Effects Of Ammonia Exposure Research Articles

The impact of ammonia and microcystin-LR on neurobehavior and glutamate/gamma-aminobutyric acid balance in female zebrafish (Danio rerio): ROS and inflammation as key pathways

Ammonia and microcystin-LR (MC-LR) are both toxins that can be in eutrophic waters during cyanobacterial blooms. While previous studies have focused on the effects of ammonia exposure on fish neurobehavioral toxicity, little attention has been given to the effects of MC-LR and combined exposures to both. This study exposed adult female zebrafish to ammonia (30 mg/L) and MC-LR (10 μg/L) alone and in combination for 30 days to investigate their neurotoxic effects and underlying mechanisms. Behavioral results showed that exposure to ammonia and MC-LR, both alone and in combination, led to decreased locomotor activity and increased anxiety in fish. Histomorphological analysis revealed the formation of thrombi and vacuolization in the brain across all exposure groups. Exposure to ammonia and MC-LR resulted in significant increases in MDA contents, decreases in Mn-SOD activities, and alterations in GSH contents compared to the control. Single and combined exposure to ammonia and MC-LR also induced the release of inflammatory factors (IL-1β and TNF-α) by activating the NOD/NF-κB signaling pathway. Furthermore, both ammonia and MC-LR significantly changed the expression of genes related to the glutamatergic and GABAergic systems, elevated Glu and GABA contents, as well as increased the Glu/GABA ratio, indicating that a shift towards increased Glu levels. Overall, these findings suggested that exposure to MC-LR and ammonia, individually and in combination, could decrease locomotor activity and increase anxiety of female zebrafish. This was likely due to brain damage from over-activated ROS and the release of pro-inflammatory cytokines, which led to a disruption in the balance of glutamatergic and GABAergic systems. However, there was no significant interaction between MC-LR and ammonia in fish neurobehavioral toxicity.

돈사 내 암모니아 농도가 육성 · 비육돈의 행동 변화에 미치는 영향

돈사 내 암모니아 농도가 육성 · 비육돈의 행동 변화에 미치는 영향

Effects of ammonia exposure on anxiety behavior, oxidative stress and inflammation in guppy (Poecilia reticulate)

Ammonia is one of the most important aquatic environmental factors, which is of great concern. In order to evaluate the effect of ammonia on guppy (Poecilia reticulate), fish were exposed to increased concentrations (0, 12.50, 25.00, 41.67, 62.50 mg/L) of ammonia for 48 h. After exposure, we measured the anxiety behavior, antioxidant enzymes and pro-inflammation genes (TNF-α, IL-1β and IL-6) of guppy. The results showed that ammonia stress induced fish anxiety, which was manifested by the increased latency to enter the upper half and decreased time spent in upper half compared with control fish. The guppy showed oxidative stress after 48 h of ammonia stress as evidenced by decreases in the activities of antioxidant enzymes and an increase in lipid hydroperoxide content. With prolonged ammonia stress, the expressions of HSP70, HSP90, TNF-α, IL-1β and IL-6 mRNA at first had an increasing trend, and then decreased, all of which were significantly higher than the control levels at 12 h and 24 h after ammonia stress (P < 0.05). Ammonia significantly upregulated these genes mRNA levels after 48 h exposure, suggesting that heat shock proteins and innate immune system may try to protect cells from oxidative stress induced by ammonia stress. Our study showed that higher ammonia exposure induced oxidative stress in exposed fish, since inhibition of antioxidant enzymes activity and increases in lipid peroxidation, and inflammation occurred. Furthermore, the results will be helpful to understand the mechanism of ammonia toxicity in guppys.

The effects of ammonia exposure on immune response, oxidative stress, and apoptosis in Procambarus clarkii

The effects of ammonia exposure on immune response, oxidative stress, and apoptosis in Procambarus clarkii

Effects of ammonia exposure on oxidative stress, immune enzyme activities, and intestinal microbiota of Pacific white shrimp Litopenaeus vannamei

Effects of ammonia exposure on oxidative stress, immune enzyme activities, and intestinal microbiota of Pacific white shrimp Litopenaeus vannamei

The effect of ammonia exposure on energy metabolism and mitochondrial dynamic proteins in chicken thymus: Through oxidative stress, apoptosis, and autophagy

Ammonia (NH3) gas is an atmospheric pollutant, produced from different sources. In poultry houses NH3 is produced from the biological process of liter, manure, and protein composition. It has been well documented that NH3 adversely effects the health of chickens. However, the underlying mechanism of NH3 toxicity on chicken thymus is still unknown. Thymus is an important immune organ, which play a critical role in eliciting protective immune responses to ensure healing process and elimination of harmful stimuli. The results showed that NH3 exposure reduced antioxidant activities and induced oxidative stress in thymus tissues. Histological observation showed normal morphology of chicken thymus in control group. In contrast, increased number of nuclear debris, vacuoles, and cristae break were seen in NH3 affected chickens. Ultrastructural analysis indicated mitochondrial breakdown, disappearance, vacuoles, and chromatin condensation in NH3 treated groups. The mRNA and protein expression of apoptosis related genes were significantly enhanced in the chicken thymus of NH3 affected chickens compared to control group. Moreover, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay results suggested that NH3 exposure increased positive stained nuclei in the chicken thymus. Meanwhile, NH3 exposure reduced the number of CD8+ T-lymphocytes, decreased the adenosine triphosphate (ATPase) activities. The mRNA and protein expression of autophagy, energy metabolism, and mitochondrial dynamics proteins were altered by NH3 exposure. In summary, these results showed that NH3 induced oxidative stress, apoptosis and autophagic cell death (ACD), which could be the possible causes of immune damage and structural impairment in chicken thymus.

Effect of ammonia exposure and acclimation on the performance and the microbiome of anaerobic digestion

In this study, the effect of ammonia (NH3) as a disturbance on the microbial communities during anaerobic digestion (AD) was examined. NH3 was progressively added into 5 stabilized semi-continuous bio-reactors containing biowaste at 5 different NH3 loading rates until an inhibitory concentration was reached, and maintained at this concentration for 3 hydraulic retention times (75 days). The performance and the microbial community of the digesters were analyzed. The digesters performances were hindered at higher NH3 loading rates, marked by lower biogas productions and the accumulation of volatile fatty acids. At the microbial community level, changes depended on the NH3 loading rate. For instance, the digester with the highest NH3 loading rate showed a hydrogenotrophic methanogenic profile resulting from the growth of Methanosarcina spp. and acetate-consuming microorganisms, as well as the restricted growth of obligate acetoclastic archaea. This work can be helpful for the design of future acclimation strategies in AD.

Effects of atmospheric ammonia on the production performance, serum biochemical indices, and liver RNA-seq data of laying ducks

ABSTRACT 1. Ammonia is a toxic gas and an air pollutant of great concern. The effects of ammonia-induced damage in ducks are rarely reported. 2. A total of 176 laying ducks were randomly allocated to one of two groups with four replicates and were exposed to ammonia at 5 ± 5 ppm (low ammonia, LA) or 75 ± 5 ppm (high ammonia, HA), respectively, for 30 days. 3. The results showed that atmospheric ammonia exposure significantly decreased body weight and laying performance (P < 0.05). It significantly changed serum biochemical indices by increasing alanine aminotransferase and aspartate aminotransferase (P < 0.05), and decreasing superoxide dismutase activity (P < 0.05). Haematoxylin and eosin staining of hepatocytes revealed severe fatty degeneration. Results of RNA-seq analyses revealed that eight genes were significantly up-regulated in the HA group, which were involved in catalytic activity, single-organism metabolic processes, oxidation-reduction processes, and carbohydrate metabolic processes. 4. These results indicated that atmospheric ammonia exposure reduced production performance, affected serum biochemical indices, and led to severe fatty degeneration in the liver of laying ducks. Differentially expressed genes in liver indicated that there were effects of ammonia exposure on the metabolism and detoxification capabilities in ducks.

Effects of ammonia exposure on growth performance and cytokines in the serum, trachea, and ileum of broilers

This study investigated the effects of ammonia (NH3) exposure (0, 15, 25, and 35 ppm) on growth performance and cytokines in the serum, trachea, and ileum of broilers. A total of 288 22-day-old male broiler chickens were assigned to 4 treatment groups with 6 replicates of 12 chickens for a 21-D trial period. Growth performance and cytokines (IL-1β, IL-6, and IL-10) concentrations in the serum, trachea, and ileum were measured in response to 3, 7, 14, or 21 D of exposure to NH3. Correlations between cytokines in the serum, trachea, and ileum and growth performance, and between tracheal and ileal cytokines, were also analyzed. Results showed that exposure to 15 ppm NH3 did not influence the growth performance, but exposure to both 25 ppm and 35 ppm NH3 decreased the growth performance compared to that of the control group. Exposure to 15 ppm NH3 for 3 D increased IL-6 concentrations and induced an inflammatory response in the trachea and ileum, whereas exposure to 15 ppm NH3 for 7 D increased IL-10 concentrations and induced an anti-inflammatory response in the ileum. Exposure to 25 ppm NH3 induced an inflammatory response in the serum, trachea, and ileum after 3 D and induced an anti-inflammatory response in the ileum after 7 D. Exposure to 35 ppm NH3 for 3 D induced both inflammatory and anti-inflammatory responses in the trachea and ileum. Furthermore, increases in cytokines in the serum, trachea, or ileum were accompanied by a decrease in BW, ADFI, ADG, and an increase of feed/gain (F/G) from 7 D to 21 D. In addition, tracheal cytokine, especially IL-1β, was positively correlated with ileal cytokine IL-1β. These results indicated that the low growth performance associated with NH3 exposure may be due in part to an increase in cytokines, and the inflammatory response in the trachea and ileum may be related to cross-talk by cytokines such as IL-6, IL-10, and, in particular, IL-1β.

Effect of Ammonia Exposure on the Non-Specific Immunity of Fresh Water Pearl Mussel Hyriopsis cumingii

Ammonia-N, the principal end-product of protein catabolism, is an important environmental toxic factor in ponds. Elevated environmental ammonia-N is very toxic to aquatic animals and has a deleterious effect on their immune system. However, its effect on their immune system remains unclear. In this study, the effects of ammonia-N (0, 5, 10 and 30 mg/L) on immune responses of Fresh Water Pearl Mussel Hyriopsis cumingii were determined. When exposed to 5 mg/L ammonia-N lysozyme activity increased significantly. Superoxide dismutase activity was highest in the 5 mg/L group followed by the 10 mg/L group. The marked decrease of Lysozyme activity of Fresh Water Pearl Mussel Hyriopsis cumingii in 10 mg/L and 30 mg/L ammonia-N groups suggests that the higher concentrations of ammonia-N reduces or inhibits their non-specific immunity. Compared to the control group, superoxide dismutase activity in 30 mg/L ammonia also decreased significantly. When exposed to 5mg/L ammonia-N, catalase, acid phosphatase and alkaline phosphatase activity enhanced. In the 10 mg/L and 30 mg/L group, ammonia-N decreased significantly The lysozyme, catalase, acid phosphatase and alkaline phosphatase activity showed a similar tendency. This suggests that in H. cumingii immunostimulatory response is enhanced at low ammoniaN concentrations. The results of this study provide a theoretical basis for disease prevention in the freshwater pearl mussel.

Ammonia exposure and subsequent recovery trigger oxidative stress responses in juveniles of Brazilian flounder Paralichthys orbignyanus.

The effects of ammonia exposure and recovery on oxidative stress parameters and histology of juvenile Brazilian flounder Paralichthys orbignyanus were evaluated. The fish were exposed to 0.12, 0.28 and 0.57mgNH3-NL-1, plus a control, for 10days followed by the same recovery time in ammonia-free water. Gill, liver and muscle samples (n=9) were collected after 1, 5 and 10days of exposure and after recovery for oxidative stress analysis (antioxidant capacity against peroxyl radicals (ACAP); glutathione S-transferase (GST) activity; lipoperoxidation levels measured through thiobarbituric acid reactive substances (TBARS) content). For histological assessment, gill, liver and brain samples were collected. Exposure to all NH3-N concentrations induced different time- and dose-dependent changes in oxidative stress parameters. Reduced antioxidant capacity of the liver and muscle and enhanced TBARS levels in the gills and liver were demonstrated. Differently, a high ammonia concentration elicited lower hepatic TBARS levels. Enhanced GST activity in all organs and increased antioxidant capacity of the gills were also observed. No ammonia-induced histopathological effects were demonstrated. After recovery, most parameters (liver ACAP, GST activity in the muscle and liver and TBARS in the gills) returned to baseline levels. However, liver TBARS and gill GST activity remained altered 0.57mgNH3-NL-1 treatment. The recovery period also led to a decrease in gill antioxidant capacity and an increase in muscle antioxidant capacity. In conclusion, a concentration of 0.12mgNH3-NL-1 induces oxidative stress and antioxidant responses in juvenile Brazilian flounder. Moreover, a 10-day recovery period is not sufficient to restore fish homeostasis.

Effects of ammonia exposure on carcass traits and fatty acid composition of broiler meat.

We aimed to study the effects of ammonia on carcass traits, organ indices and fatty acid composition of broilers. Four hundred 21-d-old male Arbor Acres broilers with initial weight 563.52 ± 2.82 g were randomly allotted to 1 of 4 groups treated with ammonia at <3 mg/kg (control), 25 ± 3, 50 ± 3, and 75 ± 3 mg/kg concentrations. Each group consisted of 4 replicates of 25 birds. Broilers from 21 to 42 d were reared on the net floor in the respiration-metabolism chambers where similar environmental conditions were maintained. At 32 and 42 d of age, carcass traits and organ indices were determined for 4 birds per pen. At 42 d of age, fatty acid composition in the breast and thigh muscle of broilers was measured. Results showed as follows: 1) At 32 d, the dressing percentage of broilers exposed to 25 and 75 mg/kg ammonia were lower than those in the control group (P < 0.05); eviscerated yield percentage of broilers in the 25 mg/kg ammonia group was also lower (P < 0.05). At 42 d, the dressing percentage of broilers in the ammonia treatments and the thigh muscle percentage of broilers in the 50 and 75 mg/kg ammonia groups were lower (P < 0.05) than those in the control. Breast muscle percentage of broilers exposed to 25 and 50 mg/kg ammonia and eviscerated yield percentage exposed to 50 mg/kg ammonia were lower than those in the control (P < 0.05). 2) The kidney index of broilers (d 32) exposed to ammonia was greater (P < 0.05) than that of the control. At 42 d, hepatic index of broilers exposed to ammonia was increased (P < 0.05), and spleen index was decreased (P < 0.05). 3) At 42 d, stearic (C18:0) and saturated fatty acids (SFA) in the thigh muscle of broilers were higher, while the unsaturated fatty acid:saturated fatty acid (U:F) ratio and unsaturated fatty acid (UFA) were lower in the 50 mg/kg ammonia treatment than in the control group (P < 0.05). In conclusion, ammonia over 25 mg/kg could decline carcass traits and immune organ indices and increase the kidney and hepatic indices. Further, exposure to 50 mg/kg ammonia could also decrease breast and thigh muscle yield percentage while increasing SFA content and decreasing UFA content in the thigh muscle of broilers.

Ammonia and urea excretion in the swimming crab Portunus trituberculatus exposed to elevated ambient ammonia-N

In the present study of the swimming crab Portunus trituberculatus exposed to 0, 1, and 5mgL−1 NH4Cl, the effects of ammonia exposure on ammonia and urea content in hemolymph; activity of H+-ATPase (subunit A) and Na+/K+-ATPase (α-subunit) (NKA) in gills; mRNA expression levels of the crustacean Rh-like ammonia transporter (Rh), K+ Channel, Na+/K+/2Cl− co-transporter (NKCC), Na+/H+-exchanger (NHE), urea transporter (UT) and vesicle associated membrane protein (VAMP) in gills were investigated. The ultrastructure of gills was also evaluated. All these results in this study showed a dose-dependent effect with ammonia exposure concentration. The data displayed a significant increase in hemolymph ammonia and urea concentrations under ammonia exposure. The up-regulation of Rh mRNA together with up-regulation of K+-channel mRNA, NKA activity, down-regulation of NKCC and NHE mRNA suggested a coordinated protective response to maintain a relatively low ammonia concentration in the body fluids during ambient ammonia exposure. The up-regulation of VAMP, H+-ATPase activity along with the ultrastructure of gills suggested a mechanism of exocytotic ammonia excretion that may exit in the gill of P. trituberculatus. An increased production of urea and the up-regulated expression of UT suggested that the crab can detoxify elevated ammonia levels in the body fluids into urea when pathways of ammonia excretion are decreased after long term ammonia exposure.

Effects of ammonia exposure on nitrogen metabolism in gills and hemolymph of the swimming crab Portunus trituberculatus

Abstract The effects of ammonia-N (control, 1 and 5 mg L − 1 ) on nitrogen metabolism in gills and hemolymph of the swimming crab Portunus trituberculatus were investigated. The results showed that mRNA expression levels of Rh protein in gills were induced significantly by ammonia-N exposure. The levels of glutamine (Gln) and urea increased significantly in gills and hemolymph of P. trituberculatus exposed to high ammonia-N. After high ambient ammonia-N exposure, hemolymph ammonia increased significantly at 6 h and declined to control level at 12 h. The levels of Gln and urea in gills and hemolymph were significantly higher than control group during the whole exposure period and showed dose and time dependent effects. In addition, the activities of key-related enzymes involved in biosynthetic pathways of Gln and urea such as glutamate dehydrogenase (GDH), glutamine synthetase (GS) and Arginase (ARG) increased remarkably in the present study. This suggests that P. trituberculatus possesses some ammonia-detoxification strategies to cope with high ambient ammonia, including an up-regulation of Rh protein in gills and conversion ammonia to Gln and urea. The levels of Gln and urea in hemolymph could be considered as suitable physical indexes to evaluate ammonia toxicity to serve anti-ammonia selective breeding in the long run.

Acute effects of ammonia exposure on selected immunological and metabolic parameters in juvenile red claw crayfish (Cherax quadricarinatus)and the post-exposure recovery

The acute effects of ammonia exposure on selected immunological and metabolic parameters in juvenile red claw crayfish,Cherax quadricarinatus as well as the post-exposure recovery were studied by using Real-time PCR technique and biochemical assays.The crayfish were first exposed to ammonia for 3 d,then half of them were sampled and the other half were moved into aerated tap water for a 7 d post-exposure recovery.The results showed that a 3 d ammonia exposure had significant impact on the activities of ACP,AKP and SOD in the muscle of juvenile C.quadricarinatus.As ammonia concentration increased,the activities of these enzymes significantly decreased.At the highest concentration(16 mg/L),they decreased to 76%,68% and 62% of the control,respectively.The mRNA expression of mitochondrial manganese superoxide dismutase(mMnSOD),cytosolic MnSOD(cMnSOD),extracellular copper/zinc SOD(exCu/ZnSOD)also showed a decreasing trend following increased ammonia concentration.In contrast,the mRNA expression of catalase(CAT),glutathione peroxidase(GPX)and glutathione transferase(GST)in muscle remained unchanged compared to the control.Dissolved protein and triglycerides in hepatopancreas significantly decreased as ammonia concentration increased.At the highest concentration,they decreased to 72% and 59% of the control.AST showed a noble elevation which was 134% of the control in 12 mg/L group.After a 7 d post-exposure recovery,ACP and AKP activities returned to the normal level in ammonia treatments.On the contrary,the activities of SOD and GPX in all ammonia treatments were significantly higher than the control.The expression of antioxidant genes was higher than the control in all ammonia treatments.Metabolic parameters showed no differences between all groups.The results indicate that high levels of ammonia might suppress activities and gene expression patterns of immune-related enzymes,leading to a loss of defence mechanism.The crayfish which had been exposed to ammonia for 3 d could not fully recover after a 7 d post-exposure recovery and oxidative stress still existed in the muscle in C.quadricarinatus.

Growth and energy storage in juvenile fathead minnows exposed to metal mine waste water in simulated winter and summer conditions

Juvenile fathead minnows ( Pimephales promelas) were exposed from 10 to 100 days post-hatch (dph) to metal mining effluent under simulated summer (20 °C and 16/8 light/dark) or winter (4 °C and 8/16 light/dark) conditions in order to test the winter stress syndrome hypothesis. The condition factor of fish at 100 dph was similar between seasons, and was greater in the summer effluent exposure group compared to the summer control. Whole body triglycerides were lower in the effluent exposure group compared to control under winter conditions, but not summer. Whole body burdens of several trace metals, notably Cu, Rb and Se, were greater in the effluent exposed fish at 100 dph and displayed seasonal differences in bioaccumulation. Fathead minnows were also exposed from 10 to 100 dph to graded concentrations of ammonia (0.02–0.40 mg unionized NH 3/L) under summer conditions in order to investigate potential effects of this component of the effluent. There was no effect of ammonia exposure on growth parameters, but an increase in whole body triglycerides was observed at the highest exposure. The seasonal differences in bioaccumulation and biological responses suggest that winter conditions may be an important modifying factor in aquatic toxicological studies.

Ammonia toxicity to the brain: Effects on creatine metabolism and transport and protective roles of creatine

Hyperammonemia can provoke irreversible damage to the developing brain, with the formation of cortical atrophy, ventricular enlargement, demyelination or gray and white matter hypodensities. Among the various pathogenic mechanisms involved, alterations in cerebral energy have been demonstrated. In particular, we could show that ammonia exposure generates a secondary deficiency in creatine in brain cells, by altering the brain expression and activity of the genes allowing creatine synthesis (AGAT and GAMT) and transport (SLC6A8). On the other hand, it is known that creatine administration can exert protective effects in various neurodegenerative processes. We could also show that creatine co-treatment under ammonia exposure can protect developing brain cells from some of the deleterious effects of ammonia, in particular axonal growth impairment. This article focuses on the effects of ammonia exposure on creatine metabolism and transport in developing brain cells, and on the potential neuroprotective properties of creatine in the brain exposed to ammonium.

Social interactions, predation behaviour and fast start performance are affected by ammonia exposure in brown trout ( Salmo trutta L.)

In fish, fast starts are brief, sudden accelerations during predator–prey encounters. They serve for escape and predation and are therefore ecologically important movements. Fast starts are generated by glycolytic muscle performance and are influenced by many internal and external factors. It is known that ammonia pollution has a major effect on the glycolytic muscle action, thus creating conditions in which fast start performance might be reduced and predation rates altered. Therefore, escape response and predation strikes were investigated in brown trout ( Salmo trutta) of 10 and 20 cm body length exposed to an elevated (1 mg l −1) ammonia concentration for 24 and 96 h. Various locomotor and behavioural variables were measured. In C-starts, i.e. an escape start where the fish bends into a C-shaped position, ammonia exposure had no effect on response latency. After 96 h of exposure, cumulative distance, maximum swimming speed and turning radius of the prey were all significantly reduced and the escape went in no definite direction. The effect of ammonia exposure was more pronounced in large fish than in small fish. Predation strikes were also affected. Distance, speed and turning radius were significantly lower in exposed fish. Agonistic behaviour of dominant fish was significantly reduced and fish spent more time resting. Predator behaviour was also altered and the number of prey captured was reduced. This study shows that ammonia exposure affects brown trout escape response mainly through a reduction in fast start velocity and through an impairment of directionality. Thus, in addition to a reduced strength of the response, ammonia exposure could also reduce the fish’s elusiveness facing a predator. Predation rate and social interactions are disrupted and predator–prey relationships could be altered.

Chronic exposure to ammonia alters basal and NMDA-induced phosphorylation of NMDA receptor-subunit NR1

Hyperammonemia is responsible for many of the neurological alterations in patients with hepatic encephalopathy by mechanisms that remain unclear. Hyperammonemia alters phosphorylation of brain protein kinase C substrates and impairs N-methyl- d-aspartate (NMDA) receptor-associated signal transduction. The aim of this work was to analyze, in rat cerebellar neurons in culture, the effects of ammonia exposure on NMDA receptor phosphorylation, MK801 binding and surface expression. Ammonia reduces MK801 binding to NMDA receptors and the surface expression of the NR1 and NR2A subunits. As phosphorylation of serines in the NR1 C1 cassette has been implied in receptor trafficking, we assessed whether hyperammonemia alters phosphorylation of these serines. Basal phosphorylation of serines 890, 896 and 897 was increased in neurons exposed to ammonia, while NMDA-induced phosphorylation of S896 and S897 was reduced. Exposure to ammonia also increased basal phosphorylation of Akt but reduced NMDA and BDNF stimulation of Akt phosphorylation. These results suggest that alterations in receptor surface expression and possibly the phosphorylation state of the NR1 subunit of NMDA receptors may contribute to the impairment by ammonia of signal transduction pathways modulated by NMDA receptors.

Operant responses of pigs to atmospheric ammonia

The motivation of Duroc×Landrace pigs, Sus scrofa, to avoid acute exposure to two concentrations of atmospheric ammonia was assessed using operant conditioning. On a fixed interval concurrent avoidance schedule, where each response (root) made on one operant manipulandum was followed by exposure to puffs of ammonia at 100 ppm, six food-motivated pigs initially avoided rooting for food reinforcement on the ammoniated manipulandum; a control manipulandum, vented only with fresh air, was preferred instead (42 and 16 roots, five and 13 reinforcements respectively; P<0.001 in each case). This initial aversion was followed by rapid acclimatization over 20 daily sessions, each lasting for 90 min ( P<0.001). The acclimatization was independent of an underlying reduction in the number of roots ( P=0.033). On a variable interval passive avoidance schedule, 12 food-motivated pigs only received food reinforcement in the presence of ammonia. Acute exposure to ammonia at a peak concentration of either 40 or 100 ppm did not influence the overall amount of food consumed ( P>0.05). However, significantly more roots were made and more food reinforcements were received in fresh air and 40 ppm ammonia than in 100 ppm ammonia (345, 365 and 241 roots, respectively, P=0.046; 43, 50 and 37 reinforcements respectively, P=0.02). This aversion was stronger after repeated testing over eight daily sessions ( P<0.001), each lasting for 90 min, yet many roots were still made and reinforcements were received on each manipulandum. The initial avoidance of 100 ppm ammonia under a concurrent operant conditioning schedule was due to the irritant rather than novel effects of ammonia exposure. This aversion was however, weak. Ammonia at 100 ppm was not completely avoided and acclimatization was rapid.