No abstract available.
Animals ; Electroshock* ; Glutamate Decarboxylase* ; Glutamate-Ammonia Ligase* ; Glutamic Acid* ; Glutamine* ; Hippocampus* ; Rats*

The purpose of this study was to determine the effect of regular exercise during dexamethasone injection in the body weight, weight of hind-limb muscles, myofibrillar protein content and glutamine synthetase activity. 180-200g female Wistar were divided into four groups: control, exercise, dexamethasone injection(dexa), and exercise during dexamethasone injection(D+E) group. The dexa group received daily subcutaneous injection of dexamethasone at a dose of 4mg/kg body weight for 7days. The exercise group ran on a treadmill for 60min/day(20minutes every 4 hours) at 10m/min and a 10degrees grade. The control group received daily subcutaneous injection of normal saline at a dose of 4mg/kg body weight for 7 days. The D+E group ran on a treadmill for 60min/day(20minutes every 4 hours) at 10m/min and a 10degrees grade during dexamethasone injection. Body weight of the control group increased significantly from days of experiment, that of the dexa group decreased significantly from day 4 of the dexa group decrease significantly from day 4 of the experiment resulting in a 82.4% decrease compared to the first day of the experiment. Body weight of the D+E group decrease significantly from day 5 of experiment resulting in a 81.77% decrease compared to the first day of the experiment. Body weights, muscle weight and myofibrillar protein content of the plantaris and gastrocnemius decrease significantly and muscle weight of the sleys tended to decrease with dexamethasone injection. Glutamine synthetase activity of the hind-limb muscles increase significantly with the dexamethasone injection. The relative weight of the soleus was comparable to the control group and that of plantaris decrease significantly and that of gastrocnemius tended to decrease compared to that of the control in the dexa group. Body weight and muscle weight of the plantaris and gastronemius of the exercise group were comparable to the control group, and the muscle weight of soleus showed a tendency to increase. The relative weight of the soleus increased significantly and that of the plantaris and gastrocnemius were comparable to the control in the exercise group. Myofibrillar protein content of the soleus and plantaris increased significantly and there was no change of GS activity of the hind-limb muscles compared to the control in the exercise group. Body weight of the D+E group was comparable to the dexa group, muscle weight of the hind-limb muscles increased significantly. Myofibrillar protein content of the soleus and plantaris increase significantly and that of the gastrocnemius tendency to increase compared to the dexa group. Body weight and muscle weight of the plantaris and gastrocnemius of the D+E group did not recover to that of the control group. Muscle weight of the soleus recovered to that of the control group. The relative weight and myofibrillar protein content of the hind-limb muscles recovered to that of the control group. From these results, it is suggested that regular exercise during dexamethasone injection might attenuate the muscle atrophy of the hind-limb muscles.
Animals ; Body Weight ; Dexamethasone* ; Female ; Glutamate-Ammonia Ligase ; Humans ; Injections, Subcutaneous ; Muscles ; Muscular Atrophy ; Rats*

Nitrogen is one of the most important nutrient elements for plants and a major limiting factor in plant growth and crop productivity. Glutamine synthase (GS) is a key enzyme involved in the nitrogen assimilation and recycling in plants. So far, members of the glutamine synthase gene family have been characterized in many plants such as Arabidopsis, rice, wheat, and maize. Reports show that GS are involved in the growth and development of plants, in particular its role in seed production. However, the outcome has generally been inconsistent, which are probably derived from the transcriptional and post-translational regulation of GS genes. In this review, we outlined studies on GS gene classification, QTL mapping, the relationship between GS genes and plant growth with nitrogen and the distribution characters, the biological functions of GS genes, as well as expression control at different regulation levels. In addition, we summarized the application prospects of glutamine synthetase genes in enhancing plant growth and yield by improving the nitrogen use efficiency. The prospects were presented on the improvement of nitrogen utility efficiency in crops and plant nitrogen status diagnosis on the basis of glutamine synthase gene regulation.
Arabidopsis ; Genes, Plant ; Glutamate-Ammonia Ligase ; genetics ; Nitrogen ; metabolism ; Oryza ; Plants ; enzymology ; genetics ; Triticum ; Zea mays

Glufosinate ammonium is the active ingredient in broad-spectrum contact herbicides such as BASTA(R) that inhibits the activity of glutamine synthetase, which is necessary for the production of the amino acid glutamine and for ammonia detoxification. Complications of glufosinate ammonium intoxication include gastrointestinal symptoms, loss of consciousness, convulsions, memory impairment, respiratory failure, and cardiovascular instability. We report herein a case of encephalopathy and reversible signal changes in the splenium of the corpus callosum, the bilateral corticospinal tracts, the hippocampi, and the cerebellar peduncles as seen in diffusion-weighted magnetic resonance imaging and fluid-attenuated inversion recovery images following BASTA(R) intoxication.
Ammonia ; Ammonium Compounds* ; Corpus Callosum ; Glutamate-Ammonia Ligase ; Glutamine ; Herbicides ; Magnetic Resonance Imaging ; Memory ; Pyramidal Tracts ; Respiratory Insufficiency ; Seizures ; Unconsciousness

As part of a study on the effects of dexamethasone and dehydroepiandrosterone (DHEA) on the biological roles of astrocytes in brain injury, this study evaluated the effects of dexamethasone and DHEA on the responses of primary cultured rat cortical astrocytes to lipopolysaccharide (LPS) and antimycin A. Dexamethasone decreased spontaneous release of LDH from astrocytes, and the dexamethasone effect was inhibited by DHEA. However, the inhibitory effect of DHEA on the dexamethasone-induced decrease of LDH release was not shown in astrocytes treated with LPS, and antimycin A-induced LDH release was not affected by dexamethasone or DHEA. Unlike dexamethasone, DHEA increased MTT value of astrocytes and also attenuated the antimycin A-induced decrease of MTT value. Glutamine synthetase activity of astrocytes was not affected by DHEA or LPS but increased by dexamethasone, and the dexamethasone-dependent increase was attenuated by DHEA. However, antimycin A markedly decreased glutamine synthetase activity, and the antimycin A effect was not affected by dexamethasone or DHEA. Basal release of (3H)arachidonic acid from astrocytes was moderately increased by LPS and markedly by antimycin A. Dexamethasone inhibited the basal and LPS-dependent releases of (3H)arachidonic acid, but neither dexamethasone nor DHEA affected antimycin A-induced (3H)arachidonic acid release. Basal IL-6 release from astrocytes was not affected by dexamethasone or DHEA but markedly increased by LPS and antimycin A. LPS-induced IL-6 release was attenuated by dexamethasone but was little affected by DHEA, and antimycin A-induced IL-6 release was attenuated by DHEA as well as dexamethasone. At the concentration of dexamethasone and DHEA which does not affect basal NO release from astrocytes, they moderately inhibited LPS-induced NO release but little affected antimycin A-induced decrease of NO release. Taken together, these results suggest that dexamethasone and DHEA, in somewhat different manners, modulate the astrocyte reactivity in brain injuries inhibitorily.
Animals ; Antimycin A* ; Arachidonic Acid ; Astrocytes* ; Brain Injuries ; Dehydroepiandrosterone* ; Dexamethasone* ; Glutamate-Ammonia Ligase ; Interleukin-6 ; Nitric Oxide ; Rats*

The toxic effect of ammonia on rCHO-GS cell decreased obviously due to the transfection of GS system in serum-free culture. The maximum cell density, 15.6 x 10(5) cells/mL was obtained in the culture with 1.42 mmol/L ammonia. The growth of rCHO-GS cell was inhibited with an increased ammonia concentration. However, a cell density of 8.9 x 10(5) cells/mL was obtained when the concentration of ammonia was 12.65mmol/L. The intracellar metabolic pathways were affected due to the decrease of the toxic effect of ammonia on rCHO-GS cell. With the increase of initial ammonia concentration from 0.36mmol/L to 12.65mmol/L, the yield coefficients of cell to glucose and lactate to glucose decreased. The activities of hexokinase (HK), pyruvate kinase (PK), and lactate dehydrogenase (LDH) increased by 43%, 140% and 25%, respectively, indicating that the utilization of glucose increased and the glycolysis pathway was more prone to efficient energy metabolism pathway. An increased activity of glutamate-pyruvate aminotransferase (GPT) showed that the conversation from glutamate to alpha-ketoglutarate was shifted to glutamate-pyruvate transamination pathway. The deamination pathway was inhibited due to a decreased activity of glutamate dehydrogenase. In addition, the number of cells in G0/G1 phase increased and the specific production rate of recombinant protein increased by 2.1-fold with the increase of initial ammonia concentration from 0.36mmol/L to 12.65mmol/L.
Ammonia ; metabolism ; toxicity ; Animals ; CHO Cells ; Cell Culture Techniques ; methods ; Cricetinae ; Cricetulus ; Culture Media, Serum-Free ; Genetic Engineering ; methods ; Glutamate-Ammonia Ligase ; genetics ; metabolism ; Glutamine ; metabolism

No abstract available.
Adenoma, Liver Cell/metabolism/*pathology/surgery ; Adult ; Glutamate-Ammonia Ligase/metabolism ; Humans ; Immunohistochemistry ; Liver Neoplasms/metabolism/*pathology/surgery ; Male ; Tomography, X-Ray Computed ; beta Catenin/*metabolism

Glutamine synthetase (GS) is a key enzyme in the regulation of glutamate neurotransmission in the central nervous system. It is responsible for converting glutamate to glutamine, consuming one ATP and NH3 in the process. Glutamate is neurotoxic when it accumulates in extracellular fluids. We investigated the effects of GS in both a spinal cord injury (SCI) model and normal rats. 0.1-ml of low (2-microM) and high (55-microM) concentrations of GS were applied, intrathecally, to the spinal cord of rats under pentobarbital anesthesia. Immediately after an intrathecal injection into the L1-L3 space, the rats developed convulsive movements. These movements initially consisted of myoclonic twitches of the paravertebral muscles close to the injection site, repeated tonic and clonic contractions and extensions of the hind limbs (hind limb seizures) that spread to the fore limbs, and finally rotational axial movements of the body. An EMG of the paravertebral muscles, fore and hind limbs, showed the extent of the muscle activities. GS (2-microM) caused spinal seizures in the rats after the SCI, and GS (6-microM) produced seizures in the uninjured anesthetized rats. Denatured GS (70 degrees C, 1 hour) also produced spinal seizures, although higher concentrations were required. We suggest that GS may be directly blocking the release of GABA, or the receptors, in the spinal cord.
Animals ; Electromyography ; Female ; *Glutamate-Ammonia Ligase/administration & dosage ; Injections, Spinal ; Male ; Rats ; Rats, Long-Evans ; Seizures/*chemically induced/physiopathology ; Spinal Cord Diseases/*chemically induced/physiopathology

BACKGROUND: Mechanisms of secondary injury (post-ischemic injury) in the central nervous system have cently reported in a vast of amount of experiments. Among many factors which give rise to post-ischemic neuronal damage, glial deterioration probably mediated by calcium paradox, could be another of the aggravating deleterious factars to the already ischemic neurophil. METHODS: Here we have designed experiment to investigate calcium paradox in astroglial cell line, humsn asttocytoma U1242MG. Intracellular calcium alterations in experimental cells were monitored by using calcium indicating dye fura-2 and epifluorescent photometry system. RESULTS: Intracellular free calcium changes during reperfusion phase after exposure to low calcium led to a prampt increase in intracellular calcium level after 10 and 30 minutes. The way of calcium entry during the reperfusion phase was mediated by the revase mode of Na+/Ca(2+) exchanger. Cells that had a reduction of reperfusate calcium to 10 uM increased cell viability. Also we observed an inverse relationship between major enzymatic activity in the astrocytoma cells (i.e., glutamine synthetase activity) and the duration of reperfusion in the the same protocols. CONCLUSIONS: A relatively small amount of intracellular calcium increase by the reverse mode of Na+/Ca(2+) exchanger during the reperfusion period is related to a limitation of enzyme activity and viability 24 hours later.
Anesthesia* ; Astrocytoma ; Brain ; Calcium ; Capnography* ; Cell Line ; Cell Survival ; Central Nervous System ; Fura-2 ; Glutamate-Ammonia Ligase ; Ions ; Neuroglia ; Neurons ; Photometry ; Reperfusion

It has been postulated that central nervous system disorders characterized by convulsive seizures are caused by alterations in one or more cerebral metabolism especially in cellular energy metabolism, electrolyte metabolism and glutamate metabolism. In the present study, alterations in cerebral energy metabolism, cellular electrolyte metabolism and glutamate metabolism were studied to investigate biochemical nature of cerebral disturbances in rats injected intraperitoneally with massive doses of penicillin. Also carried out were in vitro experiments by which direct effects of penicillin on concentrations of high energy compounds and Na+, K+-ATPase activity in the brains were determined. Intraperitoneal injections of pencillin G sodium(1,000,000 I.U. per kg body weight) to rats twice daily for 3 to 5 days resulted in significant decreases in cerebral concentrations of ATP, phosphocreatine and lactate, suggesting that penicillin induces cerebral dysfunctions by inhibiting energy production. While cerebral Na+, K+-ATPase activity and brain K+ content were significantly decreased in rats with penicllin-induced cerebral dysfunctions, brain Na+ and water contents were significantly increased. Observations that, in rats with penicillin-induced cerebral dysfunctions, the fall in high-energy phosphate contents in the brain took place as rapidly as the cation shifts indicate that alterations in both energy metabolism and electrolyte metabolism in the brain may be responsible for cerebral dysfunctions induced by penicillin. These assumptions were further supported by the findings that Na+, K+-ATPase activity and high-energy phosphate contents in the isolated cerebral hemispheres were profoundly affected by the addition of penicillin to the medium in which in vitro experiment was carried out. While the activity of glutamine synthetase in the brain was increased in rats exhibiting cerebral dysfunctions induced by penicillin, the activity of glutamine dehydrogenase was significantly decreased. Significance of changes in activities of these two brain enzymes in penicillin-induced cerebral dysfunctions was not immediately understood. It may be possible, however, that penicillin may influence glutamate contents in the brain directly orindirectly through the alteration of these two brain enzyme activities so as to modify the cerebral functions.
Adenosine Triphosphate ; Animals ; Brain ; Central Nervous System Diseases ; Cerebrum ; Energy Metabolism ; Glutamate-Ammonia Ligase ; Glutamic Acid ; Glutamine ; Injections, Intraperitoneal ; Lactic Acid ; Metabolism ; Oxidoreductases ; Penicillins* ; Phosphocreatine ; Rats ; Seizures