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PubMedDate not supplied

Alanine, glutamate, and ammonia exchanges in acutely ischemic swine myocardium.

Coronary artery disease causes an increase in glutamate uptake and alanine output by the heart. We assessed the effects of acute myocardial ischemia on alanine and glutamate exchange and ammonia production in 10 anesthetized open-chest domestic swine (46.9 +/- 0.7 kg). Coronary blood flow was controlled through an extracorporal perfusion circuit. After a nonischemic control period (aerobic) the blood flow in the left anterior descending coronary artery was reduced by 60%. Arterial and anterior interventricular venous samples where drawn before and during 35 min of ischemia. Subendocardial blood flow, measured using radiolabeled microspheres, decreased from 1.27 +/- 0.16 to 0.25 +/- 0.09 (ml/g)/min, and left-ventricular wall-thickening fell to 47% of aerobic values. Ischemia resulted in a significant increase in the rate of glucose uptake (p less than 0.05) and a switch to net lactate production (p less than 0.01). Ischemia did not affect the rates of alanine output (-0.9 +/- 1.0 vs. -0.3 +/- 0.3 mumol/min) or glutamate uptake (-0.4 +/- 1.1 vs. 0.3 +/- 0.6 mumol/min), but did increase the venous-arterial difference for ammonia (-4.1 +/- 4.1 to 52.7 +/- 5.5 microM, p less than 0.0001) and the ammonia output (-0.33 +/- 0.24 to 1.34 +/- 0.14 mumol/min, p less than 0.0001). In conclusion, acute ischemia did not stimulate greater alanine output or glutamate uptake. However, acute ischemia did cause an increase in anaerobic glycolysis rate and ammonia output, which reflects a profound disruption in myocardial energy metabolism.

Alanine↗
PubMed1991

Synergistic effect of bile acid, endotoxin, and ammonia on brain edema.

The effects of cytotoxic substances such as ammonia, bile acids and endotoxin, all of which increase in the circulating blood during fulminant hepatic failure (FHF), on the blood-brain barrier (BBB) permeability and development of brain edema were examined in the rats. Direct intracarotid injection of various bile acids resulted in the staining of the cerebral hemisphere with Evans blue as well as the increase of brain water contents. Elevation of ammonia was also observed in the cerebral hemisphere where the reversible opening of the BBB was induced by deoxycholate under hyperammonemic conditions. To see the synergistic significance of cytotoxic substances (ammonia, bile acid and endotoxin) under the more physiological condition as FHF, they were simultaneously injected into a peripheral vein. Brain uptake index of 14C-inulin and brain water content increased, and electron micrographs showed the swollen astrocytic foot processes surrounded brain capillary, but not opening of tight junction, the same as an animal model of fulminant hepatic failure. The results suggest that ammonia, bile acids and endotoxin might have a possible synergistic role in the pathogenesis of the brain edema, mainly cytotoxic, and vasogenic due to acceleration of vesicular transport, in FHF.

Ammonia↗
PubMed1996

Effect of prostaglandin E1 on ammonia concentration in blood of patients with hepatic resection.

Plasma concentrations of ammonia were examined following prostaglandin E1 (PGE1) administration in 16 patients who received hepatectomy for hepatocellular carcinoma. PGE1 at 0.01-0.04 microgram/kg/min was administered for approximately 24 hr during the perioperative periods. The ammonia concentration was reduced a day after the operation following intravenous administration of PGE1 in cirrhotic patients compared to noncirrhotic patients with or without PGE1 injection. Serum liver function scores, glutamic pyruvic transaminase, and total bilirubin concentrations were decreased after PGE1 administration. A similar ammonia response due to PGE1 was obtained after operation in cirrhotic patient when PGE1 0.5 microgram/kg was administered intravenously for 30 min. These results suggest that PGE1 administration is useful in reducing the enhanced ammonia concentration associated with hepatic resection, and it is particularly effective in the case of liver cirrhosis.

Alanine Transaminase↗
PubMed1988

Dynamic relationship between urea and glutamine synthesis in the mechanism of ammonia detoxication: a tracer study using 15NH4Cl in fulminant hepatic failure rats.

Fulminant hepatic failure (FHF) was produced in rats with intraperitoneal injection of D-galactosamine. 15NH4Cl (50 mg/kg of body weight) was injected into the rats via the tail vein. Arterial blood was drawn before and 5, 15, 30, 60 min after the injection of 15NH4Cl. 15N-ammonia, -urea, and -glutamine (amide and amino) were determined by gas chromatography and mass spectrometry. The plasma 15N-ammonia level was higher but decreased more rapidly in the FHF rats than in the control rats. This suggests that in FHF rats, the systemic vascular pool of ammonia is enlarged and ammonia clearance from blood is increased. The incorporation of 15N into urea was significantly different between the two groups. In FHF rats, the plasma urea-15N level rose 5 min after the injection, decreased at 15 min and was elevated again up to 60 min after injection. This biphasic change suggests that in FHF rats the incorporation of 15N into the extrahepatic glutamine pool is accelerated up to 15 min and that after 30 min a larger volume of glutamine-amide-15N is transferred to the urea cycle.

Ammonia↗
PubMedDate not supplied

Determination of ammonia in cerebrospinal fluid using the indophenol direct method.

We have determined ammonia in cerebrospinal fluid (CSF) with the indophenol direct method. The results were compared with an enzymatic method. The method is very simple, and precision (coefficient of variation 1.6%) and linearity (r = 0.9999, p < 0.001) of the method are excellent. The recoveries of the method are very good (within-sample recovery: range 88-93, median 93%; between-sample recovery: 88-93, median 91%). In a population of 23 neurological patients not suffering from liver disease, the reference values ranged from 8 to 26, median 18 microM. Males and females did not differ (p = 0.5). The values obtained with the indophenol method were equal to the enzymatic method (range 9-28, median 18 microM, p = 0.6). On storage in the deep freeze (-20 degrees C), there was no change in CSF ammonia concentration for at least 1 mo. When stored at 4 degrees C (refrigerator), ammonia determinations have to be performed within 2 d. CSF storage at room temperature results in artificially elevated ammonia levels and should be avoided.

Ammonia↗
PubMedDate not supplied

A membrane-based method for removal of toxic ammonia from mammalian-cell culture.

Many mammalian cells grown in culture excrete ammonia, which, when it accumulates, limits cell growth and reduces product synthesis. Common tactics for minimizing the effects of ammonia accumulation are uneconomical, requiring large quantities of media and incurring high capital costs. Solution-diffusion membranes were investigated for ammonia removal, and a supported-gas membrane was identified that could be used to remove ammonia rapidly to well below inhibitory levels. Medium treated using this membrane was reused to culture baby-hamster kidney cells, resulting in a cell growth rate that was essentially the same as that for cells grown in fresh medium.

Ammonia↗
PubMed1999

Exposure of intestinal epithelial cell HT29 to bile acids and ammonia enhances Mac-1-mediated neutrophil adhesion.

OBJECTIVE: Bile acids and ammonia (NH3/NH4+) are cytotoxic metabolic products, which are known to influence intestinal epithelial functions such as colonic chloride secretion. In this study, we have investigated the effect of bile acids and ammonia on neutrophil-intestinal epithelial adhesive interaction. MATERIALS AND METHODS: Confluently cultured HT29 cells were treated with bile acids or ammonium chloride. Then, 51Cr-labeled neutrophils were added to HT29 cell monolayers, and neutrophil adhesion was assessed by gamma-scintillation counting. RESULTS: Treatment of HT29 cells with 0.1 mM CDCA (chenodeoxycholic acid), DCA (deoxycholic acid), CA (cholic acid) or ammonium chloride but not UDCA (ursodeoxycholic acid) for 30 min increased neutrophil adhesion about 4-folds (p<0.01). The increased adhesion was inhibited 82-91% by 10 microg/ml anti-CD11b and anti-CD18 mAbs (p<0.01), but not by anti-CD11a and anti-CD54 (ICAM-1) mAbs. Interestingly, flow cytometric analysis revealed that ICAM-1 expression on HT29 cells was not changed by bile acid- or ammonia-treatment. In addition, the increased adhesion was inhibited about 65 % by proteinase K-treatment (10 microg/ml, 1 min, p<0.05) but not cycloheximide-treatment (1 microg/ml, 30 min) of HT29 cells. CONCLUSIONS: These observations indicate that exposure of HT29 cells to bile acids or ammonia induces CD11b/CD18 (Mac-1) dependent- but CD11a/CD18 (LFA-1) independent-neutrophil adhesion to intestinal epithelial cells, and ICAM-1 is unlikely involved in the interactions. Furthermore, epithelial ligand(s) for neutrophils are protein molecule(s) which are expressed on the cell surface independent of protein synthesis.

Ammonia↗
PubMed2005

Chronic toxicity of un-ionized ammonia to early life-stages of endangered Colorado pikeminnow (Ptychocheilus lucius) and razorback sucker (Xyrauchen texanus) compared to the surrogate fathead minnow (Pimephales promelas).

Ammonia-contaminated groundwater enters the Upper Colorado River from beneath the abandoned Moab Uranium Mill Tailings Pile near Moab, Utah. This reach of the Upper Colorado River was designated as critical habitat for four endangered fish species because it is one of the few existing areas with known spawning and rearing habitats. Un-ionized ammonia (NH3) concentrations frequently exceed 1.00 mg/L in backwaters adjacent to the tailings pile, which exceeds the Utah 30-d average chronic water quality criterion for un-ionized ammonia (0.07 mg/L NH3; temperature 20 degrees C; pH 8.2) by a factor of more than 10. However, there is little published information regarding the sensitivity of endangered fishes to ammonia. We conducted 28-d static renewal studies with post-swim-up larvae to determine the relative sensitivity of Colorado pikeminnow (Ptychocheilus lucius), razorback sucker (Xyrauchen texanus), and the standard surrogate fathead minnow (Pimephales promelas) to NH3. Chronic values (ChVs) for mortality and growth were determined as the geometric mean of the no observed effect concentration and the lowest observed effect concentration based on analysis of variance. The ChVs for growth of fathead minnow, Colorado pikeminnow, and razorback sucker were 0.43, 0.40, and 0.67 mg/L NH3, respectively. The ChVs for mortality of fathead minnow, Colorado pikeminnow, and razorback sucker were 0.43, 0.70, and 0.67 mg/L NH3, respectively. Therefore, the ChVs for mortality and growth were similar for fathead minnow and razorback sucker; however, the ChV for growth was lower than the ChV for mortality for Colorado pikeminnow. Maximum likelihood regression was used to calculate 28-d lethal concentrations (LCx) for each species. The 28-d LC50, LC20, and LC1 values for fathead minnow were 0.69, 0.42, and 0.13 mg/L NH3, respectively. The 28-d LC50, LC20, and LC1 values for Colorado pikeminnow were 0.76, 0.61, and 0.38 mg/L NH3, respectively. The 28-d LC50, LC20, and LC1 values for razorback sucker were 0.54, 0.38, and 0.25 mg/L NH3, respectively. The fathead minnow, Colorado pikeminnow, and razorback sucker are relatively similar in sensitivity and rank at the 35th, 49th, and 31st percentiles, respectively, of the theoretical chronic fish sensitivity distributions for NH3. The existing water quality criteria for NH3, if met by remediation activities at the Moab site, would be protective of these endangered fishes even if fish sensitivity is based on the conservative LC1 value.

Ammonia↗
PubMed2002

Effects of exogenous ammonia or free amino acids on proteolytic activity and protein breakdown products in Streptococcus bovis, Prevotella albensis, and Butyrivibrio fibrisolvens.

We studied in details the ammonia or free amino acids (AA) effects on proteolytic activity of three ruminal bacteria: enzymatic activities and protein breakdown products were measured at the end of the exponential growth phase. In Streptococcus bovis the simultaneous uptake of ammonia and probably small peptides induced a decline in total proteolytic activity as a result of changes in endopeptidasic activities. With free AA, the tendency for the endopeptidasic activities to specialise was more evident and the total proteolytic activity decreased too. In Prevotella albensis, the inhibition of proteolysis with free AA was linked to the disappearance of free endopeptidases, to the specialization of cell-associated endopeptidases and to the decrease in exopeptidases. The decrease of proteolysis in P. albensis when ammonia was added was more difficult to interpret. With ammonia or AA Butyrivibro fibrisolvens developed a distinct behavior of those expressed by the other species: the increase of the total proteolytic activity could be explained by a better balance of the endopeptidases expressed. It then clearly appeared that the expression of the proteolytic activities are linked to the nature and/or to the quantity of the nitrogen source. This leads each species to adopt its own nutritional strategy in order to adapt to the environmental conditions of the ruminal ecosystem.

Amino Acids↗
PubMed2002

Reduction of sulfide, ammonia compounds, and adhesion properties of Lactobacillus casei strain KE99 in vitro.

The ability of Lactobacillus casei strain KE99 to reduce sulfide, ammonia, and to adhere to bio-surfaces was characterized and compared with three lactobacillus reference strains. Sulfide reduction by strain KE99 in MRS broth increased exponentially after 10-h growth and reached a maximum (>300 ppm reduction) within 48 h. KE99 demonstrated a maximum reduction of sulfide under anaerobic (341 ppm) growth conditions at pH 6.0-8.0 range. Maximum anaerobic reduction of sulfide was demonstrated by L. casei 393 at pH 7.0 (272 ppm); L. rhamnosus at pH 8.0 (277 ppm); and L. reuteri at pH 7.0 (244 ppm). KE99 reduced sulfide more (p < 0.0001) in MRS broth spiked with Na2S (374 ppm) than (NH4)2S (340 ppm) salts. Ammonia reduction by strain KE99 and the three lactobacillus reference strains in MRS broth was low. Ammonia reduction reached a maximum within 36 h and remained unchanged over extended incubations of 48 h to 72 h or further. KE99 reduced ammonium sulfate (37 ppm) more readily than the nitrate (31 ppm), hypophosphate (29 ppm), or chloride (20 ppm) salts of ammonia. KE99 and the three reference strains of lactobacilli demonstrated avid binding to Bio-coat (Cn type-I, Cn type-IV, laminin, fibronectin), Matrigel, and Caco-2 cell monolayers in vitro. The number of lactobacilli binding to Caco-2 was estimated at 74/cell with strain KE99, which was significantly higher compared with 40/cell (p < 0.0001), 26/cell (0.0001), and 64/cell (p < 0.002) with L. casei 393, L. reuteri, and L. rhamnosus, respectively. The interaction of KE99 to immobilized Cn type-I was saturable and reached an equilibrium within 1 h at room temperature. KE99 binding to Cn type-I occurred at a wide pH range and was biphasic with maximum binding at pH 5.5 and 7.5. Inhibition and binding-displacement experiments with different salts and sugars suggested that the KE99 binding to immobilized Cn type-I may involve a combination of electrostatic and lectin-type interactions. KE99 effectively detached the Cn-adherent E. coli O157:H7 in the range of 55% (ATCC43895) to 76% (ATCC43894). The binding-displacement values for L. casei 393, L. reuteri and L. rhamnosus to detach Cn-adherent E. coli O157:H7 (ATCC43894) were 66 +/- 4%, 59 +/- 2%, and 64 +/- 2%, respectively. Also, a reconstituted solution of the freeze-dried KE99 preparation effectively detached the Cn-adherent E. coli O157:H7 in a dose-dependent manner that reached a binding-displacement equilibrium of 85% at a 1% wt/vol KE99 concentration.

Ammonia↗
PubMed1998

Physiological and molecular biological characterization of ammonia oxidation of the heterotrophic nitrifier Pseudomonas putida.

The heterotrophic nitrifier Pseudomonas putida aerobically oxidized ammonia to hydroxylamine, nitrite, and nitrate. Product formation was accompanied by a small but significant release of NO, whereas N2O evolution could not be detected under the assay conditions employed. The isolate reduced nitrate to nitrite and partially further to NO under anaerobic conditions. Aerobically grown cells utilized gamma-aminobutyrate as a carbon source and as a N-source by ammonification. The physiological experiments, in particular the inhibition pattern by C2H2, indicated that P. putida expressed an ammonia monooxigenase. DNA-hybridization with an amoA gene probe coding for the smaller subunit of the ammonia monooxigenase of Nitrosomonas europaea allowed us to identify, to clone, and to sequence a region with an open reading frame showing distinct sequence similarities to the amoA gene of autotrophic ammonia oxidizers.

Aerobiosis↗
PubMed2003

Effect of low oxygen inhalation on changes in blood pH, lactate, and ammonia due to exercise.

The present study examined the effect of hypoxia-induced respiratory alkalosis on exercise-induced metabolic acidosis and increases in plasma lactate and ammonia levels. Six male subjects underwent exercise of increasing intensity until exhaustion: (1) in normoxia (20.9% O(2)) (=MAX), (2) in hypoxia (12% O(2)) (=HP) in which hypoxic condition had been maintained from 60 min before to 30 min after exercise, and (3) the same intensity of exercise as HP in normoxia (=SUB). Arterialized blood was drawn from a superficial vein. Post-exercise blood pH was significantly higher in HP than in MAX ( P<0.05), although plasma lactate was at the same level. For hypoxia as compared to normoxia, regression analysis confirmed a parallel shift of plasma lactate to higher pH levels indicating the effect of respiratory alkalosis ( P<0.01). After exercise plasma levels of ammonia were lower in HP than in MAX ( P<0.05). Regression analysis between ammonia and pH revealed nearly identical changes in hypoxia and normoxia at low pH. From these results, we conclude that: (1) hypoxia-induced respiratory alkalosis attenuated exhaustive exercise-induced metabolic acidosis, (2) plasma lactate concentration was determined by the relative exercise intensity, (3) the maximum plasma ammonia concentration under exhaustive exercise was reduced at hypoxia because of respiratory alkalosis.

Adult↗
PubMed2005

Effect of hypercapnia on changes in blood pH, plasma lactate and ammonia due to exercise.

The present study examined the effects of hypercapnia on changes in blood pH, plasma lactate and ammonia due to exhaustive exercise. Six male subjects underwent exercise of increasing intensity until exhaustion: (1) breathing air = MAX (maximal exercise), or (2) under hypercapnia (HC: 21% O(2), 6% CO(2)) that had been maintained from 60 min before to 30 min after exercise = HC; and (3) exercise of the same intensity as HC in air = SUB (submaximal exercise). Arterialized blood was drawn from a superficial vein. Blood pH in HC was significantly lower than in MAX or SUB at rest, at the end of exercise and throughout recovery (P<0.05). Plasma lactate and ammonia concentration in HC was significantly lower than in MAX (P<0.05), and similar to that in SUB at the end of exercise and throughout recovery. Respiratory acidosis resulting from hypercapnia shifted the linear lactate to blood pH relationship during exhaustive exercise below that at normocapnia (P<0.001). The reduced slope of linear blood pH to ammonia relationship under hypercapnia (P<0.001) is attributed to lactic acidosis that is less, due to the lesser work intensity at the end of exhaustion, than that of normocapnia. From these results we conclude that (1) hypercapnia-induced respiratory acidosis promoted the decrease in blood pH due to lactate production throughout recovery; (2) plasma lactate concentration at maximal exercise was lowered under hypercapnia; (3) plasma ammonia concentration at maximal exercise was reduced, probably due to a less intense lactic acidosis.

Acid-Base Equilibrium↗
PubMed2000

Influence of ammonia on sodium absorption in rat proximal colon.

The influence of ammonia on sodium and chloride fluxes in rat proximal colon was studied in Ussing chamber experiments. Under short-circuit conditions, the proximal colon absorbed sodium and secreted chloride. The presence of ammonia (30 mmol 1(-1) mucosal) diminished Na+ absorption, but had hardly any influence on Cl- fluxes. Blocking the apical Na+/H+ exchanger isoform NHE2 by amiloride or HOE642 diminished absorptive Na+ and Cl- fluxes. In contrast, the NHE3-specific antagonist S3226 was ineffective. Amiloride and HOE642 also inhibited the effect of ammonia on net sodium absorption. In bicarbonate-free buffer solution, ammonia failed to alter the absorptive fluxes of sodium and chloride, but increased the secretory fluxes of Na+ and Cl-. The latter effect was blocked by HOE642. These results suggest that basal NaCl absorption in rat proximal colon depends to a large extent on NHE2. Mucosal ammonium decreases Na+ absorption and this effect can be antagonized by blocking NHE2. This observation suggests that ammonium interacts with the apical Na+/H+ exchanger, thereby diminishing sodium absorption.

Amiloride↗
PubMed2006

Amino acid challenge in patients with cirrhosis and control subjects: ammonia, plasma amino acid and EEG changes.

BACKGROUND/AIMS: The pathogenesis of hepatic encephalopathy (HE) is controversial. We have therefore studied the effect of induced hyperammonaemia in man. PATIENTS AND METHODS: 108 g of an amino acid mixture was given orally to 18 cirrhotics and 11 control subjects and changes in blood ammonia, EEG and plasma amino acids were observed. RESULTS: Basal (39+/-6 versus 14+/-2 micromol/l) and 120-min post amino acid (77+/-10 versus 27+/-4) blood ammonia concentrations in cirrhotics were significantly increased compared to healthy controls (p < 0.001). Associated with these changes there was a significant increase in the ratio of slow-to-fast wave activity indicating EEG slowing (+0.41+/-0.16; N=13 versus -0.05+/-0.08; N=8; p=0.036). As expected in cirrhotics, basal valine and leucine concentrations were decreased while phenylalanine, tyrosine and methionine were significantly increased. Although the basal molar ratio of branched chain amino acids to the aromatic amino acids phenylalanine and tyrosine was significantly decreased in cirrhotics (1.5+/-0.2 versus 3.2+/-0.2; p < 0.0001), after the challenge when EEG changes were apparent in cirrhotics, the ratio significantly increased (p < 0.005) in both groups to 2.7+/-0.3 versus 4.1+/-0.3 (p=0.002). In the combined groups, there were significant correlations between EEG ratio change and the 120-min blood ammonia concentration (r=0.498; p=0.022). CONCLUSION: The alterations in plasma amino acid patterns do not support a specific role for any of the amino acid groups in the pathogenesis of hepatic encephalopathy. They are however more in keeping with the direct or indirect role of ammonia.

Adult↗
PubMed1988

F-18 deoxyglucose and stress N-13 ammonia positron emission tomography in anterior wall healed myocardial infarction.

To evaluate myocardial blood flow and glucose utilization, N-13 ammonia (NH3) and F-18 deoxyglucose positron emission tomography scanning was performed in 22 patients with previous anterior wall myocardial infarction, using a high-resolution, multi-slice, whole-body scanner. The N-13 ammonia study was performed at rest and after exercise. The F-18 deoxyglucose study was performed at rest after fasting greater than 5 hours. The N-13 ammonia study revealed a hypoperfused area in 19 of the 22 patients (86%), that corresponded to the infarcted regions as diagnosed by electrocardiography, coronary arteriography and left ventriculography (21 patients). The hypoperfused areas expanded after exercise in 16 of 22 patients (73%). F-18 deoxyglucose uptake was observed in these hypoperfused areas, especially in patients with hypokinetic wall motion on left ventriculography and in exercise-induced hypoperfused areas. However, positron emission tomography demonstrated diffuse uptake of F-18 deoxyglucose in 3 of 8 patients with dyskinetic wall motion. Thus, metabolically active myocardium in infarcted areas or periinfarct ischemia can be visualized with F-18 deoxyglucose and stress N-13 ammonia studies.

Adult↗
PubMed1983

Ammonia utilization by a proposed bacterial pathogen in human periodontal disease, Capnocytophaga ochracea.

Capnocytophaga ochracea strain 25 was originally isolated from a patient with severe juvenile periodontitis. An NAD-specific glutamate dehydrogenase (GDH) (EC 1.4.1.2.) was found in cell-free extracts from this organism. The NADH-dependent reductive, or ammonia-assimilating activity (NADH-GDH), of the enzyme was 8-10-fold higher than its NAD-dependent oxidative, or ammonia-releasing activity (NAD-GDH), suggesting that the primary physiological role of the GDH is ammonia-fixing. Capnocytophaga ochracea GDH was purified approximately 39-fold by a rapid, single-step purification procedure using DEAE-cellulose (DE52) ion-exchange column chromatography which gave 90 per cent recovery of total enzyme units. Paper chromatography of an NADH-GDH assay mixture containing the partially purified enzyme showed that glutamate was, indeed, a product of the ammonia-assimilating reaction. The pH optimum for the NAD-GDH reaction was 9.0; that for the NADH-GDH reaction was 7.5. Although a number of mono- and divalent cations were tested, none had a large effect on either NAD-GDH or NADH-GDH activity. The NAD-GDH reaction showed a hyperbolic kinetic response to glutamate and NAD and the Km values for glutamate and NAD were 2.44 and 0.083 mM respectively. The kinetic response of the NADH-GDH reaction to NADH, alpha-ketoglutarate and ammonium chloride also obeyed Michaelis-Menten kinetics and their respective Km values were 0.069, 1.44 and 3.33 mM. Of a number of biologically-active compounds tested for their ability to modulate GDH activity, only ADP and NAD exerted much effect. The NADH-GDH activity showed a negative hyperbolic kinetic response to both ADP and NAD and Dixon plot-analysis of the NAD and ADP saturation data gave Ki values for ADP and NAD of 4.0 and 0.46 mM respectively. Both NAD and ADP appeared to exert their negative effects on NADH-GDH activity by completely inhibiting the binding of the reduced coenzyme, NADH, to the enzyme.

Ammonia↗
PubMed1989

Degradation of trichloroethylene by the ammonia-oxidizing bacterium Nitrosomonas europaea.

Suspensions of Nitrosomonas europaea are shown to cause the complete disappearance of 10 microM trichloroethylene at rates of 1 microM mg protein-1. The reaction continues at nearly this rate for many hours. Fresh cells catalyze the reaction in the absence of added ammonium (presumably utilizing endogenous ammonia or stored reductant). In older cells, trichloroethylene degradation depends on the addition of ammonia. Acetylene, 2-chloro 6-trichloromethylpyridine and alpha alpha'dipyridyl, which inhibit the oxidation of ammonia by cells, inhibit the degradation of trichloroethylene. Thus degradation of trichloroethylene is dependent on- and possibly catalyzed by the ammonia oxidizing enzyme.

Ammonia↗