was performed on liver biopsies from five patients with markedly increased liver copper concentrations. The liver cell ultrastructure was compatible with cholestasis. Liver cells contained electron dense lysosomes, which were shown to contain copper and sulphur by x-ray probe microanalysis. The characteristic organelle changes associated with copper toxicity in Wilson's disease were not observed. The biochemical, histological, and histochemical differences between PBC complicated by liver copper retention, and Wilson's disease, indicates that there are differences in the handling of copper in these disease. In this study we could find no evidence to suggest that copper plays an important role in the pathogenesis of liver dysfunction in PBC.
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PMID:Is copper hepatotoxic in primary biliary cirrhosis? 730 88

1. Rainbow trout (Salmo gairdneri) of mean initial weight 15 g were given either a low-manganese or control diet containing 1.3 and 33 mg Mn/kg dry diet respectively. 2. Weight gains over a 24-week feeding period were the same for both groups of trout. 3. Hepatosomatic index, blood packed cell volume and haemoglobin concentration, plasma protein and the activities of aspartic aminotransferase (EC 2.6.1.1) and alanine aminotransferase (EC 2.6.1.2) were unaffected by dietary Mn intake. 4. Plasma potassium and iron levels were increased in the trout given the low-Mn diet. 5. The hepatic levels of magnesium, sodium, K, zinc, copper, Mn and phosphorus were significantly reduced in the fish given the low-Mn diet. 6. In those trout given the low-Mn diet the levels of Mn and calcium in the vertebral ash were significantly reduced. 7. The hepatic activity of Cu-Zu superoxide dismutase (EC 1.15.1.1; Cu-ZnSOD) and of Mn superoxide dismutase (EC1.15.1.1; MnSOD) in cardiac muscle and liver was reduced in the group of trout given the low-Mn diet. The fall in Cu-ZnSOD and MnSOD activities coincided with reduced tissue levels of their respective metal components.
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PMID:The effect of low dietary manganese intake on rainbow trout (Salmo gairdneri). 731 45

1. A cereal-based diet containing 7.6 mg copper/kg was fed ad lib. to laying hens for up to 48 d. Four other groups were given the control diet to which was added hydrated copper sulphate to provide 250, 500, 1000 and 2000 mg added Cu/kg. 2. Hens were killed on day 0 and after 3, 6, 12, 24 and 48 d. Records were kept of body-weight, food consumption, egg production and egg weight. 3. After slaughter blood haemoglobin, packed cell volume, serum Cu and aspartate aminotransferase (AAT; EC 2.6.1.1) were measured. The liver, kidneys, a sample of breast muscle, oviduct, ovary and gizzard were weighed. Gizzard, spleen, liver and kidney tissue were examined histologically. 4. The Cu, zinc and iron concentrations of liver, kidneys and breast muscle and the manganese concentrations of liver and kidneys were determined. 5. Body-weight loss occurred at 500-2000 mg added Cu/kg diet. Egg production was depressed by level of added Cu and period of time on the Cu-containing diets. 6. Mean liver, kidney, oviduct and ovarian weights per unit body-weight were depressed by Cu in the diet and the effect increased with period of time on the diets. Mean gizzard weight per unit body-weight was increased by dietary added Cu and by time. 7. Cu concentrations in the liver were increased by dietary level of added Cu and period of time on the diet. Zn concentration in liver increased at 1000 and 2000 mg added Cu/kg diet and liver Fe concentration was increased at these levels. Histological examination of the gizzard indicated that the Cu content of the gizzard lining increased with dietary added Cu.
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PMID:Effects of level of dietary copper sulphate and period of feeding on the laying, domestic fowl, with special reference to tissue mineral content. 737 Feb 11

1. Cereal-based diets containing 0, 500, 1000 or 2000 mg added copper/kg were offered ad lib. to laying hens for 8 weeks. All the hens were subsequently offered the control diet (no added Cu, 7.5 mg Cu/kg). 2. Hens from each treatment were killed at 0, 2, 4, 6 and 8 weeks after removal of the Cu-supplemented diets. Records were kept of body-weight, food consumption and egg production. 3. After slaughter, blood haemoglobin, packed cell volume, serum Cu and asparate aminotransferase (AAT; EC 2.6.1.1) were assayed. The liver, kidneys, oviduct, ovary, gizzard, caeca and bile duct were weighed. 4. Mean Cu, zinc and iron concentration of liver, kidneys and caecal contents were determined. 5. The adverse effects of Cu on body-weight, food intake, egg production and liver, oviduct, ovary, gizzard and bile weights were rapidly reversed by removal of added Cu from the diets. 6. Greatly enhanced liver Cu concentration resulted from feeding the high-Cu diets but this effect was rapidly reversed on removal of added Cu from the diets. Liver Fe concentration showed a less marked but similar effect. 7. The Cu concentration of caecal contents was increased by Cu supplementation and rapidly reduced after withdrawal of the Cu-containing diets.
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PMID:Effects of withdrawal of copper sulphate from the diet of the mature domestic fowl with special reference to production and tissue mineral content. 741 96

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

The effects of 2,3-dimercaptopropane sulphonate (DMPS) and N-(2-mercapto-2-methylpropanoyl)-L-cysteine (bucillamine) against the renal damage induced by gold sodium thiomalate (AuTM) in adjuvant-arthritic rats were studied. Arthritic rats induced by adjuvant using Mycobacterium butyricum were injected intraperitoneally with a chelating agent (0.6 mmol/kg) immediately after intramuscular injection of AuTM (0.066 mmol/kg) every other day for 21 days. Treatment with DMPS and bucillamine prevented increases in the urinary excretion of protein, aspartate aminotransferase, and glucose and blood urea nitrogen level after AuTM injection. AuTM prevented the increase in both adjuvant-injected and uninjected hind-feet volumes. The prevention of these inflamed lesions by AuTM was not affected by DMPS and bucillamine. These chelating agents decreased the gold concentration in the kidney and liver after AuTM administration, but did not affect the hepatic and renal concentrations of copper, zinc, iron, and calcium except the renal copper level after AuTM. These findings suggest that DMPS and bucillamine are very useful antidotes for gold toxicity.
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PMID:The utility of chelating agents as antidotes for nephrotoxicity of gold sodium thiomalate in adjuvant-arthritic rats. 771 81

The accumulation process of copper (Cu) in the liver and the following metabolic disorder of Cu were examined in LEC rats, a mutant strain which accumulates Cu with age and shows spontaneous acute hepatitis and/or hepatoma. Cu concentration in the liver of female rats was approximately 220 micrograms/g liver at 2 weeks of age, decreased to 100 micrograms/g liver at 4-6 weeks, and then started to increase with age linearly to the highest concentration of 250 micrograms/g liver at 16 weeks. Although the Cu level expressed by concentration (microgram/g liver) decreased during weaning, it increased linearly with age when it was expressed by content (mg/liver), indicating a constant and preferential accumulation of Cu in the liver. Cu concentration stopped increasing at 16 weeks in the liver, followed by a sudden decrease to 1/2 the highest level. Biological markers (serum lactate dehydrogenase and glutamic-oxaloacetic transaminase activities) for liver damage started to increase, together with the appearance of signs of jaundice, when Cu attained the highest concentration. Distributions of Cu and zinc (Zn) in the supernatant fraction of the liver indicated that both metals were mostly distributed to metallothionein (MT) and, to a small extent, to superoxide dismutase on a gel filtration column throughout the course of the experiments. Serum Cu concentration started to increase in a form of ceruloplasmin, together with serum marker enzyme activities for liver damage. Cu concentration in the kidneys also started to increase after the increase of serum Cu. The results indicate that Cu accumulates in the form of MT in the liver of LEC rats to a maximum level of approximately 250 micrograms/g liver, and then decreases suddenly with the onset of acute hepatitis. The maximum level seems to be related to the capacity of MT synthesis, and acute hepatitis is assumed to occur when Cu accumulates beyond the capacity. Serum Cu started to increase, from the abnormally low level, when the metal accumulated beyond the capacity of MT synthesis in the liver, and it was partly reabsorbed by the kidneys and the rest was excreted into urine. Changes in iron and zinc levels were determined and discussed in relation to those of Cu.
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PMID:Copper metabolism leading to and following acute hepatitis in LEC rats. 771 95

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


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