Pufferfish Aquariums
Ramasamy Santhanam in Biology and Ecology of Toxic Pufferfish, 2017
Nitrogen cycle: It is the basic process of biological filtration in the aquarium. Ammonia is one of the key elements in the nitrogen cycle. Fish produce ammonia directly both as a by-product of respiration and as a waste product from the digestion of foods. Solid wastes are also converted into ammonia. It is therefore important to remove these solid wastes through mechanical filtration. Uneaten food, plant materials, and other organic items that decay in the tank are also converted to ammonia. This ammonia, a nitrogen-based compound, is extremely toxic. In any aquarium, it can build up quickly and threaten all the fish in the tank. The bacteria already accumulated in the gravel bed of the aquarium help in this regard. Nitrosomonas sp. will first act upon the ammonia (in the presence of dissolved oxygen) and convert the same into nitrite, a toxic compound. This compound in the long run tends to be a larger problem than ammonia. Subsequently another species of bacteria viz. Nitrobacter sp. converts it into nitrate, a relatively harmless compound that can be used up by plants and algae.
Acid/base balance
Bernie Garrett in Fluids and Electrolytes, 2017
When an H+ ion is secreted into the ultrafiltrate in the nephron tubule, a Na+ ion is simultaneously exchanged. This is an active process using adenosine triphosphate, and is important as it rids the body of excess acid, helps maintain pH, maintains ionic equivalence, conserves sodium, and also regenerates sodium bicarbonate for buffering. Once in the ultrafiltrate, the transport of H+ ions tends to occur by one of three methods.12,15,27 H+ ions may bind with bicarbonate to form carbonic acid and then break down into CO2 and H2O in the ultrafiltrate. Alternatively, ammonia (NH3) may be utilized as a vehicle for losing H+ ions. NH3 reacts with an H+ ion in the form ammonium (NH4) in the ultrafiltrate, combining with Cl− ions to form NH4Cl. Lastly, the phosphate buffer system may come into play, in which hydrogen phosphate (HPO42−) in the ultrafiltrate acts as an H+ acceptor, forming H2PO4− (see Figure 5.2).15,73
Liver physiology
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
The nitrogenous end-product of ammonia is ammonia. Surplus ammonia is toxic in concentrations greater than 1 ug/ml and it is converted to urea for excretion by the kidneys. Urea is synthesised from ammonia in the liver by the urea cycle, an energy-dependent process utilizing three ATP molecules per urea molecule synthesised. The nitrogenous end of ammonia combines with carbon dioxide in the liver cell mitochondria to form carbamyl phosphate, which subsequently reacts with ornithine to form citruliine (Figure 6.7). Citrulline then reacts with aspartate to form arginine, which is hydrolysed to yield water, ornithine and urea. About 30 g of urea is produced daily from 100 g of protein contained in the diet. As two hydrogen ions are produced for each molecule of urea synthesized, about 1000 mmol of hydrogen ions are formed. This H+ production may be important in neutralizing the alkali load resulting from the metabolism of neutral amino acids.
Liver transcriptome analysis reveals biological pathways and transcription factors in response to high ammonia exposure
Published in Inhalation Toxicology, 2022
Daojie Li, Shuangzhao Chen, Chun Liu, Baoxing Wei, Xiaoping Li
Ammonia is an air pollutant that can cause environmental problems, and it is also a toxic gas that can cause tissue damages in humans and animals. Ammonia in livestock farms can damage the respiratory system by direct inhalation (Wang, Wang, Chen, et al. 2020). Ammonia also affected many other organs through blood circulation system (An et al. 2019; Xing et al. 2019; Xu et al. 2020; Han et al. 2020a). Liver is an important organ for nutrient metabolism and detoxification (Reinke and Asher 2016). The pig liver is a suitable model to study the toxicity of ammonia to human liver (Lada et al. 2020). Transcriptomics is an important tool that can provide an effective information on the mechanisms of body response to environmental stresses. Through RNA extraction, fragmentation, capture, and sequencing, we can obtain the gene expression levels of the whole genome and find the key biological processes and key genes (Owens et al. 2019). Previous studies showed that a concentration of 20 ppm ammonia did not change hepatic gene expression in pigs (Cheng et al. 2014); however, ammonia at a concentration of 118–122 ppm caused liver damage and dysfunction by altering gene networks associated with oxidative stress and immune function in pigs (Zeng et al. 2021). In the present study, we explored hepatic transcriptional changes and identified some genes that may perform key biological functions in response to 80 ppm ammonia exposure in pigs.
Major component causing neurological toxicity in acute glufosinate ammonium poisoning: determination of glufosinate, 1-methoxy-2-propanol, and ammonia in serum and cerebrospinal fluid
Published in Clinical Toxicology, 2022
Seonghoon Yeon, Sung Hwa Kim, Juhyun Sim, Sunchun Kim, Yoonsuk Lee, Hyun Kim, Yong Sung Cha
We observed that in patients with GLA poisoning who developed neurological symptoms, the concentration of ammonia in the serum and the CSF was highly associated with the onset of neurological symptoms. Ammonia is a highly toxic substance, even in sub-millimolar concentrations [18], and its intracellular accumulation causes tissue necrosis and death [2]. The higher concentration of ammonia in the CSF than in the serum may be explained through the process of “ammonia trapping.” Increased levels of ammonia in the serum result in increased ammonia in the CNS through diffusion. If the amount of ammonia in the brain exceeds the removal capacity of the GS in the brain, which is largely responsible for the removal of both serum-derived and metabolically generated ammonia [19], ammonia gets “trapped,” resulting in more severe negative side effects in the brain. The increase in the CSF ammonia levels seen in GLA poisoning seems to follow a pathway similar to that seen in hepatic encephalopathy, which may occur in patients with liver cirrhosis.
Identifying areas of improvement in nursing knowledge regarding hepatic encephalopathy management
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Aalam Sohal, Victoria Green, Sunny Sandhu, Marina Roytman
- The pathophysiology of hepatic encephalopathy is multifactorial. The hypothesized neurotoxins include ammonia, tyramine, octopamine, manganese, GABA, etc., [1]; however, ammonia is the most widely recognised toxin. Ammonia is produced by the bacteria in the gastrointestinal tract and is cleared by liver. In the setting of cirrhosis, combination of declining liver function and portosystemic shunting leads to decreased ammonia clearance [11]. The ammonia crosses the blood brain leading to neuropsychiatric effects [12]. Although most of the nursing staff in our survey elected ammonia, some additionally chose urea which is not one of the toxins associated with OHE. We believe that improving the knowledge of the nursing staff on the pathogenesis of OHE would help in effective management of these complex patients during the hospitalization and after discharge.
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