ReviewMetabolic brain disease2005
Protein tyrosine nitration in hyperammonemia and hepatic encephalopathy.
Review in Metabolic brain disease, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 38 citations in OpenAlex.
- Hepatic encephalopathy.Nature reviews. Disease primers · 2022Review
- Disturbance of the Glutamate-Glutamine Cycle, Secondary to Hepatic Damage, Compromises Memory Function.Frontiers in neuroscience · 2021Review
- Emerging Roles of Carbonyl Sulfide in Chemical Biology: Sulfide Transporter or Gasotransmitter?Antioxidants & redox signaling · 2018Review
- Neurotoxicity of Ammonia.Neurochemical research · 2017Review
- Changes of the thioredoxin system, glutathione peroxidase activity and total antioxidant capacity in rat brain cortex during acute liver failure: modulation by L-histidine.Neurochemical research · 2015Article
- Phosphodiesterase-5 Inhibitors: Action on the Signaling Pathways of Neuroinflammation, Neurodegeneration, and Cognition.Mediators of inflammation · 2015Review
- Article
- Neuroinflammation and neurodegeneration in adult rat brain from binge ethanol exposure: abrogation by docosahexaenoic acid.PloS one · 2014Article
- Current pathogenetic aspects of hepatic encephalopathy and noncirrhotic hyperammonemic encephalopathy.World journal of gastroenterology · 2013Review
- Brain energy metabolism and mitochondrial dysfunction in acute and chronic hepatic encephalopathy.Neurochemistry international · 2012Review
- Ammonia increases paracellular permeability of rat brain endothelial cells by a mechanism encompassing oxidative/nitrosative stress and activation of matrix metalloproteinases.Journal of neurochemistry · 2012Article
- Hepatic encephalopathy: An approach to its multiple pathophysiological features.World journal of hepatology · 2012Article
- Exploratory investigation on nitro- and phospho-proteome cerebellum changes in hyperammonemia and hepatic encephalopathy rat models.Metabolic brain disease · 2012Article
- Signaling factors in the mechanism of ammonia neurotoxicity.Metabolic brain disease · 2009Review
- Effect of glutamine synthesis inhibition with methionine sulfoximine on the nitric oxide-cyclic GMP pathway in the rat striatum treated acutely with ammonia: a microdialysis study.Neurochemical research · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic encephalopathy is seen as a clinical manifestation of a chronic low grade cerebral edema, which is thought to trigger disturbances of astrocyte function, glioneuronal communication, and finally HE symptoms. In cultured astrocytes, hypoosmotic swelling triggers a rapid oxidative stress response, which involves the action of NADPH oxidase isoenzymes, followed by tyrosine nitration of distinct astrocytic proteins. Oxidative stress and protein tyrosine nitration (PTN) are also observed in response to ammonia, inflammatory cytokines, such as TNF-alpha or interferons, and benzodiazepines with affinity to the peripheral benzodiazepine receptor (PBR). NMDA receptor activation was identified as upstream event in protein tyrosine nitration (PTN). Cerebral PTN is also found in vivo after administration of ammonia, benzodiazepines or lipopolysaccharide and in portocaval shunted rats. PTN predominantly affects astrocytes surrounding cerebral vessels with potential impact on blood-brain-barrier permeability. Among the tyrosine-nitrated proteins, glutamine synthetase, GAPDH, extracellular signal-regulated kinase and the PBR were identified. PTN of glutamine synthetase is associated with inactivation of the enzyme. Thus, factors known to trigger hepatic encephalopathy induce oxidative/nitrosative stress on astrocytes with protein modifications through PTN. The pathobiochemical relevance of astrocytic PTN for the development of HE symptoms remains to be established.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.