Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.4.1.2 (glutamate dehydrogenase)
 4,380 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper concerns an enzymological investigation into a putative feline analogue of the human autosomal recessive disease primary hyperoxaluria type 2. The hepatic activities of D-glycerate dehydrogenase, using both D-glycerate and hydroxypyruvate as substrates, and glyoxylate reductase, which are the deficient enzyme activities in human primary hyperoxaluria type 2, were markedly depleted in four affected cats (0-6% of controls). The activities of a number of other enzymes, lactate dehydrogenase, glutamate dehydrogenase, D-amino acid oxidase, aspartate:2-oxoglutarate amino-transferase, glutamate:glyoxylate aminotransferase and alanine:glyoxylate aminotransferase (the deficient enzyme in primary hyperoxaluria type 1) were unaltered. The intracellular distribution of D-glycerate dehydrogenase and glyoxylate reductase in cat liver was shown to be cytosolic, as they are in human liver. The activities of D-glycerate dehydrogenase and glyoxylate reductase were determined in unaffected related cats and putative heterozygotes were identified. The correlation between D-glycerate dehydrogenase and glyoxylate reductase activities in the related cats and their combined deficiency in the affected cats confirmed previous suggestions that they are identical gene products.
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PMID:Enzymological characterization of a feline analogue of primary hyperoxaluria type 2: a model for the human disease. 251 73

The activities of 13 liver and 6 brain enzymes were studied in 7-12 week old CD2F1 male mice that had been fed ad libitum and standardized either to 12 hours of light (0600-1800) alternating with 12 hours of darkness (1800-0600) (LD12:12); or to a reversed light-dark cycle (darkness 0600-1800; light 1800-0600) (DL12:12). Three separate studies were performed on two different days; in each experiment, subgroups of 14 animals were sacrificed at 3-hour intervals. Livers were assayed for: isocitrate dehydrogenase, glutamate dehydrogenase, lactate dehydrogenase, alcohol dehydrogenase, glutathione reductase, glyoxylate reductase, L-alanine aminotransferase, glutamate oxalacetate transaminase, pyruvate decarboxylase, fructose-1-phosphate aldolase, fructose diphosphate aldolase, fructose 1,6-diphosphatase, and fatty acid synthetase. Brains were assayed for phosphoglucose isomerase, adenosine triphosphatase, creatine phosphokinase, pyruvate kinase, adenylate kinase, and malate dehydrogenase. All 19 enzymes demonstrated a prominent circadian rhythm in at least one experiment. Moreover, each rhythmic variable showed a statistically significant fit to a 24-hour cosine (sine) curve by the method of least squares. In general, peak activities of the liver enzymes analyzed were associated with the beginning of the dark cycle and initiation of the animal's activity, while the group of brain enzymes had peak activities which occurred at the beginning of the animals' rest span and were near the beginning of the light cycle. The phasing of each of the rhythms could be reversed within a two-week span after reversing the environmental light-dark cycle 180 degrees.
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PMID:Circadian organization of thirteen liver and six brain enzymes of the mouse. 731 49