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PubMed2004

Toxicity of ammonia to three marine fish and three marine invertebrates.

Laboratory toxicity tests were performed to obtain more data on the toxicity of ammonia to saltwater organisms. The standards for in-stream ammonia limits in marine environments presently are based on toxicity tests involving both freshwater and saltwater organisms. Acute tests (48 and 96 h) were performed at 20 degrees C, and chronic tests (7 days) were performed at 25 degrees C. Synthetic seawater and natural seawater from the Chesapeake Bay were used and compared. Included among the organisms tested were sheepshead minnow (14 days old), summer flounder (2 months old), Atlantic silverside (14 days old), mysid shrimp (less than 2 days old), ghost shrimp (10 days old), and quahog clam (9 months old). Based on these results, it seems the chronic criterion for ammonia in marine environments could be increased from 0.035 to 0.081 mg/L un-ionized ammonia, which would, of course, increase the chronic limit for total ammonia under typical saltwater conditions by a factor of 2.31. No difference was observed in the toxicity of ammonia in natural water compared to synthetic water for both the summer flounder and Atlantic silverside. Furthermore, the Atlantic silverside became more sensitive to ammonia as the salinity was increased from 14 to 22 ppt, but exhibited no change in toxicity response from 22 to 30 ppt.

Ammonia↗
PubMed1993

An ultrafiltration method for the removal of interfering agents and its application to the determination of free ammonia in solutions of oxystarch by the Berthelot reaction method.

Oxystarch was chosen as a model compound for studying biological ammonia-sequestering systems. Ammonia was determined by use of an ion-selective electrode, by L-glutamate dehydrogenase (L-GDH), and by two different Berthelot procedures, in the presence and absence of oxystarch. In the presence of total oxystarch the Berthelot method, particularly when low concentration reagents were used, detected significantly less (P < 0.10) free ammonia than either L-GDH or ion-selective electrode methods. A 0.5-kDa molecular weight cutoff sample ultrafiltration step was added prior to analysis by L-GDH and Berthelot procedures. To facilitate complete removal of oxystarch by the ultrafiltration step, oxystarch was dialyzed before use, yielding a high-molecular-weight fraction (> 1 kDa). Removal of high-molecular-weight oxystarch species and bound ammonia by ultrafiltration of samples prior to assay completely negated discrepancies between ammonia levels measured by L-GDH and both Berthelot methods. The correlation of the levels of measured ammonia, as determined by L-GDH and Berthelot methods, in mixtures with high-molecular-weight oxystarch was significantly improved by the addition of the sample ultrafiltration step. Improved correlation of results from such fundamentally different methods demonstrates the removal of interfering agents as well as the nonperturbatory nature of the improved procedure. The addition of such an ultrafiltration step may be applied to the determination of ammonia by the otherwise interference-prone Berthelot assay in mixtures with any interfering macromolecules, without the inconvenience or potential variabilities associated with distillation or diffusion procedures.

Ammonia↗
PubMed2001

A method for the determination of volatile ammonia in air, using a nitrogen-cooled trap and fluorometric detection.

A quick, cheap, and accurate method for the determination of ammonia in air is described. Ammonia and water vapor are trapped simultaneously in a gas sampling tube cooled in liquid nitrogen. Subsequently ammonia is derivatized with o-phthaldialdehyde and determined using fluorescence detection. The detection limit of ammonia in a gaseous sample is about 1 nmol per liter of gas. The recovery, using a calibration gas of 6.00 ppm ammonia in nitrogen, is 102.9 +/- 6.4%. Examples are presented in which this method is used for the determination of ammonia in environmental air and in expired air during exhaustive exercise of a human subject. It is suggested that this method can be used for the determination of volatile ammonia and other compounds in air during environmental and biological monitoring and in research.

Air↗
PubMed2002

Combined effects of algal (Chlorella vulgaris) density and ammonia concentration on the population dynamics of Ceriodaphnia dubia and Moina macrocopa (Cladocera).

Ammonia is a natural variable in ponds and lakes. Although an important source of nitrogen for microalgae, at high concentrations ammonia can affect the density and diversity of cladocerans. Using the cladocerans Ceriodaphnia dubia, and Moina macrocopa, the effect of nominal concentrations of ammonium chloride under acute and chronic exposures at different levels of algal food was tested. Regardless of food level, C. dubia was more sensitive than M. macrocopa to ammonia. In the absence of food, the median lethal concentration of ammonia (LC(50) 24 h) for C. dubia was (112 mg L(-1)) less than half that of M. macrocopa (232 mg L(-1)). When algal food (0.5 x 10(6) and 1.5 x 10(6) cells ml(-1) of Chlorella) was used, the LC(50) values were much higher for both cladoceran species. Based on the population growth studies, it was found that in controls of M. macrocopa an increase in the availability of Chlorella from 0.5 to 1.5 x 10(6) cells mL(-1) led to an increase in the maximum density from 4.7 +/- 0.2 to 16.4 +/- 1.2 ind.mL(-1), while in C. dubia the peak population density decreased from 7.9 +/- 0.6 to 5.0 +/- l.0 ind.mL(-1). An increase in ammonia concentration (10 to 40 mg L(-1) for C. dubia and 20 to 120 mg L(-1) for M. macrocopa) resulted in a corresponding decrease in peak population densities of the tested cladocerans. The rate of population increase (r) values for M. macrocopa in the controls ranged from 0.21 +/- 0.001 and 0.25 +/- 0.02 at 0.5 and 1.5 x 10(6) cells mL(-1) of Chlorella, respectively. The corresponding values of C. dubia in controls were 0.21 +/- 0.004 and 0.18 +/- 0.01. At 0.5 x 10(6) cells mL(-1) of algal food, the r values became negative under 40 and 120 mg L(-1) of ammonia for C. dubia and M. macrocopa, respectively. The role of algal food in ammonia toxicity to cladocerans was discussed. (c) 2002 Elsevier Science (USA).

Ammonia↗
PubMed1994

Neomycin reduces the intestinal production of ammonia from glutamine.

The mechanism by which neomycin treatment reduces circulating ammonia concentrations was studied in normal and portacaval shunted rats. Rats were given neomycin for 3 days and then fasted for 24 hours to eliminate feces. Neomycin decreased arteriovenous differences of ammonia across the intestine even when the intestines were empty. Neomycin treatment lowered the activity of glutaminase in the intestinal mucosa and the rate of ammonia production from glutamine by isolated intestinal segments. The intestines from portacaval shunted rats had higher glutaminase activity (by 57%), and produced ammonia from glutamine at a greater rate (by 31%), than intestines from controls. Neomycin treatment lowered glutaminase activity and ammonia production in shunted rats, but glutaminase activity still remained higher than in controls (by 23%). The data indicate that the mechanism by which neomycin lower plasma ammonia is owing, at least in part, to a direct effect on the intestines. Specifically, neomycin causes a reduction in mucosal glutaminase activity and thereby decreases the ability of the mucosa to consume glutamine and produce ammonia.

Ammonia↗
PubMed1994

Molecular mechanism of acute ammonia toxicity and of its prevention by L-carnitine.

In summary, we propose that acute ammonia intoxication leads to increased extracellular concentration of glutamate in brain and results in activation of the NMDA receptor. Activation of this receptor mediates ATP depletion and ammonia toxicity since blocking the NMDA receptor with MK-801 prevents both phenomena. Ammonia-induced metabolic alterations (in glycogen, glucose, pyruvate, lactate, glutamine, glutamate, etc) are not prevented by MK-801 and, therefore, it seems that they do not play a direct role in ammonia-induced ATP depletion nor in the molecular mechanism of acute ammonia toxicity. The above results suggest that ammonia-induced ATP depletion is due to activation of Na+/K(+)-ATPase, which, in turn, is a consequence of decreased phosphorylation by protein kinase C. This can be due to decreased activity of PKC or to increased activity of a protein phosphatase. We also show that L-carnitine prevents glutamate toxicity in primary neuronal cultures. The results shown indicate that carnitine increases the affinity of glutamate for the quisqualate type (including metabotropic) of glutamate receptors. Also, blocking the metabotropic receptor with AP-3 prevents the protective effect of L-carnitine, indicating that activation of this receptor mediates the protective effect of carnitine. We suggest that the protective effect of carnitine against acute ammonia toxicity in animals is due to the protection against glutamate neurotoxicity according to the above mechanisms.

Ammonia↗
PubMed1995

Effect of a low-carbohydrate diet on plasma and sweat ammonia concentrations during prolonged nonexhausting exercise.

The purpose of this investigation was to examine the effect of low body glycogen stores on plasma ammonia concentration and sweat ammonia excretion during prolonged, nonexhausting exercise of moderate intensity. On two occasions seven healthy untrained men pedalled on a cycle ergometer for 60 min at 50% of their predetermined maximal O2 uptakes (VO2max) firstly, following 3 days on a normal mixed diet (N-diet) (60% carbohydrates, 25% fat and 15% protein) and secondly, following 3 days on a low-carbohydrate diet (LC-diet) (less than 5% carbohydrates, 50% fat and 45% protein) of equal energy content. Blood was collected from the antecubital vein immediately before, at 30th and at 60th min of exercise. Sweat was collected from the hypogastric region using gauze pads. It was shown that plasma ammonia concentrations after the LC-diet were higher than after the N-diet at both the 30th and 60th min of exercise. Sweat ammonia concentration and total ammonia loss through the sweat were also higher after the LC-diet. The higher ammonia concentrations in plasma and sweat after the LC-diet would seem to indicate an increased ammonia production, which may be related to reduced initial carbohydrate stores.

Adult↗
PubMed1992

Ammonia regulation of phosphate-activated glutaminase displays regional variation and impairment in the brain of aged rats.

The regulation of PAG by ammonia in whole brain (Sprague-Dawley) and regional (Fischer-344) synaptosomal preparations from adult and aged animals was assessed. Whole brain synaptosomal preparations from both age groups displayed a significant decrease in PAG activity with increasing ammonium chloride concentrations, however, the aged rats exhibited a significant attenuation in ammonia-induced PAG inhibition. PAG activity measured in synaptosomes prepared from the striatum (STR), temporal cortex (TCX) and hippocampus (HIPP) was also inhibited by ammonium chloride. The STR showed the greatest degree of ammonia-induced PAG inhibition (55%) followed by the HIPP (30-35%) and the TCX (25-30%). This reduction in PAG activity was significantly attenuated in STR from aged rats at ammonium chloride concentrations greater than 50 microM and in the TCX, PAG activity was significantly attenuated in the aged rats at ammonia concentrations of 0.5 and 1.0 mM. Ammonia regulation of PAG activity in the HIPP appeared to be unaffected by age. Ammonium chloride concentrations up to 5 mM had no effect on GLU release from cortical slices, although GLN efflux was significantly enhanced. These findings suggest that isozymes of PAG may exist in different brain regions based on their differential sensitivity to ammonia. The attenuation of ammonia-induced PAG inhibition seen in aged rats may have deleterious effects in the aged brain.

Aging↗
PubMed1991

Severity of Helicobacter-induced gastric injury correlates with gastric juice ammonia.

We postulated that ammonia produced by Helicobacter pylori may contribute to gastric mucosal injury. This hypothesis was evaluated in Helicobacter-positive patients with chronic renal failure in whom a high urea concentration might amplify this phenomenon. Gastric urea and ammonia were measured, and the severity of gastritis was evaluated by counting mononuclear and polymorphonuclear cells. High gastric ammonia and low urea in Helicobacter-positive patients, and the converse in Helicobacter-negative subjects, were observed. There was a significant correlation between gastric ammonia and interstitial polymorphonuclear leukocytes infiltration (P less than 0.05), suggesting a causal link. Eradication of Helicobacter pylori was associated with a decrease of ammonia and an increase of urea (P less than 0.01). The significant correlation between the severity of gastric inflammation and the gastric juice ammonia concentration suggests that ammonia may play a pathogenic role in Helicobacter-associated gastric injury.

Ammonia↗
PubMedDate not supplied

Ammonia: key factor in the pathogenesis of hepatic encephalopathy.

There is substantial clinical and experimental evidence to suggest that ammonia toxicity is a major factor in the pathogenesis of hepatic encephalopathy associated with subacute and chronic liver disease. Ammonia levels in patients with severe liver disease are frequently found to be elevated both in blood and cerebrospinal fluid (csf). Hepatic encephalopathy results in neuropathological damage of a similar nature (Alzheimer type II astrocytosis) to that found in patients with congenital hyperammonemia resulting from inherited defects of urea cycle enzymes. Following portocaval anastomosis in the rat, blood ammonia concentration is increased 2-fold, and brain ammonia is found to be increased 2-3-fold. Administration of ammonia salts or resins to rats with a portocaval anastomosis results in coma and in Alzheimer type II astrocytosis. Since the CNS is devoid of effective urea cycle activity, ammonia removal by brain relies on glutamine formation. Cerebrospinal fluid and brain glutamine are found to be significantly elevated in cirrhotic patients with encephalopathy and in rats following portocaval anastomosis. In both cases, glutamine is found to be elevated in a region-dependent manner. Several mechanisms have been proposed to explain the neurotoxic action of ammonia. Such mechanisms include: Modification of blood-brain barrier transport; alterations of cerebral energy metabolism; direct actions on the neuronal membrane; and decreased synthesis of releasable glutamate, resulting in impaired glutamatergic neurotransmission.

Ammonia↗
PubMed1993

The action of ammonia on astrocyte glycogen and glycogenolysis.

Most of the brain glycogen, a major energy reserve that can be mobilized in response to increased neuronal activity, resides in the astrocyte, the site of the neuropathological abnormality found in hepatic encephalopathy (HE). Ammonia, a neurotoxin implicated in the pathogenesis of HE, has been reported to cause a depletion of glycogen in primary astrocyte cultures. To further investigate the action of ammonia on glycogen levels, cultured astrocytes were exposed to ammonium chloride (1-5 mM) for various times up to 7 d. Treatment with ammonia for 24 h did not alter deoxyglucose uptake, but significantly lowered peak glycogen values (found at 1.5 h following feeding with medium containing 5.5 mM glucose) in a concentration-dependent manner. This inhibitory effect was not observed after longer exposure times to ammonia. Three day treatment of cells did, however, significantly reduce norepinephrine-stimulated glycogenolysis, an effect not seen after 1 d of ammonia treatment. Part of the neurotoxic action of long term ammonia exposure in humans and experimental animals may be to inhibit the breakdown of glycogen. The effect of ammonia on astrocyte glycogen synthesis and/or breakdown may disrupt glial neuronal signaling and thus play a role in the pathogenesis of HE.

Ammonia↗
PubMed2001

Isolation and properties of obligately chemolithoautotrophic and extremely alkali-tolerant ammonia-oxidizing bacteria from Mongolian soda lakes.

Five mixed samples prepared from the surface sediments of 20 north-east Mongolian soda lakes with total salt contents from 5 to 360 g/l and pH values from 9.7 to 10.5 were used to enrich for alkaliphilic ammonia-oxidizing bacteria. Successful enrichments at pH 10 were achieved on carbonate mineral medium containing 0.6 M total Na(+) and < or =4 mM NH(4)Cl. Five isolates (ANs1-ANs5) of ammonia-oxidizing bacteria capable of growth at pH 10 were obtained from the colonies developed on bilayered gradient plates. The cells were motile and coccoid, with well-developed intracytoplasmic membranes (ICPM) and carboxysomes. At pH 10.0, ammonia was toxic for growth at concentrations higher than 5 mM NH(4)Cl. The bacteria were able to grow within the salinity range of 0.1-1.0 M of total Na+ (optimum 0.3 M). In media containing 0.3-0.6 M total Na(+), optimal growth in batch cultures occurred in the presence of a bicarbonate/carbonate buffer system within the pH range 8.5-9.5, with the highest pH limit at pH 10.5. At pH lower than 8.0, growth was slower, most probably due to decreasing free ammonia. The pH profile of the respiratory activity was broader, with limits at 6.5-7.0 and 11.0 and an optimum at 9.5-10.0. In pH-controlled, NH(3)-limited continuous culture, isolate ANs5 grew up to pH 11.3, which is the highest pH limit known for ammonia-oxidizing bacteria so far. This showed the existence of extremely alkali-tolerant ammonia-oxidizing bacteria in the soda lakes. Comparative 16S rDNA sequence analysis of the five isolates demonstrated that they possess identical 16S rDNA genes and that they are closely related to Nitrosomonas halophila (sequence similarity 99.3%), a member of the beta-subclass of the Proteobacteria. This affiliation was confirmed by comparative sequence analysis of the amoA gene, encoding the active-site subunit of the ammonia-monoxygenase, of one of the isolates. DNA-DNA hybridization data further supported that the soda lake isolates are very similar to each other and represent an alkali-tolerant subpopulation of N. halophila whose species description is herewith amended.

Ammonia↗
PubMed1999

Chronic toxicity of ammonia to the freshwater bivalve Sphaerium novaezelandiae.

The chronic toxicity of total ammonium and unionized ammonia (NH3) to the native New Zealand freshwater fingernail clam Sphaerium novaezelandiae was assessed in soft water under laboratory conditions. Control survival after 60 days was high (93%) and concentration-response relationships showed the sensitivity of S. novaezelandiae survival was markedly greater to both total and unionized ammonia (6.4x and 4.6x) after 60 days compared with the 30-day exposure at 20 degrees C. Chronic mortality and number moribund (inability to rebury) showed similar sensitivities, but reproduction was a more sensitive endpoint based on a concentration-response analysis. The survival LC50 values for total and unionized ammonia were 3.8 mg (N)/L (pH 7.5) and 0.037 mg (NH3-N)/L, and reproductive values 0.80 mg (N)/L (pH 7.5) and 0.013 mg (NH3-N)/L at 60 days. No observed effect concentration (NOEC) values for both survival and reproduction were 0.97 mg (N)/L and 0. 011 mg (NH3-N)/L, and the lowest observed effect concentration (LOEC) values were 5.4 mg (N)/L and 0.046 mg (NH3-N)/L for survival after 60 days, giving a calculated threshold effect concentration (TEC) of 2.3 mg (N)/L and 0.022 mg (NH3-N)/L. Comparison of the S. novaezelandiae chronic ammonia sensitivity data with the US EPA criteria showed the survival and reproduction TEC values for total ammonia were 1.9x higher than the chronic criterion, and the lethality value 1.4x above the unionized ammonia criterion. The findings suggest that use of the US EPA criteria would provide minimal protection for S. novaezelandiae for chronic ammonia exposure, and that development of site-specific criteria, covering a wide range of environmental conditions, may be required to adequately protect all life stages of this species.

Ammonia↗
PubMed2002

Determinants of [13N]ammonia kinetics in hepatic PET experiments: a minimal recirculatory model.

The aim of this study was the development of a modelling approach for the analysis of the systemic kinetics of the tracer nitrogen-13 ammonia administered for dynamic liver scanning. The radioactive half-life of this tracer is 9.8 min, which limits the time span in which data are available in a positron emission tomography experimental setting. A circulatory pharmacokinetic model was applied to the metabolism of ammonia in anaesthetised pigs, which incorporated data from serial measurements of [(13)N]ammonia and [(13)N]metabolite activity in arterial and portal venous blood together with blood flow rates through the portal vein and through the hepatic artery obtained over 20 min after intravenous injection of [(13)N]ammonia. Model analysis showed that up to 20 min after injection the time course of [(13)N]ammonia concentration in arterial blood is primarily determined by distribution kinetics (steady-state volume of distribution 1,856+/-531 ml kg(-1)). Simultaneous fitting of arterial ammonia and metabolite blood concentrations allowed for estimation of the hepatic [(13)N]ammonia clearance (10.25+/-1.84 ml min(-1) kg(-1)), which accounted for the formation of the circulating metabolites.

Ammonia↗
PubMed1999

High protein diet induces pericentral glutamate dehydrogenase and ornithine aminotransferase to provide sufficient glutamate for pericentral detoxification of ammonia in rat liver lobules.

The liver plays a central role in nitrogen metabolism. Nitrogen enters the liver as free ammonia and as amino acids of which glutamine and alanine are the most important precursors. Detoxification of ammonia to urea involves deamination and transamination. By applying quantitative in situ hybridization, we found that mRNA levels of the enzymes involved are mainly expressed in periportal zones of liver lobules. Free ammonia, that is not converted periportally, is efficiently detoxified in the small rim of hepatocytes around the central veins by glutamine synthetase preventing it from entering the systemic circulation. Detoxification of ammonia by glutamine synthetase may be limited due to a shortage of glutamate when the nitrogen load is high. Adaptations in metabolism that prevent release of toxic ammonia from the liver were studied in rats that were fed diets with different amounts of protein, thereby varying the nitrogen load of the liver. We observed that mRNA levels of periportal deaminating and transaminating enzymes increased with the protein content in the diet. Similarly, mRNA levels of pericentral glutamate dehydrogenase and ornithine aminotransferase, the main producers of glutamate in this zone, and pericentral glutamine synthetase all increased with increasing protein levels in the diet. On the basis of these changes in mRNA levels, we conclude that: (a) glutamate is produced pericentrally in sufficient amounts to allow ammonia detoxification by glutamine synthetase and (b) in addition to the catalytic role of ornithine in the periportally localized ornithine cycle, pericentral ornithine degradation provides glutamate for ammonia detoxification.

Ammonia↗
PubMed2005

Examination of the influence of personal traits and habituation on the reporting of complaints at experimental exposure to ammonia.

OBJECTIVE: The aim of the study is to examine the impact of personal traits and habituation on the intensity of self reported health symptoms and complaints. METHODS: Forty-three healthy male volunteers were exposed to ammonia vapours in concentrations of 0, 10, 20, 20/40, and 50 ppm on five consecutive days. To explore a possible influence of habituation on the perception of symptoms, the study group was divided into 30 men who were not familiar with the smell of ammonia, and ten participants regularly exposed to ammonia at the workplace. The perceived acute health symptoms and self-reported changes of well-being were assessed by the German version of a questionnaire of the Swedish Performance Evaluation System (SPES). Personal traits were ascertained with the positive and negative affectivity schedule (PANAS) and the Freiburger Persönlichkeits Inventar (FPI). RESULTS: There are significant associations between personal traits and the amount of complaints. Subjects with high positive affectivity report less respiratory and irritative complaints, whereas persons with negative affectivity report significantly more olfactory and respiratory symptoms. In general, the strength of these correlations decreases with higher exposure levels. At ammonia concentration above 20 ppm, these associations were no more statistically significant. During the daily exposures, the score of symptoms did not vary significantly. The perceived intensity of health symptoms and annoyance increased with the concentration of ammonia, while the self-reported dimensions of well-being decreased. Workers familiar with the smell of ammonia vapours reported less symptoms compared to naïve subjects. CONCLUSIONS: Habituation to ammonia vapours as well as personal traits influence the reporting of complaints particularly at low exposure. Both factors should be considered in the examination of chemosensory irritative compounds.

Adult↗
PubMed2005

Endogenous neuro-protectants in ammonia toxicity in the central nervous system: facts and hypotheses.

The paper overviews experimental evidence suggestive of the engagement of three endogenous metabolites: taurine, kynurenic acid, and glutathione (GSH) in the protection of central nervous system (CNS) cells against ammonia toxicity. Intrastriatal administration of taurine via microdialysis probe attenuates ammonia-induced accumulation of extracellular cyclic guanosine monophosphate (cGMP) resulting from over-activation of the N-methyl-D: -aspartate/nitric oxide (NMDA/NO) pathway, and this effect involves agonistic effect of taurine on the GABA-A and glycine receptors. Taurine also counteracts generation of free radicals, increased release of dopamine, and its metabolism to dihydroxyphenylacetic acid (DOPAC). Taurine reduces ammonia-induced increase of cell volume (edema) in cerebrocortical slices by a mechanism involving GABA-A receptors. Massive release of radiolabeled or endogenous taurine from CNS tissues by ammonia in vivo and in vitro is thought to promote its neuroprotective action, by making the amino acid available for interaction with cell membranes and/or by driving excess water out of the CNS cells (astrocytes) that underwent ammonia-induced swelling. Ammonia in vivo and in vitro affects in variable ways the synthesis of kynurenic acid (KYNA). Since KYNA is an endogenous NMDA receptor antagonist with a high affinity towards its glycine site, changes in its content may counter over-activation or depression of glutaminergic transmission observed at the different stages of hyperammonemia. GSH is a major antioxidant in the CNS whose synthesis is partly compartmented between neurons and astrocytes: astrocytic GSH is a source of precursors for the synthesis of neuronal GSH. Ammonia in vitro stimulates GSH synthesis in cultured astrocytes, which may compensate for increased GSH consumption (decreased GSH/GSSG ratio) in neurons.

Ammonia↗
PubMed2006

PET Imaging of cerebral astrocytoma with 13N-ammonia.

UNLABELLED: We performed this study in order to assess the clinical potential of (13)N-ammonia PET in patients with cerebral astrocytoma. METHODS: Dynamic 13N-ammonia PET was performed in 25 patients with suspected cerebral gliomas or recurrent cerebral astrocytomas (19 male and 6 female patients; age range 18-64 years) detected by MRI. The histopathological diagnoses were made for all cases either by biopsy or craniotomy, except for one patient with brain infarction and one patient with brain radiation necrosis confirmed by repeated MRI imaging. PET images were visually inspected, and the tumor-to-white matter count (T/W) ratios and the perfusion index (PI) of the tumors were determined. RESULTS: Six out of nine cases of low-grade gliomas were detected with 13N-ammonia PET, and three non-astrocytoma low-grade gliomas were not detected with 13N-ammonia PET. All 11 high-grade astrocytomas exhibited markedly increased uptake of 13N-ammonia. The five non-neoplastic lesions exhibited low uptake, low T/W ratios and low PI. The significant differences were observed between high-grade and low-grade gliomas with respect to both the T/W ratios and PI (T/W ratios: 5.92+/-2.27, n=11 vs. 1.66+/-0.61, n=9, P<0.01; PI: 5.22+/-1.67, n=11 vs. 1.60+/-0.54, n=9, P<0.01). There were the significant differences between the T/W ratios and PI in low-grade astrocytomas and that in non-neoplastic lesions (T/W ratios: 2.00+/-0.42, n=6 vs. 0.97+/-0.11, n=5, P<0.01; PI: 1.89+/-0.37, n=6 vs. 0.99+/-0.03, n=5, P<0.01). CONCLUSIONS: There is a substantial uptake of 13N-ammonia in cerebral astrocytomas. 13N-ammonia PET may enable differentiation between low- and high-grade astrocytomas, and has the potential to enable differentiation between low-grade astrocytomas and non-neoplastic lesions.

Adult↗