Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.4.1.2 (glutamate dehydrogenase)
 4,380 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to test the possible involvement of surface proteins on some metabolical aspects of chick glial cell differentiation in culture, perturbations were induced on the glial cell surface membrane by limited trypsinization before seeding. The developmental changes of enzymes involved in the energy metabolism of the cell: malate dehydrogenase (MDH), glutamate dehydrogenase (GDH), hexokinase (HK), lactate dehydrogenase (LDH), enolase as well as glutamine synthetase (GS) were determined in trypsin treated cells and controls. The total protein and DNA content per dish was higher in treated cells than in controls, however the protein ratio towards DNA remained unchanged. The levels of GS, GDH, LDH, and enolase activities were significantly enhanced after trypsin treatment of the cells compared to controls. The enhanced value of total LDH activity is essentially the result of the increase of M subunit containing isoenzymes. Considering that a higher level of GS activity characterizes some maturation of the glial cells (as observed during the maturation of the chick brain) it is apparent that modifications of cell surface located factors, by trypsin treatment, induce differentiation phenomena at the functional state of the glial cells in culture. This may indicate that interactions located at the cell surface are involved in the modulation of key enzymes of the energy metabolism pathway.
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PMID:Trypsinization of chick glial cells before seeding: effects on energy metabolism enzymes and glutamine synthetase. 614 Jun 46

The air-breathing ureogenic walking catfish (Clarias batrachus) faces various environmental constraints throughout the year leading to the problem of accumulation of toxic ammonia. In the present study, the possible role of conversion of accumulated ammonia to various non-essential free amino acids (FAAs) was tested in this fish under hyper-ammonia stress caused by exposing the fish at 25 mM NH(4)Cl for 7 days. Significant accumulation of ammonia of approximately two- to threefold was observed in different tissues (except in the brain), which was accompanied with the significant accumulation of non-essential FAAs in the NH(4)Cl-exposed fish. There was approximately two- to threefold increase of non-essential FAAs in different tissues and in the plasma of the NH(4)Cl-exposed fish compared to the control fish after 7 days of exposure, which was mainly attributable to the increase of Asp, Ala, Gly, Glu, Gln and taurine (Tau) concentrations in general, with certain tissue-specific variations. This was also accompanied with significant increase of activity of certain amino acid metabolism-related enzymes such as the glutamine synthetase (approx. two- to threefold), glutamate dehydrogenase (ammonia utilizing direction) (approx. twofold), aspartate and alanine aminotransaminases (approx. twofold) mainly in the liver, kidney and muscle of the NH(4)Cl-exposed fish. Thus, it appears that the walking catfish has the capacity of active conversion of accumulated ammonia to non-essential FAAs under condition of high concentrations of external ammonia. However, the increase of urea excretion rate due to active conversion of ammonia to urea via the induced urea cycle appears to be quantitatively much more important pathway than the increase of tissue levels of FAAs in dealing with a severe ammonia load.
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PMID:Role of amino acid metabolism in an air-breathing catfish, Clarias batrachus in response to exposure to a high concentration of exogenous ammonia. 1238 86

The objective of this study was to elucidate the mechanisms of acute ammonia toxicity in the aquatic Chinese soft-shelled turtle, Pelodiscus sinensis, and to examine how this turtle defended against a sublethal dose of NH(4)Cl injected into its peritoneal cavity. The ammonia and glutamine contents in the brains of turtles that succumbed within 3h to an intraperitoneal injection with a lethal dose (12.5 micromolg(-1) turtle) of NH(4)Cl were 21 and 4.4 micromolg(-1), respectively. Since the brain glutamine content increased to 8 micromolg(-1) at hour 6 and recovered thereafter in turtles injected with a sub-lethal dose of NH(4)Cl (7.5 micromolg(-1) turtle), it can be concluded that increased glutamine synthesis and accumulation was not the major cause of acute ammonia toxicity in P. sinensis. Indeed, the administration of l-methionine S-sulfoximine (MSO; 82 microgg(-1) turtle), a glutamine synthetase (GS) inhibitor, prior to the injection of a lethal dose of NH(4)Cl had no significant effect on the mortality rate. Although the prior administration of MSO led to an extension of the time to death, it was apparently a result of its effects on glutamate dehydrogenase and glutamate formation, instead of glutamine synthesis and accumulation, in the brain. By contrast, a prior injection with MK801 (1.6 microgg(-1) turtle), a NMDA receptor antagonist, reduced the 24h mortality of turtles injected with a lethal dose of NH(4)Cl by 50%. Thus, acute ammonia toxicity in P. sinensis was probably a result of glutamate dysfunction and the activation of NMDA receptors. NMDA receptor activation could also be exacerbated through membrane depolarization caused by the extraordinarily high level of ammonia (21 micromolg(-1) brain) in the brain of turtles that succumbed to a lethal dose of NH(4)Cl. One hour after the injection with a sub-lethal dose of NH(4)Cl, the brain of P. sinensis exhibited an extraordinarily high tolerance of ammonia (16 micromolg(-1) brain). The transient nature of ammonia accumulation indicates that P. sinensis could ameliorate ammonia toxicity through the suppression of endogenous ammonia production and/or the excretion of exogenous ammonia. Despite being ureogenic and ureotelic, only a small fraction of the exogenous ammonia was detoxified to urea. A major portion of ammonia was excreted unchanged, resulting in an apparent ammonotely in the experimental turtles. Since there were increases in total essential free amino acid contents in the brain, liver and muscle, it can be deduced that a suppression of amino acid catabolism had occurred, reducing the production of endogenous ammonia and hence alleviating the possibility of ammonia intoxication.
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PMID:Mechanisms of and defense against acute ammonia toxicity in the aquatic Chinese soft-shelled turtle, Pelodiscus sinensis. 1806 26