ammonia brands

Molecular formula: H3N

Renal excretion and metabolism of ammonia is critical in regulation of acid-base balance by generating bicarbonate ions and promoting renal net acid excretion, both under basal conditions and in response to acid-base disturbances. There is evidence that acute ammonia exposure activates NMDA receptor signalling pathways, and high concentrations of ammonia resulting from urea cycle enzyme deficiencies are associated with changes in astrocyte morphology due to glutamine accumulation, changes in the expression of key astrocyte proteins, and increased concentrations of neuroactive L-tryptophan metabolites. ... Ammonia plays a key role in the pathogenesis of hepatic encephalopathy, which manifests as a neuropsychiatric syndrome accompanying acute and chronic liver failure. One consequence of ammonia action on the brain is astrocyte swelling, which triggers the generation of oxidative/nitrosative stress at the level of NADPH oxidase, nitric oxide synthases and the mitochondria. A self-amplifying signaling loop between oxidative stress and astrocyte swelling has been proposed. Consequences of the ammonia-induced oxidative/nitrosative stress response are protein modifications through nitration of tyrosine residues and oxidation of astrocytic and neuronal RNA. Nitrosative stress also mobilizes zinc from intracellular stores with impact on gene expression. These alterations may at least in part mediate cerebral ammonia toxicity through disturbances of intracellular and intercellular signaling and of synaptic plasticity. Oxidative/nitrosative stress and a low-grade cerebral edema as key events in the pathogenesis of ammonia toxicity and hepatic encephalopathy may offer potential new strategies for treatment. Ammonia-induced oxidation of RNA and proteins may impair postsynaptic protein synthesis, which is critically involved in learning and memory consolidation. RNA oxidation offers a novel explanation for multiple disturbances of neurotransmitter systems and gene expression and the cognitive deficits observed in hepatic encephalopathy. SRP: Ammonia in an aqueous environment exists in equilibrium between ionized ammonium cation and the non-ionized ammonia. This equilibrium can be affected by buffers, pH, temperature, and salinity. Thus in many cases it is not possible to assign the associated toxicity to the ionized or non-ionized form of the ammonia-nitrogen. /Aqueous ammonia/ Mechanisms involved in hepatic encephalopathy (HE) still remain poorly understood. It is generally accepted that ammonia plays a major role in this disorder, and that astrocytes represent the principal target of ammonia neurotoxicity. In recent years, studies from several laboratories have uncovered a number of factors and pathways that appear to be critically involved in the pathogenesis of this disorder. Foremost is oxidative and nitrosative stress (ONS), which is largely initiated by an ammonia-induced increase in intracellular Ca(2+). Such increase in Ca(2+) activates a number of enzymes that promote the synthesis of reactive oxygen-nitrogen species, including constitutive nitric oxide synthase, NADPH oxidase and phospholipase A2. ONS subsequently induces the mitochondrial permeability transition, and activates mitogen-activated protein kinases and the transcription factor, nuclear factor-kappaB (NF-kappaB). These factors act to generate additional reactive oxygen-nitrogen species, to phosphorylate various proteins and transcription factors, and to cause mitochondrial dysfunction. This article reviews the role of these factors in the mechanism of HE and ammonia toxicity with a focus on astrocyte swelling and glutamate uptake, which are important consequences of ammonia neurotoxicity.... A new model for ammonia excretion in freshwater fish and its variable linkage to Na(+) uptake and acid excretion /is proposed/. In this model, /the Rhesus protein/ Rhag facilitates NH(3) flux out of the erythrocyte, Rhbg moves it across the basolateral membrane of the branchial i

Source: PubChem (NCBI) · compound 222