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PubMed1977

[Saliva ammonia and urea in the sheep. Effects of alimentary nitrogen additives (author's transl)].

The salivary elimination of ammonia and urea was studied in 4 permanently salivary duct fistulated sheep. Sheep were fed either a regular diet or the same diet with addition of non protein nitrogen (NPN). Individual saliva ammonia levels vary from 34 to 71 microgram N/100 ml. After intra-ruminal dosing with urea (10 g) or ammonia (2 g), the values may rise up to 1000 microgram N/100 ml. Saliva ammonia and blood ammonia changes follow the same direction. Daily saliva urea variations are correlated with feeding behaviour. NPN administration increases saliva urea and blood urea; both concentration curves are parallel.

Ammonia↗
PubMed1983

Ammonia formation in isolated rat liver mitochondria.

Studies of isolated rat liver mitochondria were undertaken in order to evaluate the importance of glutamate transport, oxidation reduction state, and product inhibition on the rates of formation of ammonia from glutamate. Uptake and efflux of glutamate across the mitochondrial membrane were measured isotopically in the presence of rotenone. Efflux was stimulated by H+ in the mitochondrial matrix and was found to be first order with respect to matrix glutamate except when the matrix pH was unphysiologically low. The data suggest that the Km of matrix glutamate for efflux is decreased by H+. Matrix H+ also appeared to stimulate glutamate uptake, but the effect was to increase both the Km of medium glutamates and Vmax. Mitochondria were incubated at 15 and 28 degrees C with glutamate and malonate. Under these conditions, glutamate was metabolized only by the deamination pathway. Flux was evaluated by assay of ammonia formation. Oxidation reduction state was varied with ADP and uncoupling agents. Matrix alpha-ketoglutarate was varied either by the omission of malonate from the incubation media or by adding alpha-ketoglutarate to the external media. Influx and efflux of glutamate could be calculated from previously determined transport parameters. The difference between calculated influx and efflux was found to be equal to ammonia formation under all conditions. It was, therefore, possible to evaluate the relative contributions of oxidation reduction state, transport, and product inhibition as effectors of ammonia formation. The contribution of transport was relatively small while oxidation reduction state exerted a large influence. alpha-Ketoglutarate was found to be a potent competitive inhibitor of ammonia production and glutamate dehydrogenase. Inhibition of glutamate dehydrogenase by alpha-ketoglutarate was judged to be a potentially important modulator of metabolic fluxes.

Ammonia↗
PubMed1984

Ammonia tolerance test used to differentiate between ascites of cirrhotic and malignant genesis.

Eighteen patients with ascites, 9 with cirrhosis of the liver and 9 with malignant disease, were subjected to the ammonia tolerance test by instillation of ammonia transrectally . Arterial blood samples were taken before and 15 and 30 min after the instillation to determine the plasma ammonia concentrations. The results show a significant difference in the plasma ammonia concentration between the two groups of patients after instillation of ammonia. Since the method is non-invasive, it is recommended as a screening test in the differentiation between ascites of cirrhotic and malignant genesis.

Adult↗
PubMed1984

Hyperplastic lesions of the primitive meninx of fathead minnows, Pimephales promelas, induced by ammonia: species potential for carcinogen testing.

In our laboratory, fathead minnows were reared from time of hatching to adulthood at 5 concentrations of ammonia in a toxicity test lasting 304 days. The ammonia concentration test range was 9.36 to 30.0 mg NH3-N/liter (0.639 to 2.17 mg NH3/liter). Intracerebral lesions were observed in fish from each ammonia concentration but not in the controls. The severity of the lesions was positively correlated with increased ammonia concentration. Massive hyperplastic lesions developed in fish tested at the 2 highest concentrations. Histologically, lesions appeared to originate from the primitive meninx, which grew into the cranial cavity, and in some fish through the cranium. Based on the orderly appearance of tissues and evidence of regression of lesions, the lesions are not considered to be neoplasms but hyperplasias of primitive meninx tissue induced as a response to ammonia exposure. Fathead minnows (Pimephales promelas) have proved useful for acute toxicity testing of environmental contaminants and have a potential usefulness in carcinogenicity testing. They are easily maintained in the laboratory, can be readily induced to spawn during their first year of life, and have a relatively short period of embryogenesis.

Ammonia↗
PubMed1983

An enzymic creatinine assay and a direct ammonia assay in coated thin films.

We developed a thin-film enzymic assay for creatinine that makes use of creatinine iminohydrolase (EC 3.5.4.21) to convert creatinine to N-methylhydantoin and ammonia. The ammonia diffuses through a semipermeable layer and is quantitated by reaction with bromphenol blue. A paired analysis of the sample on a separate coating without the enzymic reaction measures endogenous ammonia and, for samples with normal concentrations of ammonia, allows accurate determination of serum creatinine to 150 mg/L without dilution. Results of this assay (y) compare well with those by a liquid-chromatographic comparison assay (x) by linear regression (slope = 0.935, intercept = 1.13 mg/L, r2 = 0.995). It is insensitive to many substances, such as ketones and keto acids, that interfere with conventional assays. Results of the ammonia assay (y) correlate well with those by a semi-automated enzymic assay (x) based on glutamate dehydrogenase (slope = 1.068, intercept = 17.3 mumol/L, r2 = 0.985).

Ammonia↗
PubMedDate not supplied

Induced transient hyperammonemia in Rana hexadactyla with reference to the ammonia and urea excretion.

Different ammonia toxicity induced by ammonium acetate administration in frogs lead to variable excretion of ammonia and urea into the medium. When 11.45 mM/kg body weight of ammonium acetate was administered, ammonia excretion increased while urea excretion decreased. When 4.17 mM/kg body weight of ammonium acetate is administered, the urea excretion increased while ammonia excretion decreased. The possible metabolic conversion of ammonia and urea by the animal at high and low ammonium acetate administration has been discussed.

Ammonia↗
PubMed1982

Arterial and venous ammonia concentrations in the diagnosis of canine hepato-encephalopathy.

Fasting venous ammonia concentrations were measured in 105 dogs with liver disease. In 69 of these patients and in 38 normal dogs simultaneous arterial and venous ammonia concentrations were measured. In patients with liver disease ammonia values were significantly higher in arterial blood than in venous blood, therefore arterial measurements are preferable for clinical diagnosis. A significant positive correlation was demonstrated between arterial or venous concentrations and the degree of hepato-encephalopathy. In an individual patient, however, the fasting ammonia concentration is an unreliable indicator of the degree of encephalopathy. Elevated ammonia values confirm the diagnosis of hepato-encephalopathy, but normal levels do not exclude it. A strong correlation was found between the existence of encephalopathy and the presence of portosystemic collateral circulation.

Ammonia↗
PubMed1982

Excretion of ammonia by rat kidney during metabolic alkalosis.

In rat kidney, proximal tubular and final urinary ammonia concentration are finite. They are lower in animals with metabolic alkalosis than in controls. A positive correlation between ammonia concentration and water removal (as indicated by fluid to plasma ratios for inulin) was found. A comparison of tubular fluid to plasma concentration ratios for inulin and ammonia indicates that more ammonia enters proximal tubular fluid than appears in the final urine. These observations indicate that ammonia is probably secreted primarily at the level of the proximal tubule and then undergoes reabsorption at distal sites of the nephron.

Alkalosis↗
PubMed1980

Variations in blood ammonia and glutamine levels after hepatectomy and/or abdominal evisceration in the rat.

In order to specify the role of peripheral muscular tissue in ammonia metabolism, we studied, in rats, the variations of ammonia and glutamine levels in arterial and femoral venous blood after hepatectomy and abdominal evisceration with nephrectomy. In non-fasting rats this operation was immediately followed by an important hyperammonemia which was due to ammonia muscular release; glutamine blood levels increased only slightly without any modification in their arterio-femoral venous differences. The hyperammonemia induced by hepatectomy-evisceration was greatly reduced in animals which had been fasting for 48 hours but was not modified by a 72hrs preoperative sucrose feeding. These nutritional conditions did not change the blood glutamine variations which were first related to the abdominal evisceration. Indeed, in abdominal eviscerated rats without hepatectomy there was an important hyperglutaminemia with only a slight increase in blood ammonia. These results indicate that in rat 1) the liver plays an important part in skeletal muscle ammonia metabolism, 2) this metabolism is related to food ingestion, 3) the gastrointestinal tissue intervenes in glutamine metabolism.

Ammonia↗
PubMedDate not supplied

[Emission spectroscopic determination of the 15N in the ammonia and amino acids isolated from biological material].

A procedure for preparation of samples is described for emission-spectroscopic estimation of 15N in ammonia, glutamic aspartic acids, leucine and glycine using 15N-analyzer NOI-5. The assay involved separation of ammonia and amino acids by means of ion exchange chromatography, degradation of amino acids to ammonia its isolation by microdiffusion from buffers and subsequent reduction of ammonia to nitrogen. Amount of nitrogen in the samples was about 20 mg. The procedure enabled to estimate the content of 15N in ammonia and amino acids of physiological fluids.

Amino Acids↗
PubMedDate not supplied

Ammonia accumulation in platelet concentrates during storage.

Newly prepared platelet concentrates (PC) and platelet poor plasma (PPP) stored at either room temperature (RT) or 4 C were analyzed for ammonia content initially, and after storage at 24, 48, and 72 hours. These studies demonstrate that ammonia rapidly accumulates in PC stored at RT. This accumulation appears to be temperature dependent, as evidenced by the observed differences in ammonia accumulation in PC stored at 4 C and RT. Whether ammonia acts as a toxic metabolite in the inhibition of platelet function and the development of the "storage lesion," which occurs in PC stored at RT, needs further clarification. Additional studies are also necessary to establish the clinical efficacy of transfusing ammonia-containing platelet concentrates into premature neonates with immature functioning livers, and perhaps into adults with severe liver disease.

Ammonia↗
PubMed1994

Changes in blood ammonia and lactate levels during a triathlon race.

Blood ammonia and lactate concentrations were analyzed in 7 volunteer male athletes before and immediately after each segment of an endurance triathlon. The purpose of this study was to examine the effects of triathlon on ammonia and lactate blood levels and the possible correlation between both in each different event. Concentrations of blood ammonia were increased after each of the three segments, reaching a peak after the 40 km bicycle ride. Concentrations of blood lactate were also increased over baseline. However, there was a higher increase after the 1.4 km lake swim, than after the 40 km bicycle ride or after the 10 km run. No correlation was found between the levels of ammonia and lactate, suggesting that ammonia and lactate follow different metabolic patterns.

Adolescent↗
PubMed1994

Quantitative assessment of aerial ammonia toxicity to the nasal mucosa by use of the nasal lavage method in pigs.

Effects of atmospheric ammonia (NH3) on the nasal mucosa and somatic growth were investigated in pigs exposed to 4 NH3 concentrations (0; 25; 50; and 100 ppm) for 6 days in a specifically designed air-pollutant exposure chamber. Nasal lavage (NAL) was applied to quantify the ammonia-induced inflammatory response by measuring the number of neutrophils and the albumin (porcine serum albumin) concentration in the NAL liquid. In control pigs, these variables remained unchanged throughout the exposure period. In all other groups, an important ammonia concentration-related increase was recorded. The equation of the linear regression line established between the mean values of the number of neutrophils (x 10(3)) per milliliter of NAL liquid (y) recorded at the end of the exposure period and the ammonia concentrations (ppm) was: y = 69.7 + 3.3 [NH3] (r = 0.979; P < 0.020). The increase in the neutrophil count was significant (P < 0.05) at concentrations as low as 25 ppm. For albumin concentration nanograms per milliliter, the corresponding equation was: y = 574 + 14.3 [NH3] (r = 0.953; P < 0.045). However, the first significant change (P < 0.05) in this variable was only obtained for the higher concentration (100 ppm). In exposed pigs, a concentration-related depression of somatic growth was observed. The equation of the regression line plotted relating the individual values of the changes in body weight gain recorded over the exposure period expressed as percentage of the initial body weight (y) and the ammonia concentration was: y = 3.507-0.203 [NH3] + 0.001 [NH3]2 (r = 0.55; P < 0.010).(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollution, Indoor↗
PubMed1994

Concentration- and pH-dependent ammonia yields in the reaction of hydrated electrons with glycylglycine.

Competition between recombination of the radicals formed in the gamma radiolysis of water (eaq-, OH, H) and the reaction of eaq- with glycylglycine is investigated in glycylglycine solutions of various concentrations and pH. First, the concentration dependence of the ammonia yields is measured in the glycylglycine solutions of between 0.5 mM and 1.0 M. The G values of ammonia appear to reach a plateau of 2.47 +/- 0.05 molecules/100 eV at the low concentrations (1-5 mM) and increase to 3.81 +/- 0.07 molecules/100 eV at the high concentration (1 M). Secondly, the pH dependence of the ammonia yields is measured at low (1 and 5 mM) and high (0.1 and 0.2 M) concentrations of glyclyglycine. For concentrated glyclyglycine solutions, the ammonia yields increase with increasing pH, as expected based on comparison of the probabilities of the competitive reactions. However, the G values of ammonia reach a maximum at pH 9.0 and then decrease as the pH increases for dilute solutions. The lower G values at higher pH for dilute glycylglycine solutions may result from increased interspur recombination since the rate constant for the reaction of eaq- with glycylglycine is decreased and, as a consequence, the scavenging capacity of glycylglycine for eaq- decreases approximately 4.7-fold from low to high pH.

Ammonia↗
PubMed1993

Burnisher's asthma--a case due to ammonia from silverware polishing.

A 39-year-old man with no past or family history of asthma developed asthmatic symptoms five months after working as a burnisher in a hotel. He polished brass or silverware using "brasso" or "silvo" respectively. He noticed symptoms only when using "silvo". Specific bronchial provocation testing (BPT) to "brasso" was negative. Specific BPT to "silvo" produced a dual asthmatic reaction. Ammonia was present in both polishes. The ammonia-in-air levels during polishing was 8-15 ppm with "silvo" and less than 1 ppm with "brasso". A specific BPT to 12 ppm of ammonia produced an immediate asthmatic reaction. Our opinion is that he had occupational asthma from the ammonia liberated while polishing silverware with "silvo". Ammonia has been reported to cause asthma. However, there have been no previous reports of occupational asthma among burnishers doing silver polishing.

Adult↗
PubMed1977

The purine nucleotide cycle. Studies of ammonia production by skeletal muscle in situ and in perfused preparations.

Ammonia production by hind limbs of rat was studied in perfused preparations during rest, exercise, and hypoxia, and while the perfusate contained epinephrine or cyanide. Ammonia production by hind limbs was also studied in situ during rest and exercise. Strong correlations were observed between ammonia, IMP, and lactate formation. Adenylosuccinate was not present in detectable amounts in resting muscle (less than 1 nmol/g dry weight) but it appeared and rose sharply in exercising muscle, and then declined during recovery. The maximum found was about 18 nmol/g dry weight. When IMP accumulation exceeded 2.8 mumol/g dry weight, the formation of adenylosuccinate diminished, presumably because of an inhibition of adenylosuccinate synthetase by excess substrate. Exercise resulted in a greatly increased output of ammonia and a decreased output of alanine and glutamine. The tissue contents of aspartate and glutamate were decreased, while that of alanine was increased. The content of malate increased 3-fold during exercise. Epinephrine, hypoxia, and cyanide each caused an increased output of ammonia at the expense of the amino acid content of the tissue. These results provide evidence for the operation of the purine nucleotide cycle in skeletal muscle under various conditions that are associated with an increased rate of glycolysis.

Adenosine Monophosphate↗
PubMed1996

Ammonia gassing deaths--a report on two cases.

The gross postmortem features of two victims (a 17-year-old and a 33-year-old male, both of Chinese descent) who died shortly after an ammonia-gassing exposure, are presented. The findings of extensive thermal burns on the body surfaces and on the lips, conjunctivitis and opaque cornea on both eyes, oedematous and congested lungs with large areas of haemorrhages, etc, were consistent with injuries inflicted by a corrosive gas such as ammonia. The postmortem toxicological findings of elevated blood ammonia levels supported the postmortem findings. The pulmonary and femoral blood ammonia levels (0.26 mg/mL and 0.65 mg/mL) of decedent one were at least 371 times and 928 times respectively higher than normal. Similarly, the pulmonary and femoral blood ammonia levels (0.51 mg/mL and 0.43 mg/mL) of decedent two were at least 728 times and 614 times respectively higher than normal.

Accidents, Occupational↗
PubMed1996

Human blood lactate and ammonia levels after supramaximal uphill and downhill running.

The purposes of this study were 1) to confirm whether there is a difference in the levels of blood lactate and ammonia after supramaximal uphill and downhill running for the same short duration and 2) to examine the relationship between peak blood lactate levels and work/lean body mass (LBM), as well as the relationship between peak blood ammonia levels and work/LBM following supramaximal uphill and downhill running. Eight healthy, untrained male subjects performed supramaximal uphill and downhill running on a motor-driven treadmill for about 70 sec. Though there was a significant difference (p < 0.05) in running speed and work/LBM between supramaximal uphill and downhill running, no significant difference was found in exhaustion time or heart rate. Both the peak blood lactate and ammonia concentrations were significantly lower after downhill running than after uphill running (p < 0.05). Although there was no significant relationship between peak blood ammonia levels and work/LBM following either uphill or downhill running, significant linear relationships between the peak blood lactate levels and work/LBM were observed following uphill running (r = 0.74, p < 0.05) and downhill running (r = 0.72, p < 0.05). These results suggest that the differences in the blood lactate and ammonia concentration between supramaximal downhill and uphill running of the same duration may be due to the total recruitable muscle mass during exercise, and that peak blood lactate can be used as an index of anaerobic work capacity for untrained subjects under these running conditions.

Adult↗