Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. An improved procedure is reported for purification of the amine dehydrogenase from methylamine-grown Pseudomonas AM1 which yielded a product homogeneous by sedimentation and disc-electrophoretic analysis, with molecular weight of 133000. 2. The purified enzyme had absorption maxima at 280 and 430nm. On aging, a third peak appeared at 325nm, and the 430nm peak decreased in intensity. This spectrum was independent of pH. 3. Addition of 2.5mm-semicarbazide, phenylhydrazine, hydrazine or hydroxylamine produced modified spectra with maxima respectively at 400, 440, 395 and 425nm. 4. Aerobic addition of methylamine resulted in a bleaching of the 430nm peak and the appearance of a new one at 325nm. This spectral change was retained after removal of the methylamine by dialysis. The original spectrum could be restored on addition of phenazine methosulphate. 5. Addition of borohydride partially inactivated the enzyme and produced spectral changes similar to those observed with methylamine. Pre-treatment with methylamine prevented the inactivation by borohydride. The degree of inactivation could be increased by alternate phenazine methosulphate and borohydride treatments. 6. The addition of methylamine or borohydride each caused shifts in the fluorescence emission maximum from 348 to 380nm. 7. Lineweaver-Burk plots of reciprocal activity against reciprocal concentration of either of the substrates n-butylamine or phenazine methosulphate were consistent with a mechanism that involves interconversion of two free forms of the enzyme by the two substrates. 8. The enzyme, although spectrally modified, was not inactivated by dialysis against diethyldithiocarbamate, and contained about 0.27 g-atom of copper/mol, with small traces of cobalt, iron and zinc. 9. Conventional methods of resolution did not release the prosthetic group. Heat denaturation after treatment of the enzyme with methylamine liberated a yellow chromophore which did not reactivate resolved aspartate aminotransferase, and whose spectral, electrophoretic and fluorescence properties did not agree with any recognizable pyridoxal derivatives. 10. Despite the inconclusive results with the isolated chromophore, the observations on the enzyme suggest that it may contain a pyridoxal derivative bound as a Schiff's base which is converted into the pyridoxamine form on aerobic treatment with methylamine and reconverted into the pyridoxal form with phenazine methosulphate. 11. The copper detected is probably not involved in the enzyme mechanism, since most copper-chelating agents are not inhibitory, and since the enzyme does not react with oxygen.
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PMID:Microbial oxidation of amines. Spectral and kinetic properties of the primary amine dehydrogenase of Pseudomonas AM1. 512 84

The most common type of genetic relationship between cytosolic and mitochondrial isoenzymes will probably be found to be divergent evolution from a common ancestral form. This is firmly established for the aspartate aminotransferases and less directly so in other cases. The two isoenzymes of aspartate aminotransferase have evolved at roughly equal rates at the level of total amino acid sequence but certain limited surface regions of the mitochondrial form have been much more highly conserved than corresponding regions in the cytosolic protein; these regions probably play a role in topogenesis of the mitochondrial isoenzyme. It is of interest that nearly all mitochondrial proteins are initially synthesised as precursors of molecular weight greater than the mature forms. In the case of aspartate aminotransferase, and possibly of other such isoenzymes, the N-terminus of the mature protein is nearly coincident with that of the cytosolic isoenzyme. Hence during evolution either the gene for the mitochondrial isoenzyme has gained an extra coding region for this N-terminal extension or, less likely, the structural gene for the cytosolic form has suffered a sizeable terminal deletion. Cytosolic and mitochondrial superoxide dismutases have not shared a common ancestral form as shown by the fact that their primary structures are completely unrelated. On the other hand, the mitochondrial and prokaryotic enzymes are clearly related. There is now, however, evidence to suggest that some prokaryotes possess a copper/zinc enzyme related to the eukaryotic cytosolic form. Hence the possibility arises that primitive prokaryotes possessed both proteins. The copper/zinc superoxide dismutase has been retained in the cytosol of eukaryotic cells and a few bacterial species.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Structural and genetic relationships between cytosolic and mitochondrial isoenzymes. 639 70

We examined sera from 159 patients with ischemic heart disease and hypertension and from 50 apparently healthy control subjects for content of trace elements, cholesterol, triglyceride, and enzymes. Concentrations of copper, cobalt, cholesterol, and triglyceride were increased in all patients, but calcium was decreased in patients with hypertension, acute myocardial ischemia, and acute myocardial infarction. Also accompanying acute myocardial infarction were decreased concentrations of zinc and iron but increases in nickel, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. Magnesium concentration was lower in patients with acute myocardial ischemia. In acute myocardial infarction, the concentrations of copper, zinc, and iron were higher after 21-30 h (as compared with the values at 0-10 h), by which time concentrations of calcium, magnesium, cobalt, and alanine aminotransferase had decreased. The variation in concentration of trace elements in serum from cases of ischemic heart disease and hypertension corresponds to the severity of the disorder.
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PMID:Trace elements in serum from Pakistani patients with acute and chronic ischemic heart disease and hypertension. 671 25

Pretreatment with Zn is known to produce tolerance to several toxic effects of Cd. This study was designed to determine if zinc pretreatment decreased Cd-induced lethality and hepatotoxicity. Rats given 4.0 mg Cd/kg, iv, died within 10 to 20 hr while there was no mortality in rats pretreated with Zn (12 mg Zn/kg, sc, 48 and 24 hr prior to Cd challenge). Ten hr after Cd, plasma aspartate aminotransferase and sorbitol dehydrogenase activities were markedly elevated and extensive histopathologic lesions of the liver were evident in control rats while such injury was not evident in Zn-pretreated rats. To examine the mechanism of this tolerance, distribution of Cd to 14 organs and the subcellular distribution in 6 organs (liver, kidneys, intestines, heart, spleen, and testes) was determined in control and Zn-pretreated rats. Two hours after challenge (3.5 mg Cd/kg, iv, 7 microCi 109Cd/mg Cd), the distribution of Cd to the liver markedly increased after Zn pretreatment without concomitant decreases in other tissues. Zn pretreatment resulted in distribution of more Cd to hepatic cytosol and less associated with endoplasmic reticulum. Gel filtration chromatography indicated that most cytosolic Cd was bound to metallothionein. These data suggest that Zn pretreatment reduces Cd-induced hepatotoxicity which prevents the lethal effects of Cd possibly by altering the hepatic subcellular distribution of Cd.
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PMID:Zinc-induced tolerance to cadmium hepatotoxicity. 674 Jun 79

The influence of Zn on the acute hepatotoxicity of pyrrolizidine alkaloids (PAs) was determined in male rats. Zinc, 72 mumol/kg as ZnCl2, was administered ip for 3 consecutive days, followed 16 h after the last dose by a single ip injection of purified mixed PAs (80, 120, or 160 mg/kg) obtained from tansy ragwort (Senecio jacobaea). Hepatotoxicity of the PAs was assessed by measuring the activities of plasma glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) and by histological examination of the liver. There was a dose-dependent increase in plasma GOT and GTP 24 h after PA administration, whereas no significant increase of these enzymes was seen after administering Zn alone. The 7-fold increase in plasma GOT and 12-fold increase in GPT after PA (120 mg/kg) were reduced to 2.4- and 2.1-fold, respectively, by Zn pretreatment. The PA-induced liver necrosis was either reduced in severity or abolished by Zn when the PA dose was 80 or 120 mg/kg. These results suggest a protective effect of Zn against PA hepatotoxicity. The protective effect was associated with a marked increase in liver metallothionein and a significant decrease in hepatic cytochrome P-450 content, aminopyrine N-demethylase activity, and in vitro microsomal conversion of the PAs to pyrroles. Liver nonprotein sulfhydryls were unchanged. The possible role of metallothionein in the sequestration of pyrrole metabolites merits further investigation.
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PMID:Protective action of zinc against pyrrolizidine alkaloid-induced hepatotoxicity in rats. 709 90

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

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

Zinc concentrations in serum from 99 patients with acute myocardial infarction were correlated with the incidence of further complications and with activities in serum of the "cardiac" enzymes aspartate aminotransferase and lactate dehydrogenase. A significantly subnormal zinc concentration was observed for the patients, the lowest values being observed on the second and third days after infarct, particularly in patients with serious complications. Moreover, a linear correlation was observed between zinc values and enzyme activities until the fourth day after infarct. We conclude that measurement of zinc in the serum may have diagnostic value for acute myocardial infarction, although its prognostic value is still speculative.
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PMID:Zinc concentrations in serum as related to myocardial infarction. 742 47


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