Journal ArticleDOI
Chronic hyperammonemia prevents changes in brain energy and ammonia metabolites induced by acute ammonium intoxication
TLDR
It is shown that chronic hyperammonemia markedly prevents the alterations of the contents of energy and ammonia metabolites induced by acute ammonium intoxication and the mitochondrial NAD+/NADH ratio.About:
This article is published in Biochimica et Biophysica Acta.The article was published on 1993-01-22. It has received 53 citations till now. The article focuses on the topics: Hyperammonemia & Ammonium acetate.read more
Citations
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Journal ArticleDOI
Neurobiology of ammonia
TL;DR: Therapy in hyperammonemic syndromes continues to rely on ammonia-lowering strategies via peripheral mechanisms (reduction of ammonia production in the gastrointestinal tract, increased ammonia removal by muscle).
Journal ArticleDOI
Superoxide Production and Antioxidant Enzymes in Ammonia Intoxication in Rats
TL;DR: Both diminished activity of antioxidant enzymes and increased superoxide radical production could lead to oxidative stress and cell damage, which could be involved in the mechanism of acute ammonia toxicity.
Journal ArticleDOI
Brain ATP depletion induced by acute ammonia intoxication in rats is mediated by activation of the NMDA receptor and Na+,K(+)-ATPase.
Elena Kosenko,Yuri Kaminsky,Eugenio Grau,María-Dolores Miñana,Goizane Marcaida,Santiago Grisolia,Vicente Felipo +6 more
TL;DR: The results obtained suggest that ammonia‐induced ATP depletion is mediated by activation of the NMDA receptor, which results in decreased protein kinase C‐mediated phosphorylation of Na+,K+‐ATPase and, therefore, increased activity of the ATPase and increased consumption of ATP.
Journal ArticleDOI
Blocking NMDA receptors prevents the oxidative stress induced by acute ammonia intoxication
TL;DR: It is shown that MK-801, an antagonist of NMDA receptors prevents ammonia-induced changes in superoxide dismutase, glutathione peroxidase and catalase, suggesting that oxidative stress can play a role in the mechanism of ammonia toxicity.
Journal ArticleDOI
Glutamatergic and gabaergic neurotransmission and neuronal circuits in hepatic encephalopathy
Omar Cauli,Regina Rodrigo,Marta Llansola,Carmina Montoliu,Pilar Monfort,Blanca Piedrafita,Nisrin El Mlili,Jordi Boix,Ana Agusti,Vicente Felipo +9 more
TL;DR: This work reviews the alterations in the function of the neuronal circuits between basal ganglia-thalamus-cortex modulating motor activity and the role of sequential alterations in glutamatergic and GABAergic neurotransmission in these alterations.
References
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Book
Methods of Enzymatic Analysis
TL;DR: Methods of enzymatic analysis, Methods of enzymes analysis, the authors, Methods of enzyme analysis, enzymatics, methods of enzymes, and methods of analysis, method of enzymes.
Journal ArticleDOI
The Redox State of Free Nicotinamide-Adenine Dinucleotide in the Cytoplasm and Mitochondria of Rat Liver
TL;DR: The bearing of these findings on various problems, including the number of NAD(+)-NADH pools in liver cells; the applicability of the method to tissues other than liver; the transhydrogenase activity of glutamate dehydrogenase; the physiological significance of the difference of the redox states of mitochondria and cytoplasm; aspects of the regulation of theredox state of cell compartments; the steady-state concentration of mitochondrial oxaloacetate.
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Effect of acute ammonia intoxication on cerebral metabolism in rats with portacaval shunts.
TL;DR: The findings indicate that cerebral dysfunction in chronic, relapsing ammonia intoxication is not due to primary energy failure, and is suggested that ammonia-induced depletion of glutamic and aspartic acids, and inhibition of the malate-asparate hydrogen shuttle are the dominant neurochemical lesions.
Journal ArticleDOI
Kinetic evidence for multiple binding sites on phosphofructokinase.
TL;DR: The kinetic findings have been interpreted to indicate the presence of not less than seven substrate, inhibitor, and deinhibitor sites (and possibly as many as 12) in the formulation of P-fructokinase, and it would appear that these sites are so arranged that the addition of one inhibitor (ATP) makes it easier to add the other