PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27580850-3 2017 In vivo glutamine synthetase activities measured at several levels of hyperammonemia showed that this enzyme becomes saturated at blood ammonia concentration >0.9 mumol/g, and causes the elevation of brain ammonia. Ammonia 136-143 glutamate-ammonia ligase Rattus norvegicus 8-28 27580850-3 2017 In vivo glutamine synthetase activities measured at several levels of hyperammonemia showed that this enzyme becomes saturated at blood ammonia concentration >0.9 mumol/g, and causes the elevation of brain ammonia. Ammonia 209-216 glutamate-ammonia ligase Rattus norvegicus 8-28 27764760-9 2016 Decreased cell viability and GSH content and increased ROS accumulation were detected in ammonia-treated SH-SY5Y and CGNs, while ammonia-treated C6 cells showed reduced glutamate uptake, increased glutamate release, and decrease of GSH content, GS and Na+K+-ATPase activity. Ammonia 89-96 glutamate-ammonia ligase Rattus norvegicus 29-31 26220375-1 2015 Glutamine synthetase (GS) in astrocytes is critical for metabolism of glutamate and ammonia in the brain, and perturbations in the anatomical distribution and activity of the enzyme are likely to adversely affect synaptic transmission. Ammonia 84-91 glutamate-ammonia ligase Rattus norvegicus 0-20 26817210-1 2015 BACKGROUND: Ammonia metabolizing enzymes, carbamyol phosphate synthetase (CPS) and glutamine synthetase (GS), are expressed in the periportal and pericentral hepatocytes, respectively. Ammonia 12-19 glutamate-ammonia ligase Rattus norvegicus 83-103 25338921-5 2015 Transduction of MA104 epithelial or L6 myoblast/myotubes cells with Bac-GS resulted in a high expression of the GS gene, an increase in GS concentration, and a reduction of almost half of exogenously added ammonia. Ammonia 206-213 glutamate-ammonia ligase Rattus norvegicus 72-74 24292976-7 2014 Ammonia-induced protein O-GlcNAcylation was sensitive towards glutamine-synthetase inhibition by methionine sulfoximine (MSO), but was not induced by hypoosmolarity (205 mosmol/l) or CH3NH3Cl (5 mmol/l). Ammonia 0-7 glutamate-ammonia ligase Rattus norvegicus 62-82 25196365-0 2015 Assessment of glutamine synthetase activity by [13N]ammonia uptake in living rat brain. Ammonia 52-59 glutamate-ammonia ligase Rattus norvegicus 14-34 25196365-11 2015 These results indicated that [(13) N]ammonia may enable measurement of GS activity in the living brain. Ammonia 37-44 glutamate-ammonia ligase Rattus norvegicus 71-73 25106624-2 2014 In general, the ammonia metabolizing enzymes - glutaminase, glutamine synthetase, glutamate dehydrogenase, AMP deaminase, adenosine deaminase, as well as aspartate aminotransferase and alanine aminotransferase - are differentially upregulated in various brain and liver regions of the hyperammonemic rats, indicating that divergent ammonia-detoxification mechanisms are involved in the various brain regions and liver in acute hyperammonemia. Ammonia 16-23 glutamate-ammonia ligase Rattus norvegicus 60-80 24346692-0 2014 Effect of glutamine synthetase inhibition on brain and interorgan ammonia metabolism in bile duct ligated rats. Ammonia 66-73 glutamate-ammonia ligase Rattus norvegicus 10-30 24346692-2 2014 In the brain, glutamine synthetase (GS) rapidly converts blood-borne ammonia into glutamine which in high concentrations may cause mitochondrial dysfunction and osmolytic brain edema. Ammonia 69-76 glutamate-ammonia ligase Rattus norvegicus 14-34 24755687-7 2014 Glutamine synthetase (GS) and glutaminase (GA), the two brain ammonia metabolizing enzymes vis a vis ammonia and glutamate levels and profiles of all the antioxidant enzymes vis a vis oxidative stress markers were measured in the cerebral cortex and cerebellum of the control and the ALF rats. Ammonia 62-69 glutamate-ammonia ligase Rattus norvegicus 0-20 24755687-7 2014 Glutamine synthetase (GS) and glutaminase (GA), the two brain ammonia metabolizing enzymes vis a vis ammonia and glutamate levels and profiles of all the antioxidant enzymes vis a vis oxidative stress markers were measured in the cerebral cortex and cerebellum of the control and the ALF rats. Ammonia 62-69 glutamate-ammonia ligase Rattus norvegicus 22-24 24755687-7 2014 Glutamine synthetase (GS) and glutaminase (GA), the two brain ammonia metabolizing enzymes vis a vis ammonia and glutamate levels and profiles of all the antioxidant enzymes vis a vis oxidative stress markers were measured in the cerebral cortex and cerebellum of the control and the ALF rats. Ammonia 101-108 glutamate-ammonia ligase Rattus norvegicus 22-24 22167234-7 2012 These results showed an increase of GS and net glutamine accumulation under hyperammonemia, supporting the concept of their implication in cerebral ammonia detoxification. Ammonia 148-155 glutamate-ammonia ligase Rattus norvegicus 36-38 23673435-2 2013 Brain ammonia detoxification occurs primarily in astrocytes by glutamine synthetase (GS), and it has been proposed that elevated glutamine levels during hyperammonemia lead to astrocyte swelling and cerebral edema. Ammonia 6-13 glutamate-ammonia ligase Rattus norvegicus 63-83 22618691-0 2012 The role of glutamine synthetase and glutamate dehydrogenase in cerebral ammonia homeostasis. Ammonia 73-80 glutamate-ammonia ligase Rattus norvegicus 12-32 22618691-1 2012 In the brain, glutamine synthetase (GS), which is located predominantly in astrocytes, is largely responsible for the removal of both blood-derived and metabolically generated ammonia. Ammonia 176-183 glutamate-ammonia ligase Rattus norvegicus 14-34 21780187-1 2011 Glutamine synthetase (GS) is an astrocytic enzyme, which catalyzes the synthesis of glutamine from glutamate and ammonia. Ammonia 113-120 glutamate-ammonia ligase Rattus norvegicus 0-20 20689060-8 2010 The activity of glutamine synthetase (which condenses ammonia and glutamate) was found to be much higher in colonocytes than in small intestine enterocytes and was 1.6-fold higher (P = 0.0304) in colonocytes isolated from HP animals than NP. Ammonia 54-61 glutamate-ammonia ligase Rattus norvegicus 16-36 21193003-2 2011 Glutamine synthetase (GS) is highly expressed by astrocytes, and serves a neuroprotective function by converting cytotoxic glutamate and ammonia into glutamine. Ammonia 137-144 glutamate-ammonia ligase Rattus norvegicus 0-20 15326614-6 2004 Glutamate was also combined with 1 mM ammonia or with methionine sulfoximine (MSO), an inhibitor of glutamine synthetase, the enzyme that catalyzes the synthesis of glutamine from glutamate and ammonia. Ammonia 194-201 glutamate-ammonia ligase Rattus norvegicus 100-120 16530878-1 2006 BACKGROUND/AIMS: It has been proposed that, in acute liver failure, skeletal muscle adapts to become the principle organ responsible for removal of blood-borne ammonia by increasing glutamine synthesis, a reaction that is catalyzed by the cytosolic ATP-dependent enzyme glutamine synthetase. Ammonia 160-167 glutamate-ammonia ligase Rattus norvegicus 270-290 16530878-5 2006 RESULTS: Glutamine synthetase protein (but not gene) expression and enzyme activities were significantly up-regulated leading to increased de novo synthesis of glutamine and increased skeletal muscle capacity for ammonia removal in acute liver failure. Ammonia 213-220 glutamate-ammonia ligase Rattus norvegicus 9-29 16530878-7 2006 CONCLUSIONS: These findings demonstrate that skeletal muscle adapts, through a rapid induction of glutamine synthetase, to increase its capacity for removal of blood-borne ammonia in acute liver failure. Ammonia 172-179 glutamate-ammonia ligase Rattus norvegicus 98-118 16530878-8 2006 Maintenance of muscle mass together with the development of agents with the capacity to stimulate muscle glutamine synthetase could provide effective ammonia-lowering strategies in this disorder. Ammonia 150-157 glutamate-ammonia ligase Rattus norvegicus 105-125 15923062-4 2005 Thus, despite the presence of significant amounts of glutamate dehydrogenase, the overwhelming route for metabolism of ammonia entering the rat lung in vivo was the glutamine synthetase reaction. Ammonia 119-126 glutamate-ammonia ligase Rattus norvegicus 165-185 15830392-1 2005 Glutamine synthetase (GS) in the liver is restricted to a small perivenous hepatocyte population and plays an important role in the scavenging of ammonia that has escaped the periportal urea-synthesizing compartment. Ammonia 146-153 glutamate-ammonia ligase Rattus norvegicus 0-20 15830392-8 2005 In conclusion, LPS impairs hepatic ammonia detoxification by both downregulation of GS and its inactivation because of tyrosine nitration. Ammonia 35-42 glutamate-ammonia ligase Rattus norvegicus 84-86 15114044-0 2004 Contribution of glutamine synthetase to ammonia-induced apoptosis in gastric mucosal cells. Ammonia 40-47 glutamate-ammonia ligase Rattus norvegicus 16-36 15114044-1 2004 BACKGROUND/AIMS: Glutamine synthetase is a key enzyme necessary for ammonia detoxification in the brain, but excessive activation of this enzyme can be cytotoxic to neural cells as a consequence of excessive consumption of ATP and glutamate. Ammonia 68-75 glutamate-ammonia ligase Rattus norvegicus 17-37 15114044-2 2004 The stomach also expresses high levels of glutamine synthetase and this study aimed to investigate a possible pathophysiological role of glutamine synthetase in ammonia-induced gastric mucosal injury. Ammonia 161-168 glutamate-ammonia ligase Rattus norvegicus 137-157 15114044-6 2004 On the other hand, pretreatment with various concentrations of methionine sulfoximine reduced the glutamine synthetase activity in ammonia-treated RGM-1 cells, and prevented the induction of apoptosis and the reduction in intracellular ATP levels in a dose-dependent manner. Ammonia 131-138 glutamate-ammonia ligase Rattus norvegicus 98-118 15114044-7 2004 CONCLUSIONS: Our results suggested that the energy exhaustion which resulted from an overload of ammonia to glutamine synthetase may have initiated the apoptotic signaling in gastric mucosal cells. Ammonia 97-104 glutamate-ammonia ligase Rattus norvegicus 108-128 10850554-7 1999 The finding of a post-translational increase of GS in muscle following portacaval shunting suggests that, in chronic liver failure, muscle becomes the major organ responsible for the removal of excess blood-borne ammonia. Ammonia 213-220 glutamate-ammonia ligase Rattus norvegicus 48-50 12742096-4 2003 In the course of studies on the molecular mechanism of acute ammonia toxicity, we have found that glutamine synthetase activity and glutamine content in brain are modulated by NMDA receptors and nitric oxide. Ammonia 61-68 glutamate-ammonia ligase Rattus norvegicus 98-118 12579527-5 2003 The results indicate that arginine, citrulline and ornithine supplementation increased the flux of substrate through the reaction catalysed by glutamine synthetase, leading to increased glutamine production after an exhaustive bout of exercise, and of the mechanism involved in ammonia buffering. Ammonia 278-285 glutamate-ammonia ligase Rattus norvegicus 143-163 11746427-10 2001 Pretreatment with methionine sulfoximine, an inhibitor of glutamine synthetase, blocked the ammonia-induced collapse of Deltapsi(m), suggesting a role of glutamine in this process. Ammonia 92-99 glutamate-ammonia ligase Rattus norvegicus 58-78 11923223-8 2002 Ammonia-induced nitration of glutamine synthetase is associated with a loss of enzymatic activity. Ammonia 0-7 glutamate-ammonia ligase Rattus norvegicus 29-49 9538946-4 1998 Careful analysis revealed that the effect of the conditioned medium was neither due to deficiency of a component used up by the hepatocytes, nor due to glutamine or ammonia, both of which affected GS activity at concentrations above 0.5 mmol/L. Ammonia 165-172 glutamate-ammonia ligase Rattus norvegicus 197-199 10429966-5 1999 Free ammonia, that is not converted periportally, is efficiently detoxified in the small rim of hepatocytes around the central veins by glutamine synthetase preventing it from entering the systemic circulation. Ammonia 5-12 glutamate-ammonia ligase Rattus norvegicus 136-156 10429966-6 1999 Detoxification of ammonia by glutamine synthetase may be limited due to a shortage of glutamate when the nitrogen load is high. Ammonia 18-25 glutamate-ammonia ligase Rattus norvegicus 29-49 9829169-1 1998 Glutamine synthetase plays a central role in the detoxification of brain ammonia. Ammonia 73-80 glutamate-ammonia ligase Rattus norvegicus 0-20 7915704-10 1994 Serum ammonia levels showed a clear negative correlation with the specific activity of glutamine synthetase and the size of the glutamine synthetase-positive area. Ammonia 6-13 glutamate-ammonia ligase Rattus norvegicus 87-107 9336301-6 1997 The negative correlation between glutamine synthetase activity and plasma ammonia levels reported previously for cirrhotic rats (Gebhardt and Reichen, Hepatology 20:684-691, 1994) was corroborated for cirrhotic animals not treated with OA, but was no longer apparent in OA-treated cirrhotic rats. Ammonia 74-81 glutamate-ammonia ligase Rattus norvegicus 33-53 9336301-7 1997 Despite this improvement, plasma ammonia levels still varied considerably reflecting the variable accessibility and activities of glutamine synthetase in cirrhotics. Ammonia 33-40 glutamate-ammonia ligase Rattus norvegicus 130-150 9331509-4 1997 With the aim of adding lost or deficient functions and producing cell lines for the bioreactor of a hybrid artificial liver, rat glutamine synthetase (GS) gene was transfected into Chinese hamster ovary (CHO) cells, because it is able to lower the ammonia level. Ammonia 248-255 glutamate-ammonia ligase Rattus norvegicus 129-149 9107685-0 1997 FISH mapping of three ammonia metabolism genes (Glul, Cps1, Glud1) in rat, and the chromosomal localization of GLUL in human and Cps1 in mouse. Ammonia 22-29 glutamate-ammonia ligase Rattus norvegicus 48-52 9122259-10 1997 Thus, under conditions of elevated plasma ammonia an increase in the rate of glutamine synthesis occurs as a means of ammonia detoxification, and this is superimposed on the constant rate of neurotransmitter cycling through glutamine synthetase. Ammonia 42-49 glutamate-ammonia ligase Rattus norvegicus 224-244 9752723-1 1998 Glutamine synthetase, the enzyme that catalyzes the ATP-dependent conversion of glutamate and ammonia into glutamine, is expressed in a tissue-specific and developmentally controlled manner. Ammonia 94-101 glutamate-ammonia ligase Rattus norvegicus 0-20 9435573-2 1997 This response is accompanied by increased enzymatic activity of glutamine synthetase (GS), which catalyzes the synthesis of glutamine from glutamate and ammonia. Ammonia 153-160 glutamate-ammonia ligase Rattus norvegicus 64-84 9053810-0 1996 Inhibition of glutamine synthetase reduces ammonia-induced astrocyte swelling in rat. Ammonia 43-50 glutamate-ammonia ligase Rattus norvegicus 14-34 9053810-2 1996 Ammonia is rapidly incorporated into glutamine by glutamine synthetase localized in astrocytes. Ammonia 0-7 glutamate-ammonia ligase Rattus norvegicus 50-70 7487913-0 1995 Dependence of in vivo glutamine synthetase activity on ammonia concentration in rat brain studied by 1H - 15N heteronuclear multiple-quantum coherence-transfer NMR. Ammonia 55-62 glutamate-ammonia ligase Rattus norvegicus 22-42 7487913-5 1995 A linear increase of 1/v with 1/s permitted estimation of the in vivo glutamine synthetase (GS) activity at a physiological blood ammonia concentration to be 0.4-2.1 mumol/h per g. The observed ammonia-dependence strongly suggests that, under physiological conditions, in vivo GS activity is kinetically limited by sub-optimal in situ concentrations of ammonia as well as glutamate and ATP. Ammonia 130-137 glutamate-ammonia ligase Rattus norvegicus 70-90 7487913-5 1995 A linear increase of 1/v with 1/s permitted estimation of the in vivo glutamine synthetase (GS) activity at a physiological blood ammonia concentration to be 0.4-2.1 mumol/h per g. The observed ammonia-dependence strongly suggests that, under physiological conditions, in vivo GS activity is kinetically limited by sub-optimal in situ concentrations of ammonia as well as glutamate and ATP. Ammonia 194-201 glutamate-ammonia ligase Rattus norvegicus 70-90 7487913-5 1995 A linear increase of 1/v with 1/s permitted estimation of the in vivo glutamine synthetase (GS) activity at a physiological blood ammonia concentration to be 0.4-2.1 mumol/h per g. The observed ammonia-dependence strongly suggests that, under physiological conditions, in vivo GS activity is kinetically limited by sub-optimal in situ concentrations of ammonia as well as glutamate and ATP. Ammonia 194-201 glutamate-ammonia ligase Rattus norvegicus 70-90 7915704-10 1994 Serum ammonia levels showed a clear negative correlation with the specific activity of glutamine synthetase and the size of the glutamine synthetase-positive area. Ammonia 6-13 glutamate-ammonia ligase Rattus norvegicus 128-148 7910653-3 1993 Ammonia removal by brain relies on glutamine synthesis and the enzyme responsible, glutamine synthetase, has an almost exclusively astrocytic localization. Ammonia 0-7 glutamate-ammonia ligase Rattus norvegicus 83-103 8188174-3 1994 It has been postulated that the osmotic effects of glutamine, generated in astrocytes from ammonia and glutamate in a reaction catalyzed by glutamine synthetase, could mediate brain swelling. Ammonia 91-98 glutamate-ammonia ligase Rattus norvegicus 140-160 7910379-9 1994 Because the concentration of free cytoplasmic Mn(II) is poised near the Kd for Mn(II) with glutamine synthetase, a slight increase in cytoplasmic Mn(II) will directly enhance the activity of glutamine synthetase, which catalyzes removal of neurotoxic glutamate and ammonia. Ammonia 265-272 glutamate-ammonia ligase Rattus norvegicus 191-211 2007367-7 1991 Both carbamoylphosphate synthetase-I and glutamine synthetase, the ammonia-metabolizing enzymes, are expressed by all pancreatic hepatocytes; in liver, these are expressed by different populations of hepatocytes. Ammonia 67-74 glutamate-ammonia ligase Rattus norvegicus 41-61 1363168-1 1992 Glutamine synthetase (L-glutamate:ammonia ligase; EC 6.3.1.2), an enzyme catalysing the ATP-dependent formation of glutamine from glutamate and ammonia, was detected immunocytochemically only in glial (interstitial) cells of the superficial pineal gland of the rat. Ammonia 34-41 glutamate-ammonia ligase Rattus norvegicus 0-20 1681554-5 1991 Since ammonia is detoxified through the glutamine synthetase reaction, these results suggest that blood and brain ammonia concentrations are more important than the neurochemical consequences of ammonia detoxification for the etiology of cancer anorexia. Ammonia 6-13 glutamate-ammonia ligase Rattus norvegicus 40-60 1681554-5 1991 Since ammonia is detoxified through the glutamine synthetase reaction, these results suggest that blood and brain ammonia concentrations are more important than the neurochemical consequences of ammonia detoxification for the etiology of cancer anorexia. Ammonia 114-121 glutamate-ammonia ligase Rattus norvegicus 40-60 1681554-5 1991 Since ammonia is detoxified through the glutamine synthetase reaction, these results suggest that blood and brain ammonia concentrations are more important than the neurochemical consequences of ammonia detoxification for the etiology of cancer anorexia. Ammonia 114-121 glutamate-ammonia ligase Rattus norvegicus 40-60 8102050-9 1993 To estimate 15N enrichment of precursor ammonia for glutamine synthetase (GS) in astrocytes which are interposed between cerebral capillaries and neurons, 15N enrichments of blood and brain ammonia were measured by gas chromatography-mass spectrometry. Ammonia 40-47 glutamate-ammonia ligase Rattus norvegicus 52-72 8102050-12 1993 The result suggests that substrates and/or cofactors other than ammonia kinetically limit GS activity in vivo. Ammonia 64-71 glutamate-ammonia ligase Rattus norvegicus 90-92 8436955-2 1993 Recently it was shown that ammonia caused some of the metabolic signs of hepatic encephalopathy only after it was metabolized by glutamine synthetase in the brain. Ammonia 27-34 glutamate-ammonia ligase Rattus norvegicus 129-149 2865284-7 1985 Periportal glutaminase and perivenous glutamine synthetase are simultaneously active, resulting in an intercellular (as opposed to intracellular) glutamine cycle, being under the control of hormones, pH and portal ammonia and glutamine concentrations. Ammonia 214-221 glutamate-ammonia ligase Rattus norvegicus 38-58 1674354-1 1991 Glutamine synthetase catalyzes the formation of glutamine from glutamate and ammonia. Ammonia 77-84 glutamate-ammonia ligase Rattus norvegicus 0-20 1671539-3 1991 We previously showed that the specific activity of glutamine synthetase (GS), an astroglial enzyme with a key role in glutamate and ammonia metabolism in the brain, is reduced in fetal guinea pigs exposed to low levels of lead. Ammonia 132-139 glutamate-ammonia ligase Rattus norvegicus 51-71 2757524-4 1989 A model of hepatic encephalopathy can be produced using methionine sulfoximine to inhibit irreversibly the enzyme glutamine synthetase, resulting in elevated brain ammonia levels and development of Alzheimer type II astrocytosis. Ammonia 164-171 glutamate-ammonia ligase Rattus norvegicus 114-134 3225873-6 1988 Treatment with ammonia resulted in a comatose state and in a 25-40% inhibition of GAD. Ammonia 15-22 glutamate-ammonia ligase Rattus norvegicus 82-85 1982483-4 1990 We conclude that the increase in brain water content is linked to the glutamine accumulation derived from the detoxification of ammonia by glutamine synthetase. Ammonia 128-135 glutamate-ammonia ligase Rattus norvegicus 139-159 2888066-2 1987 In contrast, the brain possesses only one major enzyme for the removal of exogenous ammonia, i.e., glutamine synthetase. Ammonia 84-91 glutamate-ammonia ligase Rattus norvegicus 99-119 2888066-7 1987 These data are consistent with the hypothesis that glutamine synthetase is the major enzyme for metabolism of endogenously--as well as exogenously--produced ammonia. Ammonia 157-164 glutamate-ammonia ligase Rattus norvegicus 51-71 2888066-10 1987 In the hyperammonemic rat brain, glutamine synthetase is still the only important enzyme for the removal of blood-borne ammonia. Ammonia 120-127 glutamate-ammonia ligase Rattus norvegicus 33-53 2879838-11 1987 Our data also show that some portal vein-derived ammonia is metabolized to glutamine in the rat liver, but the amount is small (approximately 7% of that metabolized to urea) in part because liver glutamine synthetase is located in a small population of perivenous cells "downstream" from the urea cycle-containing periportal cells. Ammonia 49-56 glutamate-ammonia ligase Rattus norvegicus 196-216 2895721-1 1987 The appearance of the distribution patterns of the NH3-metabolizing enzymes carbamoylphosphate synthetase, glutamate dehydrogenase, and glutamine synthetase in the developing liver of an altricial species (rat) was compared with that in the developing liver of a closely related, precocial species (spiny mouse). Ammonia 51-54 glutamate-ammonia ligase Rattus norvegicus 136-156 22434-7 1977 In brain and kidney ammonia is detoxified mainly by the glutamate dehydrogenase and glutamine synthetase reactions whereas in the liver these enzyme reactions play a minor role. Ammonia 20-27 glutamate-ammonia ligase Rattus norvegicus 84-104 6140923-3 1983 The metabolic effects of MSO were found to be different from those of ammonia wherein a fall in the activity of glutamate dehydrogenase and an increase in the activity of glutamine synthetase was noticed. Ammonia 70-77 glutamate-ammonia ligase Rattus norvegicus 171-191 35582-1 1979 The urea cycle enzymes, carbamoyl-P-synthetase, ornithine transcarbamylase, arginase and other enzymes related to ammonia metabolism, such as glutamate dehydrogenase, glutamine synthetase and alanine and aspartate aminotransferases,have been studied in thioacetamide-induced liver disease in rats. Ammonia 114-121 glutamate-ammonia ligase Rattus norvegicus 167-187 187380-13 1976 9) It is concluded that the kidney response to an ammonia load differs from that of the liver despite the existence of a similar network of near-equilibrium reactions of (1) a lack of local availability of oxaloacetate, (2) a lower activity of alanine aminotransferase, (3) a greater in vivo activity of glutamine synthetase. Ammonia 50-57 glutamate-ammonia ligase Rattus norvegicus 304-324 4146451-23 1972 In particular, it is suggested that in acidotic rats glucose formation is the major fate of the carbon of the extra glutamine utilized by the kidney, and that inhibition of glutamine synthetase could contribute to the increase in intracellular ammonia concentration in the kidney. Ammonia 244-251 glutamate-ammonia ligase Rattus norvegicus 173-193