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)

Chronic ammonia toxicity in experimental mice was induced by exposing them for 2 and 5 days to 5 % (v/v) ammonia solution. The enzymes concerned with glutamate metabolism (aspartate-, alanine- and tyrosine aminotransferases, glutamate dehydrogenase and glutamine synthetase) and (Na+ + K+)-ATPase were estimated in the three regions of brain (cerebellum, cerebral cortex and brain stem) and in liver. Glutamate, aspartate, alanine, glutamine and GABA, RNA and protein were also estimated in the three regions of brain and liver. A significant rise in the activity of (Na+ + K+)-ATPase in all the three regions of brain along with a fall in the activity of alanine aminotransferase was noticed. Changes in the activities of other enzymes were also observed. A significant increase in alanine and a decrease in glutamic acid was observed while no change was observed in the content of other amino acids belonging to the glutamate family. As a result of this, changes in the ratios of glutamate/glutamine and glutamate + aspartate/GABA was observed. The results indicated that the brain was in a state of more depression and less of excitation. Under these conditions the liver tissue was showing a profound rise in the activity of the enzymes of glutamate metabolism. The results are further discussed.
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PMID:Chronic metabolic effects of ammonia in mouse brain. 9 19

The aim of this study was to investigate the effect of the protein synthesis inhibitor cycloheximide on the serum activities of gamma-Glutamyltransferase, Glutamate dehydrogenase and Glutamate pyruvate transaminase after bile duct obstruction in rats. The results showed that the increase of these enzyme activities after bile duct obstruction is further augmented by cycloheximide. Determinations of total bile acids in serum and liver showed that also the bile acid concentrations rise to a higher level after bile duct obstruction + cycloheximide than after bile duct obstruction alone. It is concluded that the effect of cycloheximide on the serum enzyme activities in extrahepatic cholestasis is produced via an influence on the metabolism of bile acids. This stresses the central role of bile acids for alterations of enzyme activities in extrahepatic cholestasis. Further, the effect of cycloheximide on bile acids after bile duct obstruction has not been reported before.
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PMID:Activities of APh, gamma-GT, GlDH and GPT and bile acid concentrations in serum after bile duct obstruction and cycloheximide in the rat. 168 1

At sublethal concentrations, cypermethrin caused a decrease in total proteins and an increase in free amino acids, protease, alanine aminotransferase and aspartate aminotransferase in liver, brain and gill tissues of Tilapia mossambica. Nitrogen metabolic profiles like ammonia, urea and glutamine were also elevated in all the tissues as a consequence of cypermethrin toxicity. Glutamate dehydrogenase, AMP deaminase and adenosine deaminase activity was also increased in the present study.
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PMID:Cypermethrin induced changes in nitrogen metabolism of fish, Tilapia mossambica. 187 79

In vivo studies with L-[13N]glutamate in the Walker 256 carcinosarcoma implanted under the renal capsule of female Sprague-Dawley rats demonstrate that uptake of glutamate and the rate of incorporation of the nitrogen label from this amino acid into metabolites is slower in the tumor than in nontumorous kidney tissue. Glutamate dehydrogenase, glutaminase, and alanine aminotransferase activities are significantly lower within the tumor than within the adjoining kidney. However, the tumor expresses high levels of aspartate aminotransferase, attesting to the importance of this enzyme in the metabolism of glutamate. Indeed, high performance liquid chromatographic analysis showed that the principal metabolic fate of label derived from L-[13N]glutamate in the tumor is incorporation into aspartate. Measurement of specific activity ratios of glutamate to aspartate shows that the transfer of nitrogen from glutamate to aspartate is rapid and that equilibration of label among components of the aspartate aminotransferase reaction is attained within minutes after tumor uptake. Analyses of the nontumorous portion of the implanted kidney also showed that aspartate is the major recipient of glutamate nitrogen. However, high performance liquid chromatographic analyses of deproteinized tissue revealed that glutamine and ammonia are also significant 13N-labeled metabolites formed from L-[13N]glutamate within the kidney. Proportionately lower amounts of these labeled metabolites were found in the tumor.
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PMID:Short-term metabolic fate of L-[13N]glutamate in the Walker 256 carcinosarcoma in vivo. 197 67

The effect of sub-lethal doses of Malathion and Methyl-parathion was studied on the rat liver enzymes. Intravenous administration of both insecticides at weekly interval for four weeks resulted in increase in heart and spleen weight. Short term (24 hr.) and long term (4 weeks) treatment with insecticides resulted in increased specific activities of liver enzymes, Acid phosphatase, Alkaline phosphatase, Glutamate dehydrogenase, Glutamate oxaloacetate transaminase and Glutamate pyruvate transaminase. The increase in enzyme activity was not as profound when the insecticide administration was spread over 4 weeks. Malathion had greater effect than Methyl-parathion on the biochemical parameters studied.
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PMID:Effect of malathion and methyl-parathion on rat liver enzymes. 212 8

The effect of sub-lethal doses of Malathion and Methyl-Parathion was studied on the rat liver enzymes. Intravenous administration of both insecticides at weekly interval for four weeks resulted in increase in weight of various tissues, i.e., heart and spleen. Short term (24 hr) and long term (4 weeks) treatment with insecticides resulted in increased specific activities of liver enzymes, Acid phosphatase, Alkaline phosphatase, Glutamate dehydrogenase, Glutamate oxaloacetate transaminase and Glutamate pyruvate transaminase. The increase in enzyme activity was not as profound when the insecticide administration was spread over 4 weeks. Malathion had greater effect than Methyl-parathion on the biochemical parameters studied.
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PMID:Effect of malathion and methyl-parathion on rat liver enzymes. 212 17

Previous studies have shown that "xenobiotic" compounds such as the environmental pollutant alpha-hexachlorocyclohexane (alpha-HCH) and the synthetic sex steroid cyproterone acetate (CPA) induce growth of rat liver by hypertrophy and hyperplasia. After withdrawal of the growth stimuli, liver hypertrophy was usually found to be readily reversible. Conflicting observations were made concerning the fate of liver hyperplasia: hepatic hyperplasia persisted when induced by alpha-HCH but was found to be partially reversible when induced by CPA. The present study confirms the reversibility of hepatic hyperplasia induced by CPA in rats: about 30% of liver DNA present at maximal liver enlargement disappeared within 6 days after cessation of CPA treatment. Simultaneously, a dramatic increase in the rate of cell elimination by apoptosis was found. Glutamate-pyruvate transaminase and alkaline phosphatase in serum did not show major increases, suggesting that cell death was not due to lytic membrane damage. Furthermore, if treatment with CPA was continued or resumed, the enhanced DNA content persisted and the number of apoptotic bodies was greatly reduced. These observations suggest that the occurrence of cell death is due to withdrawal of the growth stimulus CPA. It may reflect a regulatory phenomenon serving to maintain homeostasis of cell number. Further studies showed that CPA is rapidly eliminated from rat liver and serum: t 1/2 in the liver is about 11 h. In contrast, alpha-HCH was previously found to be eliminated more slowly: t 1/2 approximately 144 h. The present study revealed that alpha-HCH, CPA and nafenopin lower the number of apoptotic bodies. This suggests that inducers of liver growth can inhibit hepatocellular death by apoptosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth, regression and cell death in rat liver as related to tissue levels of the hepatomitogen cyproterone acetate. 243 63

The activity of glutamate related enzymes and the concentration of glutamine, glutamate and gamma-amino n-butyric acid (GABA) were investigated in the cerebral cortex of rats, in different stages of insulin-induced hypoglycemia. Hypoglycemia was produced by intraperitoneal injection of insulin 0.05-100 units per kg body weight. The minimum required dose to produce irreversible severe hypoglycemia was 0.5 units/kg. In 85% of the cases an insulin induced hypoglycemic convulsion, was achieved 130-150 minutes after injection. Blood glucose levels during insulin induced seizures ranged between 8-15 mg%. In the range of 0.5-100 u insulin/kg the degree of hypoglycemia and the onset of convulsions were identical. The concentration of glutamine was significantly reduced during convulsive and postconvulsive stages. Glutamate and GABA concentrations were reduced significantly in all stages of insulin-induced hypoglycemia. The decrease in glutamine concentration was concurrent with an increase in the activity of its degradative enzyme, glutaminase. This was apparent at the preconvulsive, convulsive and postconvulsive stages. The activity of other enzymes related to energy production such as glutamate dehydrogenase (GDH), glutamate transaminase (GPT) and aspartate aminotransferase (AAT) were also increased. The activity of glutamine synthase (GS) was unaffected by hypoglycemia. Insulin induced changes in glutamine, glutamate and their related enzymes could not be attributed to convulsion since a similar pattern of changes was observed in the preconvulsive and postconvulsive stages, and no changes were detected following picrotoxin-induced seizures.
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PMID:Changes in the activity of glutamate related enzymes in cerebral cortex, during insulin-induced seizures. 257 18

Serum muscle enzyme activity assays were routinely performed in 36 patients with glycogen storage diseases (15 types 1a and 1b, 12 type III, and 9 types VI and IX). Creatine phosphokinase serum activity was increased only in type III. Glutamate-pyruvate transaminase, aldolase and lactate dehydrogenase serum activities were increased in all the forms of glycogen storage disease studied. Muscle involvement may at least partly explain the increased serum enzyme activities in type III.
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PMID:[Determination of blood level of muscle enzymes in glycogenoses with liver involvement: a diagnostic criterion]. 274 13

6-Aminonicotinamide (6-AN), an antimetabolite of pyridine nucleotide synthesis, caused time dependent and regionally selective changes in the activities of the enzymes related to glutamate metabolism in the brain. The NAD+- and NADP+-linked glutamate dehydrogenase showed opposite pattern of changes in cerebellum, whereas cerebral hemispheres and brain stem exhibited similar response. Glutamate oxaloacetate transaminase (aspartate aminotransferase) and malate dehydrogenase, the functional enzymes of malate-aspartate shuttle, were decreased in soluble fraction of cerebral hemispheres and increased significantly in cerebellum after 16 hours of drug administration. Glutamate pyruvate transaminase (alanine aminotransferase) also showed an increase in the activity in cerebellum and brain stem after 8 hours of drug treatment. The EEG patterns obtained from 6-AN treated animals showed periodic bursts, turning to convulsive polyspike activity between 8-16 hours, indicating the onset of comatose-like stage. The results indicate that glutamate metabolism offers considerable anaplerotic potentials following impaired energy state after 6-AN treatment.
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PMID:6-Aminonicotinamide: EEG changes and effects on the activities of enzymes related to glutamate metabolism in rat brain regions. 287 43


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