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PubMed1985

Effect of hyperammonemia and methionine sulfoximine on the kinetic parameters of blood-brain transport of leucine and phenylalanine.

The activity of the blood-brain neutral amino acid transport system is increased in rats infused with ammonium salts or rendered hyperammonemic by a portacaval anastomosis. This effect may be due to a direct action of ammonia or to some metabolic consequence of high ammonia levels, such as increased brain glutamine synthesis. To test these possibilities we evaluated the kinetic parameters of blood-brain transport of leucine and phenylalanine in control rats, in rats after continuous 24 h infusion of ammonium salts (NH4+ = 2.5 mmol X kg-1 X h-1), and in rats treated with methionine sulfoximine, an inhibitor of glutamine synthetase, before infusion of ammonium salts. In ammonia-infused rats without methionine sulfoximine treatment, the KD and Vmax of phenylalanine transport were increased, respectively, about 170% and 80% compared to controls, whereas the Km and Vmax of leucine transport were increased, respectively, about 100% and 200%. Electron microscopy demonstrated marked swelling of astrocytic processes around brain capillaries of ammonia-infused rats; however, capillary permeability to horseradish peroxidase apparently was not increased by ammonia infusion. Administration of methionine sulfoximine before ammonia infusion inhibited glutamine synthesis and prevented the changes in transport of leucine and phenylalanine, but apparently did not reverse the perivascular swelling. These results suggest that the ammonia-induced increase in the activity of transport of large neutral amino acids across the blood-brain barrier requires glutamine synthesis in brain, and is not a direct effect of ammonia.

Ammonia↗
PubMed2000

NHE1, NHE2, and NHE3 contribute to regulation of intracellular pH in murine duodenal epithelial cells.

Na(+)/H(+)-exchangers (NHE) mediate acid extrusion from duodenal epithelial cells, but the isoforms involved have not previously been determined. Thus we investigated 1) the contribution of Na(+)-dependent processes to acid extrusion, 2) sensitivity to Na(+)/H(+) exchange inhibitors, and 3) molecular expression of NHE isoforms. By fluorescence spectroscopy the recovery of intracellular pH (pH(i)) was measured on suspensions of isolated acidified murine duodenal epithelial cells loaded with 2', 7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Expression of NHE isoforms was studied by RT-PCR and Western blot analysis. Reduction of extracellular Na(+) concentration ([Na(+)](o)) during pH(i) recovery decreased H(+) efflux to minimally 12.5% of control with a relatively high apparent Michaelis constant for extracellular Na(+). The Na(+)/H(+) exchange inhibitors ethylisopropylamiloride and amiloride inhibited H(+) efflux maximally by 57 and 80%, respectively. NHE1, NHE2, and NHE3 were expressed at the mRNA level (RT-PCR) as well as at the protein level (Western blot analysis). On the basis of the effects of low [Na(+)](o) and inhibitors we propose that acid extrusion in duodenal epithelial cells involves Na(+)/H(+) exchange by isoforms NHE1, NHE2, and NHE3.

Amiloride↗
PubMed1991

[The role of nitrogen and phosphorus in pollution of animal origin].

Despite some variability in the data, the author has been able to establish the average characteristics of animal wastes, and to formulate an overall view of nitrogen and phosphorus wastes originating from livestock, in order to compare them with other wastes. Nitrogen is originally present mainly in the form of dissolved ammonia, whereas phosphorus is present in inorganic particles. Ammonium nitrogen is toxic for the aquatic fauna and, in favourable conditions, can be oxidised into nitrates and nitrites, which are undesirable constituents, capable of affecting the health of consumers. Phosphorus and nitrogen compounds in excess of the requirements for soil fertilisation are responsible, among other things, for degrading the quality of surface water, leading to eutrophication.

Animals↗
PubMed1997

Inhibition of ultraviolet B-induced skin erythema by N-nitro-L-arginine and N-monomethyl-L-arginine.

Ultraviolet B (UVB)-irradiated human keratinocytes and human endothelial cells release nitrogen oxides, i.e. nitric oxide (NO). S-nitrosothiols, hydroxylamine (H2NOH) as well as ammonia (NH3) formed from L-arginine. Generation of these compounds was time and concentration-dependent and decreased by both N-monomethyl-L-arginine (L-NMMA) and N-nitro-L-arginine (L-NA). UVB radiation of the cells resulted in a concomitant increase of soluble guanylate cyclase (sGC) activity which was inhibited by L-NMMA and L-NA. S-nitrosothiols formed during the irradiation of the cells directly increased purified sGC activity by a mechanism characteristic of release of NO from a carried molecule. UVB-irradiated cells promptly increased thiobarbituric acid reacting substance (TBARS) (estimated as malondialdehyde. MDA) production which were inhibited by desferrioxamine. In in vivo experiments using guinea pigs subjected to UVB radiation, a Protection Factor (PF) of 2.25 +/- 0.75 was calculated when an emulsified cream formulation containing L-NMMA (1% w/w) and L-NA (1% w/w) was applied to their skin. In human volunteers subjected to UVB radiation, a dose-dependent increase of PF was observed. When an emulsified cream formulation containing L-NMMA (1% w/w) and L-NA (1% w/w) was applied to their skin the PF was 2.15 +/- 0.80: by increasing the concentration of L-NMMA (1% w/w) and L-NA (2% w/w) the PF was 4.25 +/- 1.25. The present results indicate that UVB radiation acts as a potent stimulator of human keratinocytes and endothelial cells to release nitrogen oxides that may diffuse out of the keratinocytes and endothelial cells, activating sGC in neighboring smooth muscle cells. This may be a major part of the integrated response of the skin leading to vasodilation and erythema.

Ammonia↗
PubMed1992

Ammonium ion increases the tone of rat portal vein.

1. The effect of ammonium ion on vascular tone was investigated using the portal vein isolated from rat. 2. Ammonium chloride at 10-90 mM induced a contractile response. 3. Spontaneous twitch contraction of portal strips was augmented by ammonium chloride at 10-60 mM. 4. Ammonium chloride-induced contraction was abolished in calcium-free solution or in the presence of 1 microM nifedipine. 5. Methylamine (60 mM) also induced a contractile response and augmented the spontaneous twitch contraction in rat portal vein. 6. After withdrawal of ammonium chloride or methylamine from the organ bath solution, the spontaneous twitch contraction was strongly inhibited. 7. These results suggest that ammonium compounds increase vascular tone by causing influx of extracellular calcium through the voltage-dependent calcium channel and intracellular alkalinization is involved in this process.

Ammonia↗
PubMed2004

The Rh gene family and renal ammonium transport.

PURPOSE OF REVIEW: Renal acid-base homeostasis, to a very large extent, depends on renal ammonia production and transport. A putative ammonia transporter family of proteins has recently been identified, and at least two members of this family are expressed in the renal connecting segment and collecting duct. The purpose of this review is to discuss key features of renal ammonia metabolism and transport, with particular emphasis on the transporters involved in this process. RECENT FINDINGS: The putative ammonia transporter family members, RhBG and RhCG, are expressed in the renal connecting segment and collecting duct. Basolateral RhBG is expressed by all cells in the connecting segment and cortical collecting duct, and by intercalated cells in the outer medullary and inner medullary collecting duct. Apical RhCG is expressed in the same distribution and also in the outer stripe of the outer medullary collecting duct principal cells. In all regions, the expression of RhBG and RhCG is greater in intercalated cells than in principal cells. The related protein, RhAG, appears to be an erythroid-specific protein that mediates ammonium/hydrogen ion (NH4/H) exchange. RhBG and RhCG appear to be sodium and potassium ion-independent ammonia transporters. Whether they mediate electrogenic ammonia transport or electroneutral ammonia/hydrogen ion exchange remains an active area of investigation. Finally, transport studies have identified that electroneutral ammonium/hydrogen ion exchange is present in the collecting duct. SUMMARY: The Rh glycoproteins, RhBG and RhCG, appear to mediate important roles in renal ammonia transport, and therefore in acid-base homeostasis.

Animals↗
PubMed2001

Genetics of larval urea and ammonia tolerance and cross-tolerance in Drosophila melanogaster.

Five laboratory populations of Drosophila melanogaster previously selected for over 60 generations for larval resistance to ammonium chloride (NH4Cl), and five populations selected for over 60 generations for larval resistance to urea, were investigated to determine the genetic mechanisms through which such tolerance had evolved. To examine the genetics of tolerance to urea and ammonia, egg-to-adult survivorship and developmental time were measured at two different NH4Cl levels and two different urea levels for each selection regime relative to the control lines, and among reciprocal crosses between each selection regime and the control lines. To examine tolerance to novel nitrogenous compounds (cross-tolerance), egg-to-adult survivorship and developmental time were measured at two different NH4Cl levels and two different urea levels for reciprocal crosses between the selection lines. Dominance is a major genetic factor in egg-to-adult survivorship in the presence of either urea or ammonia, while cross-tolerance to novel nitrogenous compounds also shows dominance as a major genetic mechanism controlling egg-to-adult survivorship. Dominance and X-linkage appear to be factors affecting developmental time in the presence of either urea or ammonia, although we could not exclude cytoplasmic inheritance as influencing our results. Cross-tolerance to novel nitrogenous compounds shows dominance and X-linkage as the main genetic factors controlling developmental time. We develop a simple hypothesis, in accordance with the results, that there may be two X-linked loci: one controlling urea tolerance and one controlling ammonia tolerance, and one autosomal locus exerting a pleiotropic control of tolerance. However, many other possibilities exist.

Ammonium Chloride↗
PubMed1975

Diabetogenic effect and inhibition of insulin secretion induced in normal rats by ammonium infusions.

In order to explain the abnormalities of glucose metabolism previously observed in patients with blood ammonia elevation, the effect of a transitory hyperammonemia on I.V. glucose tolerance was investigated in rats. An I.V. glucose tolerance test was performed in 3 groups of 15 rats 60 min after the beginning of a 95 min infusion of either a 2 ml isotonic NaCl solution (control group) or ammonium acetate solutions at low (0.50 mumol/kg/min. NH4+) or high doses (1.70 mumol/kg/min NH4+). The "high" NH4+ infusion produced an increase of blood ammonia to levels near 1000 mug/100 ml, a significant decrease in the K coefficient for glucose disappearance (2.53 X 10(-2) +/- 0.20 compared to 4.92 X 10(-2) +/- 0.13 in control group) and a suppression of the radioimmunological plasma insulin (I.R.I.) response to glucose. With the "low" NH4+ infusion the hyperammonemia was less pronounced (200-300) mug/100 ml), but the decrease in K(3.02 X 10(-2) +/- 0.15) and in the first phase of I.R.I. release remained significant. The decrease in glucose disappearance rate could be accounted for by the proportional decrease in insulin secretion. Thus glucose intolerance induced by ammonium acetate infusions may be due to a direct effect of NH4 + on the pancreas. These abnormalities in glucose metabolism depend on the quantity of infused ammonium.

Acetates↗
PubMed2000

pH regulation in isolated in vitro perfused rat colonic crypts.

We investigated disorders and regulation of cytosolic pH (pHi) in isolated perfused crypts from rat distal colon using the pH-sensitive dye BCECF. This preparation allows distinct examination of either luminal or basolateral transport. The effects of luminal weak organic acids and bases on pHi were examined. The physiological concentrations of both luminal CO2/HCO3- and acetic acid/acetate acidified pHi significantly, but less than when applied from the basolateral side. Corresponding changes (luminal versus basolateral) in pHi were -0.17+/-0.04 versus -0.39+/-0.04, (n=8) and -0.15+/-0.02 versus -0.41+/-0.04, (n=8), respectively. Basolateral versus luminal application of NH3/NH4+ led to a more marked change in pHi, namely 0.35+/-0.03 versus 0.008+/-0.007 pH units, (n=19). The luminal perfusion of NH3/NH4+ was controlled by applying fura-2 acid to the luminal side and at the same time recording fura-2-specific fluorescence. Hence, the influence of luminal acid/base on colonic pHi homeostasis was limited. To examine pHi regulation, we investigated the recovery from an intracellular acid load using the NH3/NH4+ pulse method. Recovery was completely dependent on basolateral Na+, indicating that luminal acid/base transport does not play a major role in pHi homeostasis. The basolateral transporters involved in pHi recovery are probably the EIPA- and HOE694-inhibitable (IC50=0.2 and 2 micromol/l, respectively) Na+/H+ exchanger NHE1 and the DIDS-inhibitable Na+-dependent HCO3- importer.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMedDate not supplied

The effect of intracellular pH on cytosolic Ca2+ in HT29 cells.

The influence of intracellular pH (pHi) on intracellular Ca2+ activity ([Ca2+]i) in HT29 cells was examined microspectrofluorometrically. pHi was changed by replacing phosphate buffer by the diffusible buffers CO2/HCO3- or NH3/NH4+ (pH 7.4). CO2/HCO3- buffers at 2,5 or 10% acidified pHi by 0.1, 0.32 and 0.38 pH units, respectively, and increased [Ca2+]i by 8-15 nmol/l. This effect was independent of the extracellular Ca2+ activity and the filling state of thapsigargin-sensitive Ca2+ stores. Removing the CO2/HCO3- buffer alkalinized pHi by 0.14 (2%), 0.27 (5%), and 0.38 (10%) units and enhanced [Ca2+]i to a peak value of 20, 65, and 143 nmol/l, respectively. Experiments carried out with Ca2+-free solution and with thapsigargin showed that the [Ca2+]i transient was due to release from intracellular pools and stimulated Ca2+ entry. NH3/NH4+ (20 mmol/l) induced a transient intracellular alkalinization by 0.6 pHunits and increased [Ca2+]i to a peak (Delta [Ca2+]i = 164 nmol/l). The peak [Ca2+]i increase was not influenced by removal of external Ca2+, but the decline to basal [Ca2+]i was faster. Neither the phospholipase C inhibitor U73122 nor the inositol 1,4,5-trisphosphate (InsP3) antagonist theophylline had any influence on the NH3/NH4+-stimulated [Ca2+]i increase, whereas carbachol-induced [Ca2+]i transients were reduced by more than 80% and 30%, respectively. InsP3 measurements showed no change of InsP3 during exposure to NH3/NH4+, whereas carbachol enhanced the InsP3 concentration, and this effect was abolished by U73122. The pHi influence on "capacitative" Ca2+ influx was also examined. An acid pHi attenuated, and an alkaline pHi enhanced, carbachol- and thapsigargin-induced [Ca2+]i influx. We conclude that: (1) an alkaline pHi releases Ca2+ from InsP3-dependent intracellular stores; (2) the store release is InsP3 independent and occurs via an as yet unknown mechanism; (3) the store release stimulates capacitative Ca2+ influx; (4) the capacitative Ca2+ influx activated by InsP3 agonists is decreased by acidic and enhanced by alkaline pHi. The effects of pHi on [Ca2+]i should be of relevance under many physiological conditions.

Ammonia↗
PubMed2007

The sugar model: autocatalytic activity of the triose-ammonia reaction.

Reaction of triose sugars with ammonia under anaerobic conditions yielded autocatalytic products. The autocatalytic behavior of the products was examined by measuring the effect of the crude triose-ammonia reaction product on the kinetics of a second identical triose-ammonia reaction. The reaction product showed autocatalytic activity by increasing both the rate of disappearance of triose and the rate of formation of pyruvaldehyde, the product of triose dehydration. This synthetic process is considered a reasonable model of origin-of-life chemistry because it uses plausible prebiotic substrates, and resembles modern biosynthesis by employing the energized carbon groups of sugars to drive the synthesis of autocatalytic molecules.

Ammonia↗
PubMed2006

Gene expression and activity of urea cycle enzymes of rat hepatocytes cold stored up to 120h in University of Wisconsin solution.

Urea cycle (UC) is the main pathway of ammonium removal. A deficiency in any of the five classical enzymes of the pathway causes a urea cycle disorder. Hepatocellular transplantation is one of the techniques applicable to treat this disorder. In the present work, we investigated the activities and the relative expression levels of two of the UC enzymes: Carbamyl phosphate synthetase I (CPSI) and ornithine transcarbamylase (OTC), in isolated hepatocytes preserved up to 120 h in University of Wisconsin (UW) solution at 0 degrees C, and during the rewarming of these suspensions. During preservation, CPSI showed differences in mRNA levels respect to time 0, while ornithine transcarbamylase remained unchanged. At the end of the rewarming, CPSI showed values of enzymatic activity and relative mRNA level comparable with the control, meanwhile, there was an increment in OTC activity. In line with these results, we found that hepatocytes cold preserved up to 120h in UW solution maintained their ability to remove an ammonium load comparable to freshly isolated hepatocytes. These data indicated that our preservation conditions up to 120h in UW solution followed by rewarming, preserves UC enzymes at levels similar to freshly isolated hepatocytes, allowing the use of these cells in bioartificial liver devices or hepatocellular transplantation.

Adenosine↗
PubMed1998

Chloride concentration in cultured hippocampal neurons increases during long-term exposure to ammonia through enhanced expression of an anion exchanger.

The effects of long-term exposure to ammonia on [Cl-]i in cultured hippocampal neurons were examined. Ammonia increased the [Cl-]i time- (>/=24 h) and concentration- (>/=2 mM) dependently, resulting in a depolarizing shift of the equilibrium potential of the GABAA receptor-Cl- channel opening (EGABA). Such an effect of ammonia was diminished by the inhibitors of Cl-/HCO3- exchangers, 0.1 mM 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS) and 0.1 mM 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), and a carbonic anhydrase inhibitor, 2 mM acetazolamide, but not by a Na+/K+/2Cl-cotransport inhibitor, 50 microM bumetanide, suggesting an enhanced Cl-/HCO3- exchange activity by ammonia. The ammonia-induced increase in [Cl-]i was also abolished by the inhibitors of protein kinase C (PKC), 0.1 microM calphostin C and 10 microM 1-(5-isoquinolinyl-sulfonyl)-2-methylpiperazine dihydrochloride (H-7), and of transcription and de novo protein synthesis, 1 microM actinomycin D and 0.5 microg/ml cycloheximide, while a PKC activator, 0.1 h microM phorbor 12-myristate 13-acetate (PMA), increased the [Cl-]i. The mRNA level of the AE3 Cl-/HCO3- exchanger was increased by ammonia in a calphostin C- and H-7-sensitive manner. The AE3-like immunoreactivity was also increased by ammonia. These findings suggest that long-term exposure to ammonia increases the expression of AE3 through the activation of PKC, resulting in an increase in [Cl-]i in neurons and a reduction of inhibitory postsynaptic potentials.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗