glutamate dehydrogenase/edema

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Inhibition of glutamine synthesis induces glutamate dehydrogenase-dependent ammonia fixation into alanine in co-cultures of astrocytes and neurons.

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It has been previously demonstrated that ammonia exposure of neurons and astrocytes in co-culture leads to net synthesis not only of glutamine but also of alanine. The latter process involves the concerted action of glutamate dehydrogenase (GDH) and alanine aminotransferase (ALAT). In the present

Morphology and mitochondrial function of the surviving myocardium following myocardial infarction in the cat.

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The surviving myocardium of the cat was studied 7 days and 6 weeks following experimental infarction. Seven days after infarction, ultrastructural alterations of the mitochondria indicative of slight hypoxic injury--clearing of the matrix and loss of dense matrix granules--were found. Together with

Ischemic tolerance in an in vivo model of glutamate preconditioning.

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Ischemia initiates a complicated biochemical cascade of events that triggers neuronal death. This study focuses on glutamate-mediated neuronal tolerance to ischemia-reperfusion. We employed an animal model of lifelong excess release of glutamate, the glutamate dehydrogenase 1 transgenic (Tg) mouse,

[Hyperextension of fetlock joints in German Holstein and German Holstein-Limousin crossbred calves].

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In two different dairy farms six calves exhibiting bilateral flexion of the fetlock joints in front or rear legs were born in 2000 to 2002. Four of the affected calves from the same farm were crossbred between German Holstein cows with red and white coat colour and a bull of the breed Limousin. The

Haematology, blood biochemistry, parasites and pathology of common eider (Somateria mollisima) males during a mortality event in the Baltic.

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A mortality event at the Christiansø colony in the Baltic proper killed 115 common eiders (Somateria mollissima) in mid-May 2016. To complement previous studies of incubating females, 39 males were necropsied and from a subsample of these a biochemical and haematological profile was obtained. The

Brain alanine formation as an ammonia-scavenging pathway during hyperammonemia: effects of glutamine synthetase inhibition in rats and astrocyte-neuron co-cultures.

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Hyperammonemia is a major etiological toxic factor in the development of hepatic encephalopathy. Brain ammonia detoxification occurs primarily in astrocytes by glutamine synthetase (GS), and it has been proposed that elevated glutamine levels during hyperammonemia lead to astrocyte swelling and

Acute Alpha-Naphthylisothiocyanate-induced Liver Toxicity in Germfree and Conventional Male Rats.

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Differences in the responses of conventional and germfree male Sprague-Dawley rats to acute injury induced by alpha-naphthylisothiocyanate (ANIT), a well-characterized biliary epithelial toxicant, were evaluated. Conventional and germfree rats were dosed once orally with 50 mg/kg of ANIT or corn oil

Ammonium metabolism in humans.

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Free ammonium ions are produced and consumed during cell metabolism. Glutamine synthetase utilizes free ammonium ions to produce glutamine in the cytosol whereas glutaminase and glutamate dehydrogenase generate free ammonium ions in the mitochondria from glutamine and glutamate, respectively.

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