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PubMed1992

Hepatocyte heterogeneity in the metabolism of amino acids and ammonia.

With respect to hepatocyte heterogeneity in ammonia and amino acid metabolism, two different patterns of sublobular gene expression are distinguished: 'gradient-type' and 'strict- or compartment-type' zonation. An example for strict-type zonation is the reciprocal distribution of carbamoylphosphate synthase and glutamine synthase in the liver lobule. The mechanisms underlying the different sublobular gene expressions are not yet settled but may involve the development of hepatic architecture, innervation, blood-borne hormonal and metabolic factors. The periportal zone is characterized by a high capacity for uptake and catabolism of amino acids (except glutamate and aspartate) as well as for urea synthesis and gluconeogenesis. On the other hand, glutamine synthesis, ornithine transamination and the uptake of vascular glutamate, aspartate, malate and alpha-ketoglutarate are restricted to a small perivenous hepatocyte population. Accordingly, in the intact liver lobule the major pathways for ammonia detoxication, urea and glutamine synthesis, are anatomically switched behind each other and represent in functional terms the sequence of the periportal low affinity system (urea synthesis) and a previous high affinity system (glutamine synthesis) for ammonia detoxication. Perivenous glutamine synthase-containing hepatocytes ('scavenger cells') act as a high affinity scavenger for the ammonia, which escapes the more upstream urea-synthesizing compartment. Periportal glutaminase acts as a pH- and hormone-modulated ammonia-amplifying system in the mitochondria of periportal hepatocytes. The activity of this amplifying system is one crucial determinant for flux through the urea cycle in view of the high Km (ammonia) of carbamoylphosphate synthase, the rate-controlling enzyme of the urea cycle. The structural and functional organization of glutamine and ammonia-metabolizing pathways in the liver lobule provides one basis for the understanding of a hepatic role in systemic acid base homeostasis. Urea synthesis is a major pathway for irreversible removal of metabolically generated bicarbonate. The lobular organization enables the adjustment of the urea cycle flux and accordingly the rate of irreversible hepatic bicarbonate elimination to the needs of the systemic acid base situation, without the threat of hyperammonemia.

Amino Acids↗
PubMed1984

Ammonia production by individual segments of the rat nephron.

Ammonia production was measured directly in 10 segments of the rat nephron to determine the relative importance of the segments as sites of renal ammonia production. Tubules were microdissected from normal rats and rats drinking 0.28 M NH4Cl or 0.28 M NaHCO3 for 3-8 d. The segments were incubated in vitro with and without 2 mM glutamine. Ammonia concentrations in the incubation fluid were measured by microfluorometry to determine ammonia production rates. All segments produced ammonia from glutamine. In normal rats, production with glutamine was highest (greater than 5 pmol/min per mm) in the proximal convoluted (S-1), proximal straight (S-3), and distal convoluted tubules, and lowest (less than or equal to 2) in cortical and medullary collecting ducts and thin descending limbs. Metabolic acidosis increased production by 60% in the S-1 segment of the proximal convoluted tubule and by 150% in the S-2 segment of the proximal straight tubule without significant effect in any other segment. Bicarbonate loading decreased production by S-1 but had no effect on S-2 or S-3. Thus, acid-base changes altered production only in specific segments of the proximal tubule. We infer that the bulk of ammonia production occurs in the proximal tubules and that production by collecting ducts can account for only a few percent of renal ammonia production and excretion in the rat.

Ammonia↗
PubMed1987

Effects of potassium on ammonia transport by medullary thick ascending limb of the rat.

Renal ammonium excretion is increased by potassium depletion and reduced by potassium loading. To determine whether changes in potassium concentration would alter ammonia transport in the medullary thick ascending limb (MAL), tubules from rats were perfused in vitro and effects of changes in K concentration within the physiological range (4-24 mM) were evaluated. Increasing K concentration from 4 to 24 mM in perfusate and bath inhibited total ammonia absorption by 50% and reduced the steady-state transepithelial NH+4 concentration gradient. The inhibition of total ammonia absorption was reversible and occurred when K replaced either Na or N-methyl-D-glucamine. Increasing K concentration in the luminal perfusate alone gave similar inhibition of total ammonia absorption. At 1-2 nl/min per mm perfusion rate, increasing K concentration in perfusion and bathing solutions had no significant effect on transepithelial voltage. With either 4 or 24 mM K in perfusate and bath, an increase in luminal perfusion rate markedly increased total ammonia absorption. Thus, both potassium concentration and luminal flow rate are important factors capable of regulating total ammonia transport by the MAL. Changes in systemic potassium balance may influence renal ammonium excretion by affecting NH+4 absorption in the MAL and altering the transfer of ammonia from loops of Henle to medullary collecting ducts.

Absorption↗
PubMed1995

Ammonia inhibits cAMP-regulated intestinal Cl- transport. Asymmetric effects of apical and basolateral exposure and implications for epithelial barrier function.

The colon, unlike most organs, is normally exposed to high concentrations of ammonia, a weak base which exerts profound and diverse biological effects on mammalian cells. The impact of ammonia on intestinal cell function is largely unknown despite its concentration of 4-70 mM in the colonic lumen. The human intestinal epithelial cell line T84 was used to model electrogenic Cl- secretion, the transport event which hydrates mucosal surfaces and accounts for secretory diarrhea. Transepithelial transport and isotopic flux analysis indicated that physiologically-relevant concentrations of ammonia (as NH4Cl) markedly inhibit cyclic nucleotide-regulated Cl- secretion but not the response to the Ca2+ agonist carbachol. Inhibition by ammonia was 25-fold more potent with basolateral compared to apical exposure. Ion substitution indicated that the effect of NH4Cl was not due to altered cation composition or membrane potential. The site of action of ammonia is distal to cAMP generation and is not due simply to cytoplasmic alkalization. The results support a novel role for ammonia as an inhibitory modulator of intestinal epithelial Cl- secretion. Secretory responsiveness may be dampened in pathological conditions associated with increased mucosal permeability due to enhanced access of lumenal ammonia to the basolateral epithelial compartment.

Ammonia↗
PubMedDate not supplied

Urinary ammonia plus urinary urea nitrogen as an estimate of total urinary nitrogen in patients receiving parenteral nutrition support.

Nitrogen balance has historically been estimated by using urinary urea nitrogen (UUN) multiplied by a factor of 1.25 to account for nonurea nitrogen present in the urine. Recently, the reliability of UUN as an estimate of nitrogen losses has been questioned and the use of total urinary nitrogen (TUN) has been proposed as a more accurate measure of urinary nitrogen losses. However, analysis of TUN losses is not readily available in many hospital laboratories. Because ammonia is the major fluctuating component of urinary nonurea nitrogen and equipment to measure urinary ammonia is available in most hospitals, this study was undertaken to determine whether urinary ammonia plus UUN provides a clinically useful approximation of TUN. Twenty-four-hour urine samples acidified with boric acid during collection from 20 patients (a total of 42 samples) receiving total parenteral nutrition were analyzed for UUN, ammonia, and TUN. The UUN values ranged from 4.9 to 42.4 g/24 h. The mean difference between TUN and UUN was 1.99 +/- 0.27 g/24 h. The mean difference between TUN and UUN plus ammonia was 0.78 +/- 0.27 g/24 h. Thus, UUN alone accounted for 90% and the combination of UUN plus urinary ammonia accounted for 96% of TUN. These data suggest that UUN plus ammonia does provide a greater level of reliability as an estimate of TUN than UUN alone.

Ammonia↗
PubMed1986

Evaluation by scoring and computerized morphometry of lesions of early Mycoplasma pulmonis infection and ammonia exposure in F344/N rats.

To evaluate lesions of ammonia exposure and Mycoplasma pulmonis infection in gnotobiotic F344/N rats, groups of rats were inoculated with M. pulmonis, exposed to 76 micrograms/liter (100 parts per million) ammonia, or both, or served as controls. Six rats from each group were killed 3, 5, 7, and 9 days after inoculation and their respiratory organs prepared for histologic examination. Lesions were assessed by subjective scoring and computerized morphometry, and results obtained by the two methods were compared to assess agreement of results. Lesions were limited to the nasal passages. Ammonia exposure resulted in hyperplastic and degenerative changes in the anterior nasal epithelium. Lesions of mycoplasmosis were more severe in ammonia-exposed than unexposed rats, but qualitative differences in lesions were not apparent. Results of the two methods agreed in assessment of submucosal inflammatory cell accumulation. Epithelial lesions were difficult to evaluate by both methods in infected, ammonia-exposed rats. In evaluation of lesions of ammonia exposure alone, agreement was adequate. Both methods indicated that exudates were significantly greater in ammonia-exposed infected rats than in non-exposed infected rats. Thus, scoring and morphometry provided similar assessments of differences in lesion severity among the treatment groups.

Ammonia↗
PubMed2002

Nitrogen metabolism and excretion in the mangrove killifish Rivulus marmoratus I. The influence of environmental salinity and external ammonia.

At a field site in Belize, mangrove killifish Rivulus marmoratus inhabit hypersaline waters (up to 48 per thousand containing approximately 1 mmol l(-1) ammonia. We tested the hypotheses that R. marmoratus modify their nitrogen metabolism and excretion (i) by accumulating free amino acids (FAAs) and urea in the tissues during hyperosmotic stress and (ii) by shifting to ureotelism and accumulating FAAs during hyperammonia stress. Urea excretion (J(Urea)) (but not ammonia excretion, J(Amm)) displayed a diurnal pattern, with significantly less (75 %) urea excreted at night than during the day in both laboratory-reared clones and wild-caught killifish. When fish were exposed to hypersaline conditions (45 per thousand sea water), J(Urea) was significantly reduced and tissue urea and FAA levels were elevated compared with those of control fish (15 per thousand sea water). When R. marmoratus were exposed to 0, 1, 2, 5 and 10 mmol l(-1) NH(4)Cl (pH 8) for 48 h, no differences were found in J(Urea). Remarkably, prolonged exposure (10 days) to 5 mmol l(-1) NH(4)Cl (pH 8) did not result in an elevation of tissue ammonia levels. In addition, tissue urea and total FAA levels did not differ between control and ammonia-exposed fish after > or =4 days. We propose that the euryhaline R. marmoratus retain urea and FAAs within their tissues in response to extreme osmotic stress. In contrast to many ammonia-tolerant fishes, R. marmoratus do not shift to ureotelism during prolonged hyperammonia stress, nor do they convert nitrogenous wastes into FAAs. The data suggest that killifish continue to eliminate ammonia despite an unfavourable blood-to-water gradient, thereby avoiding accumulation of ammonia.

Amino Acids↗
PubMed2002

Nitrogen metabolism and excretion in the mangrove killifish Rivulus marmoratus II. Significant ammonia volatilization in a teleost during air-exposure.

The mangrove killifish Rivulus marmoratus can tolerate prolonged periods of air-exposure (>1 month). During these periods of emersion, we hypothesized that R. marmoratus would convert potentially toxic ammonia into urea and free amino acids (FAAs). In air-exposed fish, both ammonia (J(Amm)) and urea (J(Urea)) excretion continued at approximately 57 % and 39 %, respectively, of submerged rates. Remarkably, approximately 42 % of the total ammonia excreted during air-exposure was through NH(3) volatilization. Ammonia did not accumulate in whole-body tissues of air-exposed fish, but levels of both urea and some FAAs (primarily alanine and glutamine) were up to twofold higher after 10 days. The activities of the ornithine-urea cycle enzymes carbamoyl phosphate synthetase III and ornithine transcarbamylase increased (by approximately 30 % and 36 %, respectively) in whole-body tissues of air-exposed fish, while levels of arginase remained unchanged. The activities of enzymes involved in amino acid and oxidative metabolism were not significantly different between control and air-exposed fish. Partitioning of the anterior and posterior ends of immersed fish revealed that just over half (57 %) of the total nitrogen (ammonia+urea) was excreted through the anterior end of the fish, presumably via the branchial tissues, while emersed fish increased excretion via the posterior end (kidney+skin). R. marmoratus do not undergo a shift towards ureotelism during air-exposure. Rather, we propose that R. marmoratus are able to survive on land for extended periods without significant ammonia accumulation because they continuously release ammonia, partially by NH(3) volatilization.

Air↗
PubMed2002

Glutamine synthetase expression in liver, muscle, stomach and intestine of Bostrichthys sinensis in response to exposure to a high exogenous ammonia concentration.

A previous study provided evidence that the adaptive strategy used by the teleost fish Bostrichthys sinensis (sleeper) for detoxifying ammonia during extended periods of air exposure was to synthesize and store glutamine, primarily in the muscle, accompanied by an increase in glutamine synthetase (GSase) activity in liver. The aim of the present study was to assess the effect on GSase expression in various tissues of exposure of B. sinensis to exogenous ammonia. Exogenous ammonia increases internal ammonia concentrations in fish, mimicking environmental situations such as air exposure that preclude loss of ammonia across the gills, and thus triggering alternative mechanisms for ammonia detoxification. The results reveal relatively high levels of GSase activity, not only in liver but also, unexpectedly, in muscle, and even higher levels in intestine and, in particular, stomach. Exposure to ammonia results in significant increases in GSase activity, GSase protein and GSase mRNA levels in all of these tissues except stomach. The amino acid sequences of GSases from liver and stomach deduced from the cDNA sequences are essentially identical and are >97 % identical to the amino acid sequences of GSases from Gulf toadfish (Opsanus beta) and marble goby (Oxyeleotris marmoratus).

Amino Acid Sequence↗
PubMed1992

Gas phase derivatization of ammonia with 4-fluoro-7-nitrobenzo-2-oxa-1,3-diazole and its application to urease assay.

An ammonia-specific and rapid fluorometric method for determination of ammonia and urease activity was developed. The method is designed to assay ammonia levels or urease activity for the rapid diagnosis of Helicobacter pylori infection. 4-Fluoro-7-nitrobenzo-2-oxa-1,3-diazole was used to derivatize ammonia and 4-amino-7-nitrobenzo-2-oxa-1,3-diazole was analysed by high performance liquid chromatography at an excitation wavelength of 455 nm and an emission wavelength of 520 nm. Derivatization was designed to react with ammonia gas produced in a strong alkaline pH sample. The fluorescent intensity was linear in the range of 0.1-10 mM ammonia per tube when the reaction was carried out for 15 min at 37 degrees C. Urease activity, judged as the amount of ammonia production from urea, could be measured at 25 ng per tube (S/N = 1.5) with Jack bean meal urease. Because of its rapidity, this assay is potentially superior to the current standard method in use in clinical settings.

4-Chloro-7-nitrobenzofurazan↗
PubMed2000

Pretreatment of wastepaper and pulp mill sludge by aqueous ammonia and hydrogen peroxide.

Pretreatment of two different softwood-based lignocellulosic wastes (newsprint and Kraft pulp mill sludge) was investigated. Pretreatment was done by aqueous ammonia and hydrogen peroxide (H2O2), two delignifying reagents that are environmentally benign. Three different treatment schemes were employed: aqueous ammonia alone (ammonia recycled percolation [ARP]), mixed stream of aqueous ammonia and H2O2, and successive treatment with H2O2 and aqueous ammonia. In all cases there was a substantial degree of delignification ranging from 30 to 50%. About half of the hemicellulose sugars were dissolved into the process effluent. Retention of cellulose after pretreatment varied from 85 to 100% for newspaper feedstock and from 77 to 85% for the pulp mill sludge. After treatment with aqueous ammonia alone (ARP), the digestibility of newspaper and the pulp mill sludge was improved only by 5% (from 40 to 45% for the former and from 68 to 73% for the latter), despite a substantial degree of delignification occurring after the ARP process. The lignin content thus did not correlate with the digestibility for these substrates. Simultaneous treatment with H2O2 and aqueous ammonia did not bring about any significant improvement in the digestibility over that of the ARP. A successive treatment by H2O2 and ARP showed the most promise because it improved the digestibility of the newspaper from 41 to 75%, a level comparable to that of alpha-cellulose.

Ammonia↗
PubMed1992

Ultrafiltrate analysis confirms the specificity of the selected method for plasma ammonia determination.

The specificity of the direct enzymatic determination of plasma ammonia has hitherto not been unequivocally confirmed, because a suitable comparison method was lacking. Therefore a method variant was elaborated, which includes ultrafiltration to eliminate the high-molecular-mass components regarded as potential sources of unspecificity in the direct measurement procedure according to Rattliff, C.R. & Hall, F. F. (Select. Meth. Clin. Chem. 9, 85-90 (1982)). As the distribution of ammonia during plasma ultrafiltration is markedly influenced by pH and protein concentration, plasma pH is adjusted to 5.5 where the distribution ratio is 1 and nearly independent of actual protein concentration. Acidification significantly diminishes the spontaneous increase of ammonia in plasma at 2-4 degrees C, and the plasma ultrafiltrate is virtually stable. Taking into consideration the slow ammonia formation during sample preparation, excellent agreement was found between ammonia concentrations measured in plasma and in plasma ultrafiltrate, using samples with an apparently normal matrix (n = 30), dysproteinaemia (n = 32) or paraproteinaemia (n = 8). Our data show that the protein matrix of the sample does not cause significant unspecificity in the direct "endpoint" procedure for ammonia determination nor does it affect imprecision. In samples with added bilirubin (up to 252 mumol/l), haemolysate (haemoglobin up to 3.87 g/l) or lipid emulsion (triacylglycerol up to 3.86 mmol/l) ammonia values determined directly in plasma differed maximally by 4% from ultrafiltrate values. A simplified procedure for the ultrafiltration of plasma may be used routinely in clinical service in cases of grossly icteric, haemolytic or turbid samples.

Ammonia↗
PubMed2004

Short-term low-carbohydrate diet dissociates lactate and ammonia thresholds in men.

A low-carbohydrate (L-CHO) diet has been shown to shift the lactate threshold toward higher workloads. The aim of the present study was to examine the effect of an L-CHO diet on the ammonia threshold and to compare it with the lactate threshold in men. The plasma catecholamine threshold was also measured. Eight young, untrained men participated in the study. Two exercise tests with graded workload were performed. The workload was increased every 3 minutes by 40 W until volitional exhaustion. The first test was performed after 3 days of a controlled mixed diet. After the first test, the mixed diet was switched to a L-CHO diet. Three days later the same test was repeated. The blood concentration of lactate, ammonia, noradrenaline, and adrenaline was measured before and after each workload in both groups. It was found that the concentration of the examined compounds in the blood increases exponentially with graded workload after each kind of diet. This led us to calculate the blood ammonia, lactate, epinephrine, and norepinephrine thresholds. The thresholds were defined as points at which the concentration of a given compound starts to increase in a nonlinear fashion, which is calculated using 2 segmental linear regressions. After the mixed diet, the threshold for each compound occurs at the same workload. The L-CHO diet resulted in dissociation of the lactate threshold from the ammonia threshold: the lactate threshold was shifted toward a higher workload, whereas the ammonia threshold was shifted toward a lower workload. The norepinephrine threshold was also shifted toward a lower workload, and the epinephrine threshold remained unchanged. The results obtained indicate that an L-CHO diet accelerates production of ammonia and delays production of lactate during graded exercise, as well as that diet must be strictly controlled when ammonia and lactate thresholds are measured.

Adult↗
PubMed2003

Effects of pore-water ammonia on in situ survival and growth of juvenile mussels (Lampsilis cardium) in the St. Croix Riverway, Wisconsin, USA.

We conducted a series of in situ tests to evaluate the effects of pore-water ammonia on juvenile Lampsilis cardium in the St. Croix River (WI, USA). Threats to this river and its associated unionid fauna have accelerated in recent years because of its proximity to Minneapolis-St. Paul, Minnesota, USA. In 2000, caged juveniles were exposed to sediments and overlying water at 12 sites for 10 d. Survival and growth of juveniles was significantly different between sediment (mean, 47%) and water column (mean, 86%) exposures; however, these effects were unrelated to pore-water ammonia. During 2001, juveniles were exposed to sediments for 4, 10, and 28 d. Pore-water ammonia concentrations ranged from 0.3 to 62.0 microg NH3-N/L in sediments and from 0.5 to 140.8 microg NH3-N/L within exposure chambers. Survival (mean, 45, 28, and 41% at 4, 10, and 28 d, respectively) and growth (range, 3-45 microm/d) of juveniles were highly variable and generally unrelated to ammonia concentrations. Although laboratory studies have shown unionids to be quite sensitive to ammonia, further research is needed to identify the route(s) of ammonia exposure in unionids and to understand the factors that contribute to the spatial variability of ammonia in rivers.

Ammonia↗
PubMed2003

Effects of ammonia on juvenile unionid mussels (Lampsilis cardium) in laboratory sediment toxicity tests.

Ammonia is a relatively toxic compound generated in water and sediments by heterotrophic bacteria and accumulates in sediments and pore water. Recent data suggest that unionid mussels are sensitive to un-ionized ammonia (NH3) relative to other organisms. Existing sediment exposure systems are not suitable for ammonia toxicity studies with juvenile unionids; thus, we modified a system to expose juveniles to ammonia that was continuously infused into sediments. This system maintained consistent concentrations of ammonia in pore water up to 10 d. Juvenile Lampsilis cardium mussels were exposed to NH3 in pore water in replicate 96-h and 10-d sediment toxicity tests. The 96-h median lethal concentrations (LC50s) were 127 and 165 microg NH3-N/L, and the 10-d LC50s were 93 and 140 microg NH3-N/L. The median effective concentrations (EC50s) (based on the proportion affected, including dead and inactive mussels) were 73 and 119 microg NH3-N/L in the 96-h tests and 71 and 99 microg NH3-N/L in the 10-d tests. Growth rate was substantially reduced at concentrations between 31 and 76 microg NH3-N/L. The lethality results (when expressed as total ammonia) are about one-half the acute national water quality criteria for total ammonia, suggesting that existing criteria may not protect juvenile unionids.

Age Factors↗
PubMed1998

Dietary carbohydrates alter the fecal composition and pH and the ammonia emission from slurry of growing pigs.

We investigated the effects of dietary carbohydrates on the composition and pH of fecal material and on the ammonia emission from the slurry of growing pigs. Thirty-four barrows (BW approximately 40 kg) were randomly allotted to 1 of 10 diets. A basal diet was formulated to meet all requirements for protein, amino acids, minerals, and vitamins. The control diet was composed of the basal diet plus heat-treated cornstarch. In the other diets, the cornstarch in the control diet was replaced with three levels of either coconut expeller, soybean hulls, or dried sugar beet pulp. Feces were collected separately from urine in a balance experiment. Feces were mixed with a standardized urine (ratio of 1:2.5, wt/wt) to form a slurry. A sample of this slurry was placed in an in vitro system to determine the pH and the ammonia emission for 16 d at 20 degrees C. The fecal and slurry DM contents decreased (P < .001) and the total VFA concentrations increased (P < .001) when the level of dietary carbohydrates increased. The pH and the ammonia emission decreased as the level of carbohydrates increased (P < .001). The addition of soybean hulls to the diet had the greatest effect on reducing the pH and ammonia emission (P < .001), and the effects of sugar beet pulp and coconut expeller were approximately the same. A linear relationship was found between the intake of dietary nonstarch polysaccharides (NSP) and the ammonia emission (P < .001). For each 100-g increase in the intake of dietary NSP, the slurry pH decreased by approximately .12 unit and the ammonia emission from slurry decreased by 5.4%. We conclude that replacing cornstarch in the diet with components that have a high concentration of fermentable carbohydrates increases the VFA concentration of feces and slurry and reduces the pH and ammonia emission from the slurry of growing pigs.

Ammonia↗
PubMed1980

Effects of air and fluid flow rates on removing different concentrations of urea and ammonia from fluid by gas absorption in a capillary hemodialyzer.

Urease converts urea into ammonium and bicarbonate. Alkalinization converts ammonium into free ammonia which can be removed as a gas. Our approach is to use a capillary hemodialysis as a gas absorption unit with liquid moving through the blood compartment and air through the dialysate compartment to extract ammonia gas. This paper examines the effects of air flow rate, fluid flow rate, and concentrations of ammonia (and urea) in the fluid. It was observed that increasing air flow rate or dialysate flow rate increases the mass transfer rate for ammonia especially at low ammonia concentration levels. Ammonia removal rate increases with air flow rate linearly. Ammonia removal rate increases with increasing fluid flow rate, but reaches a plateau when flow rate was above 500 ml/mn.

Air↗
PubMed1976

Influence of aminooxyacetate administration on ammonia-induced metabolic disturbances in the rat liver.

The purpose of the present report was to investigate the effects of aminooxyacetate administration to rats on the ammonia-induced disturbances in the substrate levels and in the activities of the enzymes involved in glutamine metabolism. 1.--Aminooxyacetate enhances the accumulation of ammonia following an ammonia load and prevents the other substrate level changes induced by ammonia. Thus, this transaminase inhibitor suppresses ammonia detoxication by formation of aminoacids as well as by urea synthesis. 2.--A significant decrease of glutamine synthetase activity is observed only after administration of both aminooxyacetate and ammonium chloride. 3.--Like in rats injected with ammonium chloride alone, an ammonia-induced activation of liver glutaminase I is found in inhibitor-pretreated rats. This result confirms the specific enhancement of glutaminase I activity by ammonia in excess.

Acetates↗