The effect of pellet size on the ammonia loss from urea applied to forest soil

Summary Using diluted phosphoric acid- and glycerol-treated polyurethane plastic foam discs as static ammonia absorbers, the extent of ammonia loss from applied urea was determined on forest soil under field conditions. The investigation, which primarily involved a comparison of urea materials of two different pellet sizes (2–4 mg and 2060 mg urea per pellet, respectively), extended over a period of 28 days. The urea was applied to the soil surface at a rate of 200 kg N per hectare.It was found that the gaseous ammonia loss from the large-pellet urea (tablets) was markedly lower than that from the small-pellet urea during the first two weeks of exposure. On extending the observation period to four weeks, this difference in cumulative ammonia loss decreased successively. After 28 days' exposure, at a daily mean temperature of 13°C, the volatile loss amounted to 20 and 22 per cent, respectively. An addition of 5% (w/w) of a solution of concentrated orthophosphoric acid, or a fine-crystalline ortho-boric acid to the large-pellet urea, resulted in a reduction of the loss to half the value. The possibilities of controlling the ammonia loss from urea by combining the large pellet size with the addition of urease inhibitors are discussed. re]19721012     

Assessment of volatilization loss of ammonia from surface-applied urea on forest soil by N15 recovery

Summary Using vertically isolated micro-plots the isotopic recovery technique was tested for assessing the extent of ammonia volatilization loss from N¹⁵-labelled urea applied on the forest floor (Pinus silvestris L.). The size of the ammonia loss was obtained as a difference between the amounts of labelled urea N added and the amounts of labelled N recovered in the soil profile after 13, 31, and 39 days's exposure, respectively. Urea materials of two different pellet size were used: granulated small pellets (280 pellets per gram) and tablets (2.06 g each). The nitrogen application rate was 200 kg N per hectare. The recovery data for 13 days' exposure indicated a volatilization loss, which for the small pellet urea was 24.9 per cent and for the tabletted urea 12.1 per cent. The corresponding figures for the 31 days' exposure, during which the total amount of precipitation was 14 mm, were 15.1 and 26.9 per cent, respectively. The pattern of labelled N distribution in the soil profile examined showed that during the period of exposure in question a leaching loss of labelled N was rather unlikely. It was demonstrated, furthermore, that nitrogen from the tabletted urea had diffused to a greater depth of the soil than that from the small-pellet urea. Nitrogen from the small-pellet urea was to a large extent recovered in the litter layer. On exposure to heavy rain the tabletted urea was subjected to the highest leaching loss. An addition of 10 per cent (w/w) of metaphosphoric acid or sublimed sulphur to the tabletted urea did not result in any further reduction of the volatilization loss. The merits and limits of the isotopic recovery technique are discussed.     

Acute and chronic exposure to ammonia and olfactory acuity for n-butanol in the pig

An associative learning method (using a food reward) was developed to measure pigs' olfactory acuity for n-butanol, a standard odourant in human olfactometry. The pig could press two operant paddles but it only received a food reward when it pressed the one over which n-butanol was released. Once each pig had reached a training criterion (10 consecutive roots on the correct paddle on each of two consecutive sessions) this method was used to assess the impact of acute and chronic exposure to an atmosphere containing approximately 40 parts per million (ppm) ammonia gas, compared to fresh air, on its ability to perceive different concentrations of n-butanol. These were presented using a staircase pattern, i.e. if the pig gained or failed to gain a food reward on two consecutive occasions the concentration was reduced or increased, respectively. Acute exposure for approximately 45min to about 40ppm ammonia had no effect (P>0.05) on the lowest detected concentration (LDC) of n-butanol in six pigs. The geometric mean LDC was 1.23 parts per trillion (ppt) in approximately 40ppm ammonia and 2.09ppt in fresh air. The LDC of three pigs increased, i.e. acuity fell, from 5.1 to 175.5ppt over 24 days of exposure to congruent with40ppm ammonia. Ammonia had no effect on one of the other pigs and the high variability in the LDC for the remaining two pigs produced no meaningful assessment of its impact. Subsequent removal to fresh air for a further 24 days led to partial recovery of acuity in one of the three pigs that had shown evidence of olfactory impairment but not in the other two. Collectively our findings suggest that chronic, but not acute, exposure to congruent with40ppm ammonia can interfere with olfactory perception in some pigs (50% of our sample) and that this loss of acuity is not necessarily reversible.     

Air-breathing catfish, Clarias batrachus upregulates glutamine synthetase and carbamyl phosphate synthetase III during exposure to high external ammonia

We assessed the possible upregulation of glutamine synthetase (GS) and typical 'fish type' carbamyl phosphate synthetase III (CPS III) in detoxification of ammonia in different tissues of the walking catfish (Clarias batrachus) during exposure to 25 mM NH(4)Cl for 7 days. Exogenous ammonia led to an increase in ammonia and urea concentrations in different tissues. The results revealed the presence of relatively high levels of GS activity in the brain, liver and kidney, unexpectedly, also in the muscle, and even higher levels in the intestine and stomach. Exposure to high external ammonia (HEA) caused significant increase of activities of GS, CPS III and CPS I-like enzymes, accompanied with the upregulation of GS and CPS III enzyme proteins in different tissues. Exposure to HEA also led to a sharp rise of plasma cortisol level, suggesting being one of the primary causes of upregulation of GS and CPS III enzymes activity. Liver perfusion experiments further revealed that exposure to HEA enhances the capacity of trapping ammonia to glutamine and urea by the liver of walking catfish. These results suggest that the upregulation of GS and CPS III activity in walking catfish during exposure to HEA plays critical roles to ameliorate the toxic ammonia to glutamine, and also to urea via the induced ornithine-urea cycle possibly through the involvement of cortisol.     

Chronic exposure to ammonia alters pathways modulating phosphorylation of microtubule-associated protein 2 in cerebellar neurons in culture

Hyperammonemia is considered the main cause for the neurological alterations found in hepatic failure. However, the mechanisms by which high ammonia levels impair cerebral function are not well understood. It has been shown that chronic hyperammonemia impairs signal transduction pathways associated with NMDA receptors and also alters phosphorylation of some neuronal proteins. The aim of the present work was to analyze the effects of chronic exposure to ammonia on phosphorylation of microtubule-associated protein 2 (MAP-2) in intact neurons in culture and to assess whether modulation of MAP-2 phosphorylation by glutamate receptor-associated transduction pathways is altered in neurons chronically exposed to ammonia. It is shown that chronic exposure to ammonia increases basal phosphorylation of MAP-2 by approximately 70%. This effect seems to be due to a decreased tonic activation of NMDA receptors and of calcineurin. Chronic exposure to ammonia also alters the modulation of MAP-2 phosphorylation by NMDA receptors and metabotropic glutamate receptors. In neurons exposed to ammonia, treatment with NMDA for 30 min induced a significant decrease in phosphorylation of MAP-2. Activation of metabotropic glutamate receptors with (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid significantly increased phosphorylation of MAP-2 in control neurons, whereas in neurons exposed to ammonia the response was the opposite, with 1-aminocyclopentane-1,3-dicarboxylic acid inducing a dephosphorylation of MAP-2. These results indicate that ammonia alters significantly signal transduction pathways associated with different types of glutamate receptors. This would lead therefore to significant alterations in glutamatergic neurotransmission, which would contribute to the neurological alterations found in hyperammonemia and in hepatic encephalopathy.     

非离子氨和亚硝酸氮对虾虎鱼仔鱼的急性毒性及安全浓度评价

目的检测非离子氨和亚硝酸氮对鱼类的生态毒性效应。方法在水温（25±1）℃、溶氧（6.07～6.77）mg/L、盐度30～31、pH8.0～8.2的条件下,采用半静水式生物毒性试验方法研究了非离子氨和亚硝酸氮对裸项栉虾虎鱼（Ctenogobius gymnauchen）仔鱼的急性毒性效应（非离子氨浓度梯度设置为0、0.413、0.735、1.309、2.329、4.147 mg/L,亚硝酸氮浓度梯度设置为0、3.0、4.14、5.713、7.884、10.88 g/L）。结果非离子氨和亚硝酸氮暴露后仔鱼出现呆滞、侧游、呼吸困难、体色变白、身体弯曲等中毒症状,且随着暴露浓度的升高与暴露时间的延长,死亡率逐渐增加,存在明显的剂量效应关系和时间效应关系;非离子氨和亚硝酸氮对裸项栉虾虎鱼仔鱼96 hLC50分别为9.1 mg/L和12.405 g/L,其安全浓度分别为0.91 mg/L和1.2405 g/L。结论裸项栉虾虎鱼对非离子氨和亚硝酸氮具有较强的耐受力,非离子氨对裸项栉虾虎鱼仔鱼的毒性显著大于亚硝酸氮。     

CHANGES IN VESICULAR DOPAMINE-β-HYDROXYLASE RESULTING FROM TRANSMITTER RELEASE

—Exposure of rats to 3°C for up to 30 min leads to a decrease of 30 per cent in the dopamine-β-hydroxylase activity of the vesicular pellet of the heart; this is greater than can be accounted for by loss of soluble DBH from the two populations of noradrenaline storage vesicles known to be present in the heart. Cold exposure in the presence of α-methyltyrosine causes a much smaller reduction in dopamine-β-hydroxylase activity; this suggests that there is a decrease in transmitter release when synthesis is inhibited. The noradrenaline concentration of the vesicular pellet rises briefly during cold exposure and is then maintained at control levels; the early rise is absent in the presence of α-methyltyrosine. The use of the noradrenaline : dopamine-β-hydroxylase ratio as an index of saturation of vesicular storage capacity suggests that during cold exposure an increased synthesis rate leads to increased filling of vesicles.     

The African lungfish, Protopterus dolloi, detoxifies ammonia to urea during environmental ammonia exposure

The African lungfish, Protopterus dolloi, was able to maintain a low level of blood plasma ammonia during exposure to high concentrations of environmental ammonia. After 6 d of exposure to 30 or 100 mM NH(4)Cl, the total ammonia concentrations in the blood plasma were 0.288 and 0.289 mM, respectively, which were only 1.7-fold greater than the control value of 0.163 mM. In addition, accumulation of ammonia occurred only in the muscle, but not in the liver. This was achieved in part through urea synthesis, as reflected by significant increases in urea contents in the muscle, liver, and plasma of the experimental animals. In contrast with plasma ammonia, the plasma urea concentrations of specimens exposed to 30 or 100 mM NH(4)Cl for 6 d increased 15.4-fold and 18.8-fold, respectively. Taken together, these results suggest that P. dolloi upregulated the rate of urea synthesis to detoxify ammonia during environmental ammonia exposure and that the increased rate of urea synthesis was fast enough to compensate for the rate of endogenous ammonia production plus the net influx of exogenous ammonia in these experimental animals. Simultaneously, there were increases in the rates of urea excretion in the experimental animals between day 2 and day 6 of environmental ammonia exposure. Interestingly, the rates of urea excretion in specimens exposed to 100 mM NH(4)Cl were lower than those exposed to 30 mM NH(4)Cl, despite the presumably greater load of ammonia to be detoxified to urea in the former situation. It would appear that P. dolloi was regulating the rate of urea excretion during ammonia exposure to retain urea, which might have some physiological functions under environmental stresses yet to be determined. There were decreases in the contents of glutamate, glutamine, and total free amino acids in the liver of the experimental animals, which indirectly suggest that a reduction in the rate of proteolysis and/or amino acid catabolism would have occurred that might lead to a decrease in ammonia production. Our results suggest that, unlike marine elasmobranchs and coelacanths, which synthesize and retain urea for osmoregulatory purposes, the ureogenic P. dolloi was adapted to synthesizing and excreting urea for the purpose of ammonia detoxification.     

Loss of Ammonia Monooxygenase Activity in Nitrosomonas europaea upon Exposure to Nitrite

Nitrosomonas europaea, an obligate ammonia-oxidizing bacterium, lost an increasing amount of ammonia oxidation activity upon exposure to increasing concentrations of nitrite, the primary product of ammonia-oxidizing metabolism. The loss of activity was specific to the ammonia monooxygenase (AMO) enzyme, as confirmed by a decreased rate of NH₄⁺-dependent O₂ consumption, some loss of active AMO molecules observed by polypeptide labeling with ¹⁴C₂H₂, the protection of activity by substrates of AMO, and the requirement for copper. The loss of AMO activity via nitrite occurred under both aerobic and anaerobic conditions, and more activity was lost under alkaline than under acidic conditions except in the presence of large concentrations (20 mM) of nitrite. These results indicate that nitrite toxicity in N. europaea is mediated by a unique mechanism that is specific for AMO.     

Ambient ammonia effect on catalytic potential of muscle and gill AMP deaminase in fish

AMP deaminase activity was inhibited in gill and muscle of Sarotherodon mossambicus, subjected to a week-long exposure to sublethal concentration of ambient ammonia. pH-dependent kinetic studies revealed decreased catalytic efficiency of the enzyme due to altered active site density and ionization pattern in the fish tissues at different phases of ammonia exposure.     

Metabolic and immune responses in Chinese mitten-handed crab (Eriocheir sinensis) juveniles exposed to elevated ambient ammonia

The toxicity of ammonia to Eriocheir sinensis juveniles was determined. The 24 h-, 48 h-, 72 h-, 96 h-LC(50) values of total ammonia (TAN) were 251.68, 217.61, 156.05, and 119.67 mg L(-1), respectively. Following these results, crabs were then exposed for a 2-day period to 20, 40, 60 and 80 mg L(-1) TAN and sampled at 3, 6, 24 and 48 h for changes in metabolic parameters (including haemolymph ammonia concentration, glucose, lactate, urea, triacylglycerol, glutamine, and glutamate levels) and immunity indicators (the total of haemocyte count and superoxide dismutase activity). Results showed a distinct linear relationship between ambient ammonia and haemolymph ammonia and a notable increase in haemolymph ammonia content after ammonia exposure. Compared with the control group, lower concentration of triglycerides and significantly higher glucose, urea, and lactate level in haemolymph were observed when ambient ammonia increased. This suggested a reduced use of carbohydrates through anaerobic metabolism and an increase in the use of lipids to satisfy the metabolic demand. A significant surge of the ammonia metabolic product, glutamate, was observed after 3 h ammonia exposure, and the compensatory response to reduced glutamate was manifested by increased glutamine synthesis. During the same period, total haemocyte count decreased while ambient ammonia increased. Superoxide dismutase (SOD) activity in haemolymph was stimulated by lower ambient ammonia concentration after short time exposure and depressed by higher ammonia concentration. Therefore, haemolymph ammonia accumulation resulted in an increase in energy demand and a depression in immune capacity. The mechanism to detoxification of ammonia may be to transform ammonia to urea and glutamine.     

Nitrogen metabolism and excretion in the swamp eel, Monopterus albus, during 6 or 40 days of estivation in mud

Monopterus albus inhabits muddy ponds, swamps, canals, and rice fields, where it can burrow into the moist earth, and it survives for long periods during the dry summer season. However, it had been reported previously that mortality increased when M. albus was exposed to air for 8 d or more. Thus, the objective of this study was to elucidate the strategies adopted by M. albus to defend against ammonia toxicity during 6 or 40 d of estivation in mud and to evaluate whether these strategies were different from those adopted by fish to survive 6 d of aerial exposure. Ammonia and glutamine accumulations occurred in the muscle and liver of fish exposed to air (normoxia) for 6 d, indicating that ammonia was detoxified to glutamine under such conditions. In contrast, ammonia accumulation occurred only in the muscle, with no increases in glutamine or glutamate contents in all tissues, of fish estivated in mud for 6 d. Similar results were obtained from fish estivated in mud for 40 d. While estivating in mud prevented excessive water loss through evaporation, M. albus was exposed to hypoxia, as indicated by significant decreases in blood P(O(2)), muscle energy charge, and ATP content in fish estivated in mud for 6 d. Glutamine synthesis is energy intensive, and that could be the reason why M. albus did not depend on glutamine synthesis to defend against ammonia toxicity when a decrease in ATP supply occurred. Instead, suppression of endogenous ammonia production was adopted as the major strategy to ameliorate ammonia toxicity when M. albus estivated in mud. Our results suggest that a decrease in O(2) level in the mud could be a more effective signal than an increase in internal ammonia level during aerial exposure to induce a suppression of ammonia production in M. albus. This might explain why M. albus is able to estivate in mud for long periods (40 d) but can survive in air for only <10 d.     

Role of amino acid metabolism in an air-breathing catfish,Clarias batrachus in response to exposure to a high concentration of exogenous ammonia

The air-breathing ureogenic walking catfish (Clarias batrachus) faces various environmental constraints throughout the year leading to the problem of accumulation of toxic ammonia. In the present study, the possible role of conversion of accumulated ammonia to various non-essential free amino acids (FAAs) was tested in this fish under hyper-ammonia stress caused by exposing the fish at 25 mM NH(4)Cl for 7 days. Significant accumulation of ammonia of approximately two- to threefold was observed in different tissues (except in the brain), which was accompanied with the significant accumulation of non-essential FAAs in the NH(4)Cl-exposed fish. There was approximately two- to threefold increase of non-essential FAAs in different tissues and in the plasma of the NH(4)Cl-exposed fish compared to the control fish after 7 days of exposure, which was mainly attributable to the increase of Asp, Ala, Gly, Glu, Gln and taurine (Tau) concentrations in general, with certain tissue-specific variations. This was also accompanied with significant increase of activity of certain amino acid metabolism-related enzymes such as the glutamine synthetase (approx. two- to threefold), glutamate dehydrogenase (ammonia utilizing direction) (approx. twofold), aspartate and alanine aminotransaminases (approx. twofold) mainly in the liver, kidney and muscle of the NH(4)Cl-exposed fish. Thus, it appears that the walking catfish has the capacity of active conversion of accumulated ammonia to non-essential FAAs under condition of high concentrations of external ammonia. However, the increase of urea excretion rate due to active conversion of ammonia to urea via the induced urea cycle appears to be quantitatively much more important pathway than the increase of tissue levels of FAAs in dealing with a severe ammonia load.     

Strategies for surviving high concentrations of environmental ammonia in the swamp eel Monopterus albus

The swamp eel Monopterus albus lives in muddy ponds, swamps, canals, and rice fields in the tropics. It encounters high concentrations of environmental ammonia (HEA) during dry seasons or during agricultural fertilization in rice fields. This study aimed at determining the tolerance of M. albus to environmental ammonia and at elucidating the strategies that it adopts to defend against ammonia toxicity in HEA. In the laboratory, M. albus exhibited very high environmental ammonia tolerance; the 48-, 72-, and 96-h median lethal concentrations of total ammonia at pH 7.0 and 28 degrees C were 209.9, 198.7, and 193.2 mM, respectively. It was apparently incapable of actively excreting ammonia against a concentration gradient. In addition, it did not detoxify ammonia to urea, the excretion of which would lead to a loss of nitrogen and carbon, during ammonia loading. The high tolerance of M. albus to HEA was attributable partially to its exceptionally high tolerance to ammonia at the cellular and subcellular levels. During the 144 h of exposure to 75 mM NH(4)Cl at pH 7.0, the ammonia contents in the muscle, liver, brain, and gut of M. albus reached 11.49, 15.18, 6.48, and 7.51 mu mol g(-1), respectively. Such a capability allowed the accumulation of high concentrations of ammonia in the plasma (3.54 mu mol mL(-1)) of M. albus exposed to HEA, which would reduce the net influx of exogenous ammonia. Subsequent to the buildup of internal ammonia levels, M. albus detoxified ammonia produced endogenously to glutamine. The glutamine contents in the muscle and liver reached 10.84 and 17.06 mu mol g(-1), respectively, after 144 h of exposure to HEA, which happened to be the highest known for fish. Unlike urea, the storage of glutamine in the muscle during ammonia loading allowed its usage for anabolic purposes when the adverse environmental condition subsides. Glutamine synthetase activity increased significantly in the liver and gut (2.8- and 1.5-fold, respectively) of specimens exposed to HEA for 144 h. These results suggest that the liver was the main site of ammonia detoxification and the gut was more than a digestive/absorptive organ in M. albus. Monopterus albus did not undergo a reduction in amino acid catabolism during the first 24 h of ammonia exposure. However, assuming a total inhibition of excretion of endogenous ammonia, there was a deficit of -312 mu mol N between the reduction in nitrogenous excretion (3,360 mu mol N) and the retention of nitrogen (3,048 mu mol N) after 72 h of aerial exposure. The deficit became much greater after 144 h, reaching a value of -3,243 mu mol N. These results suggest that endogenous ammonia production in M. albus was suppressed in order to prevent the newly established internal steady state concentration of ammonia from rising to an intolerable level after an extended period of exposure to HEA.     

The effect of sub-lethal ammonia exposure on fed and unfed rainbow trout: the role of glutamine in regulation of ammonia

Many species of fishes have evolved mechanisms for coping with ammonia caused by either high ammonia environments or an inability to excrete nitrogenous wastes. Rainbow trout (Oncorhynchus mykiss), have not been known to have such a mechanism. The present study investigated whether rainbow trout can use amino acid synthesis and storage to cope with ammonia. Experiments were performed on fed and unfed rainbow trout under both control and elevated ammonia conditions (0 and 10 mgN/l (total ammonia nitrogen), pH 7.2). The results indicate that both feeding and ammonia exposure increased plasma ammonia significantly 6 h postprandial and post ammonia exposure. After 48 h the fed/ammonia exposed fish had plasma ammonia levels that were not significantly different than the fed/control fish. Plasma ammonia was reduced by more than 50%, attributable to ammonia being converted to glutamine in brain, liver and muscle tissue. Feeding alone also increased glutamine levels in brain tissue. Activity of glutamine synthetase in brain and liver was increased corresponding to an increase in glutamine concentrations when fish were exposed to ammonia. This is the first report showing that rainbow trout can detoxify endogenous and exogenous ammonia.     

Ammonia induces aquaporin-4 rearrangement in the plasma membrane of cultured astrocytes

Aquaporin-4 (AQP4) is a water channel protein mainly located in the astroglial plasma membrane, the precise function of which in the brain edema that accompanies hepatic encephalopathy (HE) is unclear. Since ammonia is the main pathogenic agent in HE, its effect on AQP4 expression and distribution in confluent primary astroglial cultures was examined via their exposure to ammonium chloride (1, 3 and 5 mM) for 5 and 10 days. Ammonia induced the general inhibition of AQP4 mRNA synthesis except in the 1 mM/5 day treatment. However, the AQP4 protein content measured was dependent on the method of analysis; an apparent increase was recorded in treated cells in in-cell Western assays, while an apparent reduction was seen with the classic Western blot method, perhaps due to differences in AQP4 aggregation. Ammonia might therefore induce the formation of insoluble AQP4 aggregates in the astroglial plasma membrane. The finding of AQP4 in the pellet of classic Western blot samples, plus data obtained via confocal microscopy, atomic force microscopy (using immunolabeled cells with gold nanoparticles) and scanning electron microscopy, all corroborate this hypothesis. The effect of ammonia on AQP4 seems not to be due to any osmotic effect; identical osmotic stress induced by glutamine and salt had no significant effect on the AQP4 content. AQP4 functional analysis (subjecting astrocytes to a hypo-osmotic medium and using flow cytometry to measure cell size) demonstrated a smaller water influx in ammonia-treated astrocytes suggesting that AQP4 aggregates are representative of an inactive status; however, more confirmatory studies are required to fully understand the functional status of AQP4 aggregates. The present results suggest that ammonia affects AQP4 expression and distribution, and that astrocytes change their expression of AQP4 mRNA as well as the aggregation status of the ensuing protein depending on the ammonia concentration and duration of exposure.     

Nitrogenous fertilizer transformations in the sudan Gezira soil

Summary and Conclusions Direct measurements were made of losses of ammonia during the transformation of urea and ammonium sulphate, surface-applied to alkaline Gezira soil in containers incubated in the field, under different rates of nitrogen application and moisture conditions.The highest rate of ammonia loss occurred during the first week after application with both fertilizers, thereafter decreasing to lower values. The cumulative ammonia loss was higher with higher application of nitrogen. Ammonium sulphate gave consistently higher ammonia losses than urea and losses from open soil system were generally less than from soil in polythene bags.With lowest irrigation level used, ammonia loss attained a sizeable value throughout the incubation period with both fertilizers. With the higher moisture levels, the magnitude of ammonia loss decreased appreciably, much more so with urea than with ammonium sulphate. Induced drying and rewetting prolonged the duration of loss and increased the magnitude of cumulative loss. An appreciable loss of ammonia may take place from fertillzed Gezira Soil under warm conditions, low moisture levels and high fertilizer concentration; this may be the case with patchy fertilizer distribution and frequent light showers during early summer. It is advisable to apply the urea or ammonium sulphate when conditions are most favourable for nitrification.     

Glutamate transporters in hyperammonemia

Evidence suggests that increases in brain ammonia due to congenital urea cycle disorders, Reye Syndrome or liver failure have deleterious effects on the glutamate neurotransmitter system. In particular, ammonia exposure of the brain in vivo or in vitro preparations leads to alterations of glutamate transport. Exposure of cultured astrocytes to ammonia results in reduced high affinity uptake sites for glutamate due to a reduction in expression of the astrocytic glutamate transporter GLAST. On the other hand, acute liver failure leads to decreased expression of a second astrocytic glutamate transporter GLT-1 and a consequent reduction in glutamate transport sites in brain. Effects of the chronic exposure of brain to ammonia on cellular glutamate transport are less clear. The loss of glutamate transporter activity in brain in acute liver failure and hyperammonemia is associated with increased extracellular brain glutamate concentrations which may be responsible for the hyperexcitability and cerebral edema observed in hyperammonemic disorders.     

Changes in the selected hematological parameters and gill Na/K ATPase activity of juvenile crucian carp Carassius auratus during elevated ammonia exposure and the post-exposure recovery

The increase in concentration of ammonia in lake water during the degradation of algal blooms may last for several weeks and thus cause chronic toxicity to aquatic organisms. The purpose of this study was to assess the chronic toxicity of ammonia on the selected hematological parameters and gill Na⁺/K⁺ ATPase activity of juvenile crucian carp Carassius auratus during elevated ammonia exposure and the post-exposure recovery. Juvenile crucian carp were exposed in different ammonia solutions for 45 days and then immediately transferred to pristine freshwater to initiate a 15-day recovery period. Results showed sub-lethal ammonia significantly deters growth and a 15-day recovery period was not sufficient for the fish to compensate for the loss of growth. The fish exhibited a continuous decrease in red blood cell (RBC), the total hemoglobin (Hb), and gill Na⁺/K⁺ ATPase activity as the concentration of NH₃-N increased. After the 15-day recovery period, RBC, Hb, and gill Na⁺/K⁺ ATPase activity had recovered to similar levels as the controls.     

Effect of acute and chronic exposure to ammonia on different larval instars of Anopheles darlingi (Diptera: Culicidae)

Anopheles darlingi (Diptera: Culicidae) is the most important vector of malaria in South America and has already been found in peri‐urban areas that commonly contain toxic nitrogenous compounds, such as ammonia. The adaptation of mosquitoes to polluted breeding sites can increase their distribution and affect the dynamics of vector‐borne diseases such as malaria. Therefore, the present study investigated the tolerance of larval instars of An. darlingi to ammonia under acute and chronic exposure conditions. Anopheles darlingi larval mortality, development time, and pupal and adult production using larvae of the 1^st (L1) and 3^rd (L3) instar were assessed as both acute and chronic effects of exposure to different concentrations of ammonia. Lethal concentrations (LCs) for L1 larvae were lower than LCs for L3 larvae. In general, higher ammonia concentrations caused an increase in larval mortality, especially in chronically exposed L1 larvae. The larval development time in L1 and L3 was longer with chronic treatment and decreased with increasing concentrations of ammonia. The number of pupae was very low for acutely exposed L1 and L3 larvae. Likewise, the probability of adult production decreased with increasing ammonia concentrations. This is the first report on the tolerance of An. darlingi to pollutants.