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PubMed1988

Preferential interaction among lens proteins as evidenced from accessibility of crystallins to ammonia gas.

Different crystallins (alpha, beta H, beta L and low molecular weight--LMW) were isolated from bovine lenses. The study of accessibility of the lyophilized solid proteins to ammonia gas was conducted in a high-vacuum vapor sorption apparatus. The sorption and desorption isotherms obtained were used to calculate the sorptive capacity and retentive capacity (hysteresis and irreversibly sorbed ammonia gas) of the different proteins. Individual crystallins were used to study the accessibility of the self-aggregates. Protein mixtures (beta H + beta L; alpha + LMW, etc.) were employed to study the accessibility of binary, tertiary and finally quaternary systems to ammonia vapor. Finally lyophilized thin sections of the bovine lenses were exposed to ammonia vapor. Comparing the sorptive and retentive capacities of self- and hetero-aggregates gave an indication of the preferred interactions among lens proteins in free solution, and by inference in situ, in the lens fibers.

Absorption↗
PubMed1989

Continuous intravenous ammonia infusion as a model for the study of hepatic encephalopathy in rabbits.

To obtain a more precise pathophysiological evaluation of the role of ammonia in acute hepatic encephalopathy, we compared the plasma ammonia concentrations and electroencephalographic recordings (EEGs) of rabbits with surgically induced acute hepatic failure (AHF, n = 10) and normal rabbits administered an infusion of ammonium acetate (NH4-Ac, n = 7) over a 10-hr period. AHF was surgically induced by portocaval shunting followed by hepatic artery ligation 48 hr later. In the infusion group the dose of NH4-Ac, initially 0.78 mmol/kg/hr, was increased every 2 hr by 0.13 mmole/kg/hr during a 10-hour period to simulate the arterial NH3 concentrations observed in AHF. Ammonia levels in rabbits administered the NH4-Ac infusion were identical to those observed in AHF, with the exception of the higher initial value in the AHF group. Moreover, the mean rates of increase in grade of encephalopathy in the two groups were similar, although the EEG grades in the infusion group were significantly less at all time points. In conclusion, this study demonstrates that a more pathophysiological approach to identification of the putative toxins in hepatic encephalopathy is feasible. Some of the EEG abnormalities of acute hepatic encephalopathy in rabbits are presumably due to hyperammonemia; the encephalopathy observed in AHF at zero time is probably caused by the previously constructed portocaval shunt via an undefined, but possibly also ammonia-related, mechanism.

Acetates↗
PubMed1986

Effect of hyperketonemia on renal ammonia excretion in man.

The effect of DL-sodium beta-hydroxybutyrate (Na BOHB) on urinary ammonia excretion was studied in seven chronically acidemic human subjects. Metabolic acidosis was induced by the ingestion of 0.1 g/kg body weight of ammonium chloride for three days. On the morning of day 4, baseline blood and urine samples were collected during three 30-minute periods. Na BOHB (1 mmol/kg, pH = 7.4) was then infused over 20 minutes, and this was followed by a continuous infusion at the rate of 10 mumol/kg min for 160 minutes. Urinary ammonia excretion decreased by 35% (P less than 0.001) while urine pH rose slightly from 5.49 to 5.82 (P less than 0.002). Venous pH increased from 7.31 to 7.38 (P less than 0.005) and bicarbonate concentration from 19 to 25 mEq/L (P less than 0.002). Four subjects were restudied with an infusion of Na beta-OHB (pH adjusted to 4.4 with the addition of HCI). Venous pH and bicarbonate concentration did not change significantly while urine pH decreased from 5.25 to 4.90 (P less than 0.001). Urinary ammonia excretion fell by 34% (P less than 0.01) despite the decline in urine pH and the absence of change in blood pH and bicarbonate concentration. Three subjects were restudied with sodium bicarbonate (0.52 to 0.85 mEq/min) infusion. Despite similar increases in blood pH and plasma bicarbonate concentration as observed with Na beta-OHB at pH = 7.4, urinary ammonia excretion did not fall significantly. In an attempt to simulate the change in redox potential and NAD+ to NADH ratio that occurred during the metabolism of beta-hydroxybutyrate to acetoacetate, sodium lactate was given to four subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1989

Effects of hyperthermia on the peripheral metabolism of ammonia and glutamine.

Although there are a number of physiological states associated with an increase in body temperature, eg, nonseptic and septic fever or exercise, the effects of hyperthermia on intermediary metabolism in vivo have received little attention. The current study was undertaken to examine the peripheral metabolism of ammonia and ammonia-related amino acids using a model of exogenously induced mild hyperthermia in nonfebrile subjects. Arteriovenous levels of metabolites were measured in subjects with known cerebrovascular insufficiency. Peripheral exchange of these metabolites was monitored before, during, and after hyperthermia to an average temperature of 38.5 degrees C. All subjects showed an increase in plasma ammonia and glutamate. There was also an associated peripheral production of ammonia and an uptake of glutamine and alanine by the skeletal muscle tissues. The exchange of glutamate was not affected. These findings indicate that hyperthermia is associated with a nitrogen-sparing effect, the mechanism of which is yet unknown.

Acid-Base Equilibrium↗
PubMed1983

The effect of ammonia on stalk cell formation in submerged monolayers of Dictyostelium discoideum.

It has been shown that ammonia inhibits stalk cell formation in monolayers of V12M2, and it was suggested that this inhibition was due to an antagonism of the differentiation-inducing factor (DIF) (Gross, J.D. et al., Nature, 303, 244-246, 1983). However, the results presented here indicate that ammonia inhibition is independent of DIF concentration, and that it occurs well in advance of the period of DIF requirement. Ammonia completely inhibits DIF accumulation and inhibits stalk cell differentiation, but there is no inhibition of prespore cell formation. These results imply the existence of an early ammonia-sensitive event that influences terminal cell type differentiation.

Ammonia↗
PubMed1994

Principles of an efficient new method for the removal of ammonia from animal cell cultures using hydrophobic membranes.

To overcome ammonia inhibition in animal cell culture, a method utilizing porous polytetrafluoroethylene membranes with an associated pH gradient was investigated. Model experiments without cells were carried out in three different reactor configurations suitable for animal cell culture processes to characterize mass transfer properties of the process. The actual fluxes of ammonia across the membrane are of the same order of magnitude as the typical ammonia production rate in an animal cell process, thus indicating the potential of the method for preventing the accumulation of toxic ammonia in cell culture.

Ammonia↗
PubMed1983

Stimulation of uric acid production and depression of increase in plasma glutamine concentration by insulin in chickens infused with ammonia.

1. A single intraportal injection of insulin remarkably stimulated uric acid production in the chicken infused with ammonium acetate and significantly depressed the increase in plasma glutamine concentration by the infusion of ammonia (P less than 0.01 at 20 min, P less than 0.05 at 40 min after the start of infusion). 2. The increases in ammonia concentration in the blood and kidney during the infusion of ammonia were not affected by the insulin pretreatment. 3. The depressive effect of insulin on the increase in plasma glutamine concentration by ammonia may be due to the acceleration by insulin of incorporation of glutamine into biosynthetic pathway of uric acid in the chicken.

Acetates↗
PubMed1984

Ammonia absorption from the intestine in adult cockerels.

Two ml of w mM ammonium acetate solution was introduced into 10 cm chicken intestinal sack having Meckel's diverticulum in the middle part. After the introduction, blood ammonia concentration in the mesenteric vein draining the sack reached a maximal increase within 5 min and returned to the initial level in 30 min. The difference of ammonia concentration between cardiac and mesenteric venous blood also showed a similar tendency. About 91% of the ammonia introduced into the intestinal lumen disappeared in 30 min. Amino acid metabolism in intestinal tissue appears to be affected by the introduction of ammonia into the intestinal lumen.

Absorption↗
PubMed1976

Further observation on the possible relationship between migraine and serum ammonia levels.

Although patients diagnosed as having migraine, have been studied extensively, there is no definite proof of a primary biochemical abnormality which is of significance in the pathogenesis of migraine. Several authors have suggested that increased serum ammonia levels may play a decisive role in the pathogenesis of migraine. This possibility was first put forth by Russell, who studied a single family with ornithine carbamyl transferase deficiency and 8 juveniles with migraine, RUSSELL'S finding was supported by a preliminary study carried out by one of the authors in which hyperammo-naemia was found in 22 adults during migraine attacks. In order to etknd these earlier findings, serum ammonia levels were determined in 35 adults with either classic or complicated migraine and in 20 healthy adults. No significant difference was found between the patients (44 microgram/100 ml +/- 13.9) and the controls (74 microgram/100 ml +/- 9.5). Ammonia level was determined in 10 patients within two hours of the onset of an acute migraine and was unchanged (65 microgram/100 ml). This study suggests that alterations in serum ammonia level are not important in the pathogenesis of migraine in adults.

Adult↗
PubMed1994

Attenuation of ammonia toxicity in mice by PK 11195 and pregnenolone sulfate.

Ammonia and benzodiazepines are thought to be involved in the pathogenesis of hepatic encephalopathy. The present study was undertaken to evaluate the effect of various benzodiazepine-receptor ligands and neurosteroids on ammonia toxicity in mice. Administration of ammonium acetate (8-15 mmole/kg; i.p.) to Swiss Webster mice resulted in a dose-dependent increase in mortality. Pretreatment with the central benzodiazepine receptor agonist clonazepam or the antagonist Ro15-1788 (7 mg/kg each; i.p.) had no significant effect on the lethal response to 10 mmole/kg ammonium acetate. However, pretreatment with the putative antagonist of the peripheral-type benzodiazepine receptor, PK 11195 (10 mg/kg; i.p.), reduced mortality from 50 to 10%. Ro5-4864 (10 mg/kg; i.p.), an agonist of the peripheral-type benzodiazepine receptors, had no effect on ammonia toxicity. The neurosteroid, pregnenolone sulfate (20 mg/kg; i.p.) reduced mortality from 50 to 25%. The non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 (2 mg/kg; i.p.), had no effect on the lethal response to ammonium acetate. The results from the present study suggest a role for peripheral-type benzodiazepine receptors and specific neurosteroids in the alleviation of ammonia toxicity in mice.

Ammonia↗
PubMed1977

Ammonia inhibits protein secretion in isolated rat hepatocytes.

The general secretion of proteins by isolated rat hepatocytes in suspension is inhibited by colchicine, anoxia, or ammonia (NH4Cl). The inhibition by ammonia is accompanied by the cytoplasmic retention and swelling of protein secretory vesicles, suggesting that ammonia accumulates in the vesicles and thereby prevents their translocation to the cell periphery. General protein synthesis appears to be relatively unaffected by ammonia.

Ammonia↗
PubMed1979

Ammonia overloading in hepatocytes isolated from liver of fetal and adult rats.

Ammonia overloading was investigated during glucose and fructose metabolism in isolated hepatocytes under a variety of metabolic conditions. In all assay conditions, the glycolytic flux and oxygen uptake was not modified by 10 mM ammonia. In hepatocytes isolated from rats fed as libitum, the presence of ammonia caused a decrease in the production of lactate (pyruvate); this effect was not observed in anaerobic incubations, in hepatocytes isolated from starved animals, or in fetal hepatocytes. In spite of an overproduction of urea, ammonia detoxification also takes place by the synthesis of alanine, glutamate and aspartate. Addition of 1 mM aminooxyacetate, an inhibitor of aminotransferases, to the incubation medium prevents the formation of these amino acids, and also prevents the decrease of lactate in hepatocytes isolated from fed animals.

Alanine↗
PubMed1980

Radioimmunochemical determination of carbamoyl-phosphate synthase (ammonia) content of adult rat liver.

1. Rabbit antiserum was raised against purified carbamoyl-phosphate synthase (ammonia) from rat liver. 2. The antiserum proved to be specific in double-diffusion test and reacted in an in situ immunohistochemical test on rat liver proteins fractionated on a sodium dodecyl sulphate polyacrylamide gel only in the region where carbamoyl-phosphate synthase (ammonia) migrated. 3. This antiserum was used for setting up a radioimmunochemical determination of carbamoyl-phosphate synthase (ammonia) in cetyltrimethylammonium bromide extracts of rat liver. To obtain reproducible results in this assay it was necessary to treat the unlabelled ligand with sodium dodecyl sulphate and dithiothreitol. This treatment led to a large increase in the percentage of labelled ligand displaceable by added unlabelled ligand. 4. Radioimmunochemical determination showed that adult rat liver (3-month old) contains 5.5 mg carbamoyl-phosphate synthase (ammonia) protein per gram wet weight.

Animals↗
PubMed1977

The phosphorylation of thymidine and the synthesis of histones in ammonia-treated eggs and egg fragments of the sea urchin.

Unfertilized sea urchin eggs may be preloaded with workable amounts of 3H-thymidine. After fertilizing the eggs or treating the eggs with ammonia, the preloaded thymidine is incorporated into DNA in amounts that are proportional to the number of chromosomes that are replicated. The phosphorylation of the internal thymidine is turned on by fertilization and ammonia treatment, but 3H-TTP does not accumulate because it is immediately used for nuclear DNA synthesis. Accumulation of 3H-TTP occurs only in ammonia-treated enucleate fragments in which no nuclear DNA synthesis can occur. Along with the phosphorylation of thymidine, the synthesis of histones occurs in ammonia-treated enucleate egg fragments.

Ammonia↗
PubMed1989

Ammonia-induced injury in pure cultures and natural populations of coliform bacteria.

Ammonia-induced injury was investigated in pure cultures of Escherichia coli and Enterobacter aerogenes, and in natural coliform populations obtained from the oligotrophic Luxapallila and the eutrophic Sunflower Rivers in northern Mississippi. Pure cultures were affected by ammonia exposure as indicated by changes in the injury ratio (IR) of CFU on m-T7 agar/CFU on m-Endo agar. Ammonia concentrations between 0 and 20 (mg NH3-N/1) had little or no effect and concentrations between 40 and 80 caused the greatest injury. Natural coliform populations from the oligotrophic river were more prone to ammonia-induced injury than those from the eutrophic river. The results stress the need for the routine use of m-T7 media and the enumeration of injured cells when using the membrane filter procedure to ascertain domestic water quality.

Ammonia↗
PubMed1991

A quantitative index of regional blood flow in canine myocardium derived noninvasively with N-13 ammonia and dynamic positron emission tomography.

To derive a quantitative index of regional myocardial blood flow, the arterial input function of the flow tracer N-13 ammonia and the regional myocardial N-13 activity concentrations were noninvasively determined in 29 experiments in eight dogs. N-13 ammonia was administered intravenously and cross-sectional images were acquired dynamically using an ECAT III positron emission tomograph with an effective in-plane resolution of 13.46 mm full-width half-maximum. Time-activity curves were derived from the serial images by assigning regions of interest to the left ventricular myocardium and left ventricular blood pool. Tracer net extractions were estimated from the myocardial time-activity concentrations at various times after tracer injection and the integral of the arterial input function. Myocardial blood flow was altered by intravenous dipyridamole, morphine, propranolol and partial or complete occlusion of the left anterior descending coronary artery, and ranged from 9 to 860 ml/min per 100 g. Estimates of tracer net extractions were most accurate when determined from the myocardial N-13 activity concentrations at 60 s divided by the integral of the arterial input function to that time. These estimates correlated with regional myocardial blood flows determined independently by the microsphere technique by y = x (1 - 0.64(e-114/x); SEE = 22.9; r = 0.94). First pass extraction fractions of N-13 ammonia determined noninvasively with this approach declined with higher flows in a nonlinear fashion and were similar to those determined invasively by direct intracoronary N-13 ammonia injections. The findings indicate that an accurate index of regional myocardial blood flow can be obtained noninvasively by high temporal sampling of arterial and myocardial tracer activity concentrations with positron emission tomography. They also provide a basis for the in vivo application of tracer kinetic principles to derive quantitatively and noninvasively regional rates of functional processes in human myocardium.

Ammonia↗
PubMed1989

Failure of sodium benzoate to alleviate plasma and liver ammonia in rats.

The intraperitoneal administration of L-norvaline and L-methionine-SR-sulfoximine to rats caused an increase in the concentration of ammonia in plasma as well as in liver. These compounds interfere with urea and glutamine formation, respectively. Subsequent injection of sodium benzoate failed to alleviate ammonia levels, and on the contrary, caused a further increase. Sodium benzoate itself, when administered, resulted in higher levels of ammonia in plasma and liver of the rats. Administration of glycine to rats treated with benzoate did not lower ammonia levels indicating that other factors besides glycine may also be necessary for the removal of sodium benzoate.

Ammonia↗
PubMedDate not supplied

Examination of 7-ethoxycoumarin deethylation and ammonia removal activities in 31 hepatocyte cell lines.

Aiming the selection of possible candidates for the reactor cells in a hybrid artificial liver, we investigated the activities of 7-ethoxycoumarin deethylation and ammonia removal in 31 hepatocytes cell lines established from the human, rat, mouse, and chicken, compared with freshly isolated rat hepatocytes. Rat liver homogenate and hepatocytes showed 7-ethoxycoumarin deethylation activity of 0.925 and 1.840 nmol/mg protein/min, respectively. Two human hepatoblastoma cell lines, Hep G2 and HuH 6, showed the activity of 0.190 and 0.027 nmol/mg protein/min, respectively. While the rat hepatocytes efficiently removed added ammonia form the culture medium, no ammonia removal activity was detectable in any cell line with the assay conditions in this study. Ammonia removal activity, possibly catalyzed by the urea cycle, is likely to be harder to restore than the drug metabolizing system in the course of cell immortalization.

Ammonia↗