Rise In Ammonia Levels Research Articles

Taurine can play a positive role in growth, liver health and resistance to Aeromonas hydrophila of yellow catfish Pelteobagrus fulvidraco exposed to ammonia stress for a long time

Ammonia is an important environmental pollutant that is toxic to most aquatic animals, and nutrient manipulation is an effective regulatory pathway. To assess the influence of taurine supplementation on growth, liver detoxification and anti-bacterial infection of yellow catfish subjected to ammonia exposure for a long time, three experiment diets with different taurine levels (0.50, 1.00, and 2.00 %) were formulated and fed to fish (7.28 ± 0.05) g under three ammonia levels (0.00, 25.00 and 50.00 mg/L total ammonia nitrogen) for 56 days. The results showed that hepatic glycogen and whole-body protein contents were reduced, suggesting that energy deficiency caused by ammonia poisoning plays an important role in growth inhibition; elevated serum alanine aminotransferase and aspartate aminotransferase levels suggest liver injury, which may be caused by oxidative stress (decreased activities of superoxide dismutase and catalase, and expressions of SOD and CAT) and inflammation (increased contents of tumor necrosis factor α, interleukin 1 and interleukin 8, and expressions of TNF α, IL 1 and IL8), analysis of tissue sections further confirmed this finding. Furthermore, after injection with Aeromonas hydrophila, cumulative mortality increased proportionally with the rise in ammonia levels, the observed decrease in serum complements C3, C4, immunoglobulin M, and antibody titer contents emerged as a crucial factor contributing to the decreased disease resistance. The exogenous taurine was found to alleviate the negative impact of the above-mentioned ammonia poisoning. This study provides valuable insights into the mechanism of ammonia-induced aquatic toxicology in fish.

THE EFFECT OF DIFFERENT ZONING IN A CLOSED-HOUSE CAGE ON MICROCLIMATE CONDITIONS AND BROILER PERFORMANCE

Closed-house cages have zones in them that have different conditions. Zoning in cages has different temperatures, humidity, speed, and ammonia levels and affects broiler performance. This study aims to determine the effect of different zoning on microclimate conditions and broiler performance in closed-house cages. This research was carried out from June 9, 2023 – to July 6, 2023, at the closed-house cage “Chicken Farm Janna” in Taipa Village, North Palu District, Palu City, Central Sulawesi Province. This study used 396 broiler samples aged 1-28 days with a DOC (Day-old chick) weight of ± 37 grams/head. The strain used is Lohman produced by PT. Japfa Comfeed Indonesia. This study used a t-test with 2 treatments and 9 repeats. The treatment studied is Z1 = Zone 1-60 meters from the inlet and Z2 = Zone 60-120 meters from the inlet. The results of the t-test show that different zoning has a significant influence (t count >t table) on microclimate conditions and broiler performance in closed-house cages. Different zoning exerts a real influence on microclimate conditions and the performance of broilers in closed-house cages. In the closed house cage, the zone opposite the inlet (zone 2) results in a temperature rise, a rise in ammonia levels, a drop in humidity, a loss in body weight, and an increase in mortality.

Ammonia Level and Mortality in Acute Liver Failure: A Single-Center Experience.

BACKGROUND Acute liver failure (ALF) is an emergent condition that requires intensive care and manifests in particular by significant elevation in serum ammonia level. Patients with ALF with concomitant renal failure experience a further rise in ammonia levels due to decreased kidney excretion. The aim of this study was to evaluate the relationship between elevated ammonia levels and mortality and to characterize the subgroup of ALF patients who develop acute kidney injury (AKI) and require renal replacement therapy. MATERIAL AND METHODS This was a retrospective study of 36 consecutive patients admitted to Johns Hopkins Hospital's intensive care units from December 2008 to May 2013 who presented with grade III and IV hepatic encephalopathy (HE). Patients who developed AKI and required hemodialysis (HD) were compared to those without AKI. Patients with chronic kidney disease were excluded. RESULTS Sixteen patients developed AKI and underwent HD (HD group). Median ammonia levels in the HD and non-HD groups were not significantly different (p=0.95). In the HD group, 4 patients underwent liver transplantation (LT) and 3 of them survived the hospitalization. Among the 12 HD patients who did not receive LT, 6 (50%) survived. Out of 20 non-HD patients, 3 were transplanted, all of whom survived the hospitalization. Among the 17 non-HD patients who did not receive LT, 14 (82%) survived. Admission ammonia level (>120 µmol/L) was associated with higher mortality rate (OR=7.188 [95% CI 1.3326-38.952], p=0.026) in all patients. CONCLUSIONS Admission ammonia level is predictive of mortality in ALF patients with grade 3-4 HE.

Enhanced renal vein ammonia efflux after a protein meal in the pig

Background/Aims: The intake of dietary protein has been associated with increased arterial ammonia levels. However, the origin of this rise in ammonia levels is unknown. This study was designed to examine whether this increase is caused by ammonia formed by the gut escaping hepatic clearance, or ammonia formed by the kidney and subsequently released into the circulation. Methods: Splanchnic and renal fluxes of ammonia and amino acids were studied in 10 pigs that were fed in a randomized cross-over design with a protein meal ( n=8), a meal with an equimolar amount of free amino acids ( n=8) or an iso-osmolar NaCl solution ( n=6). Results: After the protein meal, and less pronounced after the amino acid meal, arterial ammonia levels increased from approximately 25 to 75 μmol/l. Arterial pH changes and splanchnic ammonia release were negligible. The renal vein ammonia efflux increased after the protein meal (0.67±0.10 to 1.94±0.35 μmol/kg bw/min) and to a lesser degree after the amino acid meal (to 1.20±0.39 μmol/kg bw/min). Renal uptake of alanine, and not glutamine, increased stoichiometrically, paralleling the enhanced renal vein ammonia efflux. Conclusions: Arterial ammonia increases after a meal in pigs, coinciding with a negligible splanchnic ammonia release, but increased renal vein ammonia efflux. Thus, post-prandial plasma ammonia levels appear to be mainly related to renal ammoniagenesis. Alanine appears to be the main precursor for this renal ammoniagenesis in the pig.

In vitro ammonia utilization and urea synthesis by rat liver after portacaval shunt.

The objective of this study was to study in vitro ammonia utilization and urea synthesis by the rat liver after portacaval shunt (PCS) in comparison to controls. This study is part of a series of experiments to investigate metabolic derangements in the liver following PCS. Sixteen male Wistar rats weighing 150-230 g were used. PCS was performed on 8 and the rest served as sham-operated controls. The experiments were performed 4 weeks postoperatively. The usually monitored postoperative parameters after PCS like body weight, rise in ammonia levels in the peripheral blood, atrophy of mesenteric fat, atrophy of the liver, etc., were comparable to other PCS series. Liver slices (1 x 2 x 1 mm) were prepared from each rat liver and incubated in Krebs-Henseleit buffer. After incubation, ammonia utilization in the controls was 162.88+/-20.12 micromol/g dry weight/h while in PCS rats it was 81.35+/-2.64 micromol/g dry weight/h (p < 0.0001). The rate of urea synthesis in controls was 122.54+/-12.93 micromol/g dry weight/h whereas in the PCS group it was 14.99+/-2.21 micromol/g dry weight/h (p < 0.0001). These results indicate a significant decline in the capacity of the liver for ammonia utilization as well as urea synthesis after PCS.

Hyperglucagonemia and Hyperammonemia: Which Is the Chicken and Which the Egg?

Elevated plasma ammonia level in hepatic cirrhosis has been attributed to a lack ofconversion of enteric ammonia into urea or to its entry into systemic circulation via portasystemic shunting, or to both. It is exaggerated by excessive protein intake. Because hyperglucagonemia is well documented in cirrhosis and a protein meal is an effective glucagon secretogogue, plasma glucose, insulin, glucagon, and ammonia levels were determined in 50 cirrhotic patients after an overnight fast. Effects of a protein meal were also assessed in 20 of these patients. Plasma glucose was normal and remained unaltered after a protein meal. Insulin, glucagon and ammonia levels were elevated, but only in patients with advanced liver dysfunction. Ammonia levels correlated significantly with glucagon (r = 0.61, p &lt; 0.001), but not with insulin or glucose levels. Insulin and glucagon levels rose after a protein meal in all patients and controls, whereas a significant rise in the ammonia level occurred only in decompensated cirrhotics. Elevation of the ammonia level was significantly correlated with fasting glucagon (r = 0.54, p &lt; 0.05), as well as with glucagon response (r = 0.65, p &lt; 0.01), but not with basal insulin or insulin response. Furthermore, the rise in ammonia level occurred too early to be accounted for by enteric generation. Finally, direct effects of glucagon administration on plasma glucose and serum ammonia were examined in 15 cirrhotic patients. Glucose response was significantly blunted in cirrhotic patients as compared with normal subjects, whereas serum ammonia rose promptly but only in cirrhotics with maximum rise being noted in cirrhotic patients with advanced liver dysfunction. This study, therefore, suggests that hyperglucagonemia may contribute significantly to hyperammonemia in hepatic cirrhosis.

Elevated plasma ammonia level in hepatic cirrhosis: Role of glucagon

Elevated plasma ammonia level in hepatic cirrhosis has been attributed to a lack of conversion of enteric ammonia into urea or to its entry into systemic circulation via portasystemic shunting, or to both. It is exaggerated by excessive protein intake. Because hyperglucagonemia is well documented in cirrhosis and a protein meal is an effective glucagon secretogogue, plasma glucose, insulin, glucagon, and ammonia levels were determined in 50 cirrhotic patients after an overnight fast. Effects of a protein meal were also assessed in 20 of these patients. Plasma glucose was normal and remained unaltered after a protein meal. Insulin, glucagon, and ammonia levels were elevated, but only in patients with advanced liver dysfunction. Ammonia levels correlated significantly with glucagon (r = 0.61, p < 0.001), but not with insulin or glucose levels. Insulin and glucagon levels rose after a protein meal in all patients and controls; whereas a significant rise in the ammonia level occurred only in decompensated cirrhotics. Elevation of the ammonia level was significantly correlated with fasting glucagon (r = 0.54, p < 0.05), as well as with glucagon response (r = 0.65, p < 0.01), but not with basal insulin or insulin response. Furthermore, the rise in ammonia level occurred too early to be accounted for by enteric generation. Finally, direct effects of glucagon administration on plasma glucose and serum ammonia were examined in 15 cirrhotic patients. Glucose response was significantly blunted in cirrhotic patients as compared with normal subjects, whereas serum ammonia rose promptly but only in cirrhotics, with maximum rise being noted in cirrhotic patients with advanced liver dysfunction. This study, therefore, suggests that hyperglucagonemia may contribute significantly to hyperammonemia in hepatic cirrhosis.